Vox Meditantis

Ida Henrietta Hyde (1857–1945) invented the microelectrode in 1921, a glass micropipette fine enough to penetrate individual cells and record their electrical responses – a tool that would become foundational to modern neuroscience. By the time the technology existed to fully exploit her invention in the 1940s and 1950s, her contribution had been forgotten, and men who independently rediscovered similar devices received Nobel nominations for work she had pioneered decades earlier. Yet Hyde’s story encompasses far more than this singular injustice: she was the first woman to receive a doctorate in science from Heidelberg University, the first to conduct research at Harvard Medical School, and the first elected to the American Physiological Society, where she remained the sole female member for eleven years.

This interview takes place on 25th October 2025, when Hyde would be 168 years old. She reflects on her contributions to electrophysiology, the obstacles she overcame, and what it means to invent something revolutionary before the world is ready to recognise it.

Welcome, Dr Hyde. Thank you for joining us today. I’d like to begin by asking about your beginnings in Chicago. You worked in a hat factory for seven years – can you describe what that labour was like, and how you managed to hold onto dreams of university education whilst doing such work?

The factory was on West Van Buren Street. I started at fourteen as an apprentice milliner after the Great Fire of 1871 took our home and my mother’s shop. The fire came on a Sunday evening – I remember the wind, how it carried embers across entire city blocks. By Tuesday, there was nothing but ash where we’d lived. Mother tried to rebuild, but there wasn’t enough capital, and I was the eldest. My brother Ben needed schooling, and someone had to bring in wages.

The work itself wasn’t complicated – trimming, shaping felt, attaching ribbons and wiring – but it was monotonous, and the air was thick with lint and dye fumes. My hands were always stained. I worked ten hours daily, six days weekly, earning perhaps three dollars per week initially, more as I gained skill. What kept me tethered to something beyond that factory floor was a book I found during my lunch break, discarded in a packing crate – an English translation of Humboldt’s Views of Nature. I’d sit on the loading dock, eating bread, reading about the geography of plants, the structure of volcanoes, the interconnectedness of natural systems. It was like discovering that the world extended infinitely beyond the walls where I spent my days sewing hat brims.

I began saving carfare. The factory was three miles from our lodgings, and I walked both ways, tucking those pennies into a tin box under my bed. I attended evening courses at the Chicago Athenaeum – basic mathematics, grammar, a bit of natural history – and eventually saved enough to sit the entrance examinations for the University of Illinois. I was twenty-four by then. Most of my cohort were eighteen.

You completed only one year at Illinois before your brother’s illness forced you to withdraw. How did you cope with that loss of momentum, and what sustained you through the seven years you spent teaching elementary school in Chicago whilst waiting for another chance?

It was wrenching. I’d finally entered the world I’d been reading about – lectures on comparative anatomy, access to laboratory specimens, conversations with people who cared about ideas – and then Ben fell ill with what we thought might be consumption. There was no question of continuing; he needed care, and our mother was working herself to exhaustion. I withdrew mid-term and nursed him for the better part of a year.

When he recovered, I took a position teaching third and fourth grades in the Chicago public schools. The salary was modest but steady, and it allowed me to keep saving. What sustained me, I think, was realising that teaching wasn’t merely a delay – it was its own form of inquiry. The children I taught had no exposure to the natural world beyond the soot-covered streets of Chicago. I began bringing specimens into the classroom: leaves, insects preserved in alcohol, a bird’s nest, once a jar containing a frog I’d caught near the river. I developed a curriculum we called “Science in the Schools” – nature studies integrated into elementary education. It was rudimentary by university standards, but it was systematic. I taught them to observe, to ask questions, to notice patterns.

That work, I later realised, was training me in pedagogy, in thinking about how knowledge is constructed and communicated. When I finally returned to university – at Cornell, in 1889, at age thirty-one – I wasn’t just a student. I was someone who understood how to design an investigation, how to explain complex ideas simply, how to persist.

At Cornell and then Bryn Mawr, you studied under some of the most prominent biologists of the era – Thomas Hunt Morgan, Jacques Loeb. What drew you specifically to physiology, and how did you come to focus on the electrical properties of cells?

Morgan was brilliant, meticulous, utterly absorbed in embryological questions. Loeb was different – provocative, interested in mechanistic explanations for life processes, convinced that biology could be made quantitative. He was working on artificial parthenogenesis in sea urchins at the time, demonstrating that chemical and physical stimuli could substitute for fertilisation. That reductionist impulse, the idea that you could isolate variables and measure them, appealed to me.

Physiology seemed to sit at the intersection of chemistry, physics, and biology. It asked: how do living systems work? Not merely what they’re made of, but what mechanisms govern their function. I was particularly drawn to questions of excitability – how nerve and muscle cells respond to stimuli, how they transmit signals, how their behaviour changes under different conditions.

Whilst at Woods Hole during my Bryn Mawr summers, I worked on jellyfish – Hydromedusa – studying their pulsation rhythms and the development of their nervous systems. Jellyfish have a nerve net rather than a centralised brain, and you could see, quite directly, how electrical impulses propagated through their tissues. If you stimulated one region, the contraction would spread in waves. That visible, almost tangible connection between electrical stimulus and muscular response fascinated me.

By the time I went to Germany in 1893, I was convinced that understanding cellular excitability – particularly the electrical behaviour of individual cells – was essential to understanding how organisms coordinate their activities.

Let’s discuss your time in Germany. You arrived at Strassburg with a fellowship from the Association of Collegiate Alumnae, expecting to work with Professor Goette on embryology. What happened when you arrived and discovered that German universities didn’t admit women?

It was absurd, frankly. Professor Goette had invited me. He’d read my work on jellyfish development, which corroborated findings he’d published in a dispute with another embryologist, and he wanted me to continue that line of investigation in his laboratory. The invitation was enthusiastic, unequivocal.

When I arrived in Strassburg, I learnt that the university had never matriculated a woman. German universities operated under the assumption that women lacked the intellectual stamina for advanced study – this was explicit policy, not merely custom. Professor Goette petitioned the university administration on my behalf, and after considerable delay, they agreed I could work in his laboratory – but not attend lectures, not take examinations, not officially enrol. I was, in effect, tolerated as a curiosity.

The situation at Strassburg became untenable when it became clear that I couldn’t sit for a doctoral examination there, regardless of the quality of my research. So I transferred to Heidelberg, where I hoped the situation might be different. It was not.

At Heidelberg, you wanted to study physiology under Wilhelm Kühne, one of the most prominent physiologists in Europe. He’s remembered now for his work on enzymes and muscle physiology. What was his response when you requested to join his laboratory?

Kühne was opposed. Not on scientific grounds – he’d not seen my work – but on principle. He told colleagues he would “never allow skirts in his lectures.” That was the phrase used: skirts. Not women, not female students, but skirts, as though we were articles of clothing rather than people.

I was barred from attending his physiology lectures, barred from participating in laboratory demonstrations, barred from accessing the equipment directly. What I did instead was this: I befriended Kühne’s laboratory assistants – young men who were themselves doctoral candidates – and I borrowed their lecture notes. Every evening, they’d pass me their transcriptions of Kühne’s lectures, along with sketches of the experimental setups they’d observed. I’d copy these by hand, studying them in my lodgings, teaching myself physiology from second-hand accounts.

For laboratory work, I’d arrive early in the morning or late in the evening, when Kühne wasn’t present, and I’d use the equipment under the supervision of his assistants. They were, by and large, sympathetic – some found Kühne’s stance ridiculous – but they couldn’t openly defy him. I conducted experiments on the circulation and respiration of aquatic organisms, measuring heart rates under different conditions, observing how oxygen availability affected muscle contractility. I recorded everything meticulously, knowing that my work would be scrutinised far more rigorously than that of my male peers.

You mentioned that when a colleague asked Kühne whether he’d grant you a degree if you passed the examination, he agreed – jokingly. How did that eventual examination unfold?

It was four hours long. Oral examination by a committee of professors, not just Kühne but faculty from zoology, chemistry, and anatomy. They could ask me anything within the entire scope of natural sciences as understood at that time.

I was asked to explain the mechanism of muscle contraction, to describe the chemical composition of blood, to discuss the embryological development of vertebrate circulatory systems, to solve problems involving osmotic pressure and gas exchange. They tested whether I understood not just rote facts but underlying principles – whether I could reason through problems I’d not encountered before.

At one point, Kühne asked me to describe how I would design an experiment to test whether a particular physiological response was due to nervous innervation or intrinsic muscle properties. It was a fair question, but it required me to think through experimental controls, potential confounding variables, measurement techniques – essentially to demonstrate that I could design and interpret research independently.

I passed. Kühne, to his credit – or perhaps to his surprise – honoured his word. I received my doctorate in February 1896. The degree wasn’t awarded “summa cum laude,” which was the highest distinction, because the university senate decided that honour couldn’t go to a woman. Instead, they invented a new phrase: Multa Cum Laude Superavit – “she overcame with much praise.” I was thirty-eight years old.

After Heidelberg, you worked at the Zoological Station in Naples, then at Harvard Medical School – where you were the first woman to conduct research. Can you describe what it meant to be “first” in these institutions, and whether that visibility felt like an advantage or a burden?

Both, perpetually. At Naples, I was funded by a research table I’d helped establish specifically for American women scientists – the Naples Table Association, which we founded in 1897. That table provided me with laboratory space, access to marine specimens, and a stipend, but it also marked me as someone requiring special accommodation. I was visible in a way my male colleagues were not. Every mistake I made would be interpreted as evidence of female incapacity; every success would be framed as exceptional.

At Harvard, I worked under William Townsend Porter in the Physiology Department from 1897 to 1898. I was permitted to conduct research – note the phrasing – but not to hold a faculty appointment, not to teach, not to supervise students. I published an article in the inaugural issue of the American Journal of Physiology in 1898, titled “The Effect of Distention of the Ventricle on the Flow of Blood through the Walls of the Heart.” That work examined how increased pressure within the heart’s chambers affected coronary circulation – essentially, whether the heart could adequately perfuse its own muscle tissue when it was overfilled.

The findings were significant: excessive distention compromised coronary flow, which had implications for understanding heart failure. But the article was published, and I moved on. There was no possibility of staying at Harvard, no trajectory towards tenure. I was grateful for the opportunity but acutely aware that I was being tolerated, not integrated.

In 1899, you joined the University of Kansas, where you founded the Department of Physiology and served as its chair for over two decades. That appointment, at age forty-one, seems to have been your first real institutional home. What was it like to finally have autonomy over your research and teaching?

It was liberating, and it was isolating. Kansas needed physiologists for its developing medical school, and they were willing to hire me because my credentials were impeccable and because, frankly, they couldn’t attract male candidates of equivalent stature to a regional university in the Midwest. I was appointed associate professor of physiology in 1899, promoted to full professor and department chair in 1905.

For the first time in my career, I had my own laboratory. I could design my own curriculum, order equipment, set research priorities. I taught medical students the fundamentals of physiology – circulation, respiration, nervous system function – and I continued my own research on the effects of alcohol, caffeine, and other substances on physiological systems. I published a textbook, Laboratory Outlines of Physiology, in 1910, which was used at Kansas and at several other institutions.

But Kansas was far from the centres of physiological research – Harvard, Yale, Johns Hopkins, the Marine Biological Laboratory at Woods Hole. I attended conferences when I could, maintained correspondence with colleagues, but I wasn’t part of the daily intellectual exchange that drives innovation. I had few graduate students, limited funding for equipment, and no peers within the department – I was the department. That autonomy came at the cost of intellectual community.

Let’s discuss the microelectrode. In 1921, you published a paper in Biological Bulletin describing a device you’d developed: a glass micropipette filled with mercury, fine enough to interact with individual cells, capable of electrical stimulation, fluid injection, and recording cellular responses. Can you walk us through how you designed this instrument and what problem you were trying to solve?

The problem was this: physiologists had spent decades studying nerve and muscle tissues by stimulating them with electrodes, recording their responses with galvanometers, observing their contractions under microscopes. But those methods measured aggregate responses – the behaviour of entire muscles, whole nerves. If you wanted to understand how individual cells functioned, you needed tools that could interact with cells at that scale.

By the early 1920s, microscopists had developed techniques for manipulating individual cells – there was a device called the Barber micropipette, developed here at Kansas by Marshall Barber, which could be used to isolate single bacterial cells. I realised that a similar principle could be adapted for physiological work. What I needed was a glass capillary tube drawn out to a very fine tip – on the order of three to four micrometres in diameter – filled with a conductive medium, that could be positioned near or against a cell and used to deliver stimuli or record responses.

The technical challenge was achieving tips fine enough to interact with individual cells without damaging them, whilst maintaining electrical conductivity. I used mercury-filled glass capillaries. Mercury is conductive, and its meniscus – the curved surface inside the capillary – moves in response to electrical current. By applying current, I could move the mercury meniscus toward or away from the tip, which allowed me to expel fluids from the pipette, withdraw fluids into it, or deliver electrical stimulation.

I fabricated the pipettes by hand, drawing out glass tubing over a flame until the bore narrowed sufficiently, then filling them with mercury through a zinc-zinc sulphate junction to maintain conductivity. The apparatus included both an active electrode (the fine-tipped pipette) and an indifferent electrode placed elsewhere in the solution.

And what organism did you use to test this device?

Vorticella – a ciliated protozoan with a contractile stalk. It’s a single-celled organism, about fifty to one hundred micrometres long when extended, and its stalk can contract rapidly when stimulated, coiling like a spring. The contraction is mediated by a structure called the spasmoneme, which runs through the stalk and responds to mechanical or chemical stimuli.

Vorticella was ideal for testing the microelectrode because it was large enough to manipulate under a microscope, its responses were visible and rapid, and I could vary the strength of electrical stimulation and observe whether the contraction was graded or all-or-none.

What did you find?

That the contractions were graded, not all-or-none. If I applied a weak electrical stimulus, the stalk would contract partially; stronger stimuli produced stronger contractions. This contradicted earlier work by Pratt, who had shown that contractions in individual muscle fibres were all-or-none – you either trigger an action potential or you don’t, with no intermediate states.

What I was demonstrating was that Vorticella‘s spasmoneme behaved differently from vertebrate muscle fibres. Its contractile response was proportional to stimulus intensity, which suggested a different physiological mechanism – likely a calcium-mediated process rather than a sodium-potassium action potential, though we didn’t have the biochemical tools to confirm that in 1921.

Your paper described the microelectrode’s construction in considerable detail and suggested multiple potential applications – injecting or removing fluids from cells, electrically stimulating specific cellular components. But you published only this single paper on the device and never followed up with additional studies. Why?

Several reasons, none of them satisfying. First, the technology required to fully exploit the microelectrode didn’t exist in 1921. To record intracellular electrical activity with precision, you need high-impedance amplifiers, drift-free DC circuitry, and oscillographs capable of displaying rapid voltage changes. None of that was available. The electronics of the 1920s were designed for telegraphy and radio transmission, not for measuring millivolt-level changes inside cells.

What I could do with the microelectrode in 1921 was limited: I could stimulate cells, I could inject or withdraw small volumes of fluid, but I couldn’t make stable intracellular recordings of membrane potential. So whilst I could demonstrate the device’s potential, I couldn’t show the kinds of discoveries it would enable.

Second, I was retiring. I’d been at Kansas for twenty-two years, and in 1920, at age sixty-three, I stepped down from my position. The physiology department was being restructured – merged with another department, led by a committee rather than an individual chair – and there was pressure, never stated outright, for me to leave. I spent my final years traveling, conducting independent research in California, but I no longer had access to a fully equipped laboratory, graduate students, or institutional support for developing new methodologies.

Third – and I think this is the hardest part to articulate – I didn’t realise how important the microelectrode would become. In 1921, it was a clever tool, a methodological advance, but its revolutionary potential wasn’t yet apparent. I’d published the description, made it available to other researchers, and moved on to other questions.

In the 1940s, Judith Graham and Ralph Gerard at the University of Chicago independently developed glass micropipette electrodes for intracellular recording. Gerard was nominated for a Nobel Prize in the 1950s for that work. By the time electronics had advanced sufficiently for microelectrodes to transform neurophysiology – enabling Hodgkin and Huxley’s Nobel Prize-winning work on action potentials, Eccles’s studies of synaptic transmission, and eventually Neher and Sakmann’s patch-clamp technique, which won another Nobel in 1991 – your 1921 paper had been forgotten. How do you reflect on that erasure?

With a mixture of resignation and anger, if I’m being honest. When I read about Gerard’s work in the 1940s, receiving accolades for developing a technique I’d described in 1921, I felt invisible. Not merely overlooked, but erased. As though my contribution had never existed.

Part of me understands the logic: Gerard’s microelectrodes, refined by Gilbert Ling, were technically superior to mine. They used potassium chloride solutions rather than mercury, achieved finer tips, and were paired with amplifiers that could record intracellular potentials reliably. By the time Hodgkin visited Gerard’s laboratory in 1948 and learnt the technique, the microelectrode had become a standard tool, and the electronics had finally caught up to enable the kinds of experiments I’d envisioned.

But the principle was mine. The idea that you could use a fine-tipped glass pipette to interact with individual cells, to stimulate them, to record their responses – that originated in 1921, not 1946. When the Nobel Prize was awarded to Hodgkin, Huxley, and Eccles in 1963, when Neher and Sakmann won in 1991 for patch-clamp recording, my name didn’t appear in the historical accounts. The microelectrode had become an anonymous tool, its origins lost.

What troubles me most is that this wasn’t an accident. Independent rediscovery is common in science – multiple researchers often arrive at similar ideas when the intellectual groundwork has been laid. But when women’s contributions are rediscovered, they’re not credited as precedents. Instead, the men who come later are celebrated as inventors, and the women who came first are footnoted, if mentioned at all.

You once wrote an essay titled “Before Women Were Human Beings,” published in 1938, reflecting on your experiences in German universities. That’s quite a powerful title. Can you elaborate on what you meant by it?

It was meant literally. In the 1890s, German universities operated on the assumption that women were not fully rational beings – not capable of abstract thought, not suited for intellectual labour, not deserving of the same educational opportunities as men. This wasn’t subtext; it was explicit policy.

When I arrived in Strassburg and Heidelberg, I encountered professors who genuinely believed that women’s brains were structurally different from men’s in ways that precluded higher learning. There was a body of pseudoscientific literature – craniometry, theories of variability – arguing that women’s intellectual capacity was inherently limited. These weren’t fringe beliefs; they were mainstream academic opinion.

What “Before Women Were Human Beings” tried to capture was the surreal experience of navigating an intellectual world that simultaneously acknowledged your competence – because I passed examinations, published research, earned a doctorate – and denied your full humanity. I could demonstrate mastery of physiology, but I couldn’t sit in a lecture hall. I could design experiments, but I couldn’t access laboratory equipment during regular hours. I was competent enough to earn a degree, but not competent enough to be granted the highest honours.

The essay was also a record for future generations. I wanted to document the specific, absurd humiliations women of my era faced, so that younger scientists wouldn’t have to wonder whether they were imagining the obstacles or being overly sensitive. The discrimination was real, it was structural, and it was intended to exclude us.

You were the first woman elected to the American Physiological Society in 1902, and you remained the only female member until 1913. What was that isolation like?

Exhausting. Every conference, every meeting, every social gathering associated with the Society, I was the only woman in the room. Often literally – there would be fifty, sixty men, and me.

There were practical indignities: the Society’s meetings were sometimes held in locations that didn’t have women’s lavatories, because women weren’t expected to attend scientific conferences. Dinners were held at men’s clubs that didn’t admit women, so I’d be excluded from the informal conversations where collaborations were formed and ideas exchanged.

But the deeper issue was intellectual isolation. I had no female colleagues to consult, no one who shared my particular vantage point, no one with whom I could discuss not just scientific questions but the experience of navigating a profession that didn’t want us there. When a second woman, Mabel Purefoy FitzGerald, was elected in 1913, it felt like an enormous relief – as though I’d been holding my breath for eleven years.

You devoted considerable energy to creating opportunities for other women scientists – co-founding the Naples Table Association, establishing scholarships at Kansas and Cornell, endowing the Ida H. Hyde Woman’s International Fellowship through the American Association of University Women. Over one hundred women received support through the programmes you created. Do you see that work as separate from your scientific research, or as part of the same mission?

It’s the same mission. Science advances when talented people have access to training, resources, and opportunities to contribute. Excluding half the population on the basis of sex is not just unjust; it’s intellectually wasteful.

Every woman I supported through a scholarship or fellowship represented research that might not otherwise have been conducted, discoveries that might not otherwise have been made. Some of those women went on to distinguished careers; others left science due to marriage or family obligations or lack of institutional positions. But all of them added to the collective body of knowledge.

That said, I’m acutely aware that the time I spent on advocacy and institution-building was time I wasn’t spending on my own research. Service work – mentoring students, organising fellowships, writing letters of recommendation, serving on committees – is essential but invisible. It doesn’t produce publications, doesn’t generate citations, doesn’t earn Nobel Prizes. Men of my generation, by and large, didn’t do this work; they had wives, secretaries, and institutions that managed those tasks for them. Women scientists of my era did service work because no one else would, and because we understood that creating pathways for the next generation was as important as our own individual achievements.

But I do sometimes wonder what I might have accomplished if I’d had those years back, if I’d been able to focus solely on research.

Let’s discuss a few specific scientific contributions beyond the microelectrode. Your 1898 paper in the American Journal of Physiology examined the relationship between ventricular distention and coronary blood flow. What were the key findings, and why did that question matter?

The heart is a peculiar organ: it’s a pump that must perfuse itself whilst it’s working. Coronary arteries supply blood to the heart muscle, but those arteries are compressed during systole – when the heart contracts. So coronary flow occurs primarily during diastole, when the heart is relaxed.

The question I was investigating was: what happens when the ventricles are overfilled – when there’s excessive pressure inside the heart’s chambers? Does that improve or impair coronary flow?

The prevailing assumption at the time was that increased ventricular pressure would push more blood into the coronary arteries, improving perfusion. But my experiments suggested the opposite: excessive distention of the ventricles compressed the coronary vessels running through the heart wall, reducing blood flow to the myocardium. This had clear implications for heart failure: when the heart becomes dilated, unable to empty effectively, it can’t adequately supply its own muscle tissue with oxygen, which further impairs contractility.

The work was technically demanding. I used isolated mammalian hearts – canine hearts, primarily – perfused with saline under controlled pressure. I measured coronary flow rates whilst varying ventricular distention, using manometers to track pressure changes and graduated cylinders to quantify outflow. The results were consistent: beyond a certain threshold, increased distention reduced coronary perfusion.

That finding became part of the foundation for understanding cardiac mechanics – the relationship between preload, afterload, and myocardial oxygen supply. It’s not the kind of work that generates headlines, but it’s the meticulous accumulation of physiological knowledge that enables later clinical advances.

You also conducted extensive research on the effects of alcohol, caffeine, and narcotics on physiological systems. What motivated that line of investigation, and what did you discover?

Those were substances with obvious social and medical relevance. Alcohol consumption was pervasive, caffeine was ubiquitous, and narcotics – particularly opiates – were widely used for pain management. Yet their physiological mechanisms were poorly understood.

I studied their effects on heart rate, blood pressure, respiration, and reflexes, using animal models – primarily dogs and frogs – because I could control dosages and isolate variables. What I found was that these substances had dose-dependent effects that varied depending on the physiological system examined.

Alcohol, for example, initially acts as a stimulant – increasing heart rate, dilating blood vessels – but at higher doses it becomes a depressant, slowing cardiac function and impairing respiratory reflexes. Caffeine increases heart rate and contractility, but excessive doses can induce arrhythmias. Narcotics depress respiration, which is why opiate overdoses are lethal – the body loses the drive to breathe.

These findings were relevant to medicine: understanding how substances affect physiology helps clinicians manage intoxication, predict drug interactions, and design safer therapies. But the work was also intellectually satisfying because it revealed that physiological responses are not binary. They’re context-dependent, shaped by dose, route of administration, individual variability, and interactions between multiple systems.

I want to ask about something you mentioned earlier: mistakes. You said that teaching at Chicago taught you that knowledge is constructed, that inquiry involves failure. Can you describe a professional misjudgement or failed experiment that taught you something important?

Early in my research at Woods Hole, I was studying the rhythmic pulsations of jellyfish – trying to determine whether their contractions were myogenic, originating in the muscle tissue itself, or neurogenic, driven by nerve impulses. I designed an experiment where I would sever different regions of the nerve net and observe whether pulsations continued.

What I failed to account for was that jellyfish tissues have remarkable regenerative capacity. I’d sever a nerve tract, observe that pulsations ceased, and conclude that the severed region was essential – but then, hours later, the pulsations would resume. I initially interpreted this as experimental error, assuming my cuts hadn’t been precise enough.

It took me weeks to realise that what I was observing wasn’t experimental failure but biological regeneration. The nerve net was regrowing, reconnecting the severed regions. Once I understood that, I redesigned the experiment to account for regeneration, conducting observations immediately after cuts and tracking recovery over time.

That experience taught me to interrogate unexpected results rather than dismissing them. What looks like a failed experiment is often an accurate measurement of something you hadn’t anticipated – a phenomenon you didn’t know existed. Curiosity requires humility: the willingness to admit that your initial hypothesis might be wrong, that nature is more complex than your models, that the most interesting discoveries often emerge from anomalies.

Looking at the trajectory of your field – from your 1921 microelectrode to modern intracellular recording, patch-clamp techniques, deep brain stimulation for Parkinson’s disease – how do you feel about the role your invention ultimately played, even if your name was omitted from the story?

Conflicted. On one hand, the microelectrode I developed in 1921 became foundational to modern neuroscience. Every time a researcher inserts an electrode into a neuron to record its activity, every time a surgeon uses microelectrode recording to guide deep brain stimulation for Parkinson’s disease, every time a patch-clamp experiment characterises an ion channel – they’re using descendants of the tool I invented. The principle I established is embedded in those techniques, even if my name isn’t.

On the other hand, scientific credit isn’t just about ego. It’s about whose contributions are deemed valuable, whose names get attached to methods, whose careers are legitimised by recognition. When Gerard received Nobel consideration for microelectrode work, when Hodgkin and Huxley won the Prize for action potential research enabled by microelectrodes, when Neher and Sakmann won for patch-clamp – those honours reinforced a narrative where innovation comes from men at elite institutions. My absence from that narrative told a different story: that women’s contributions, particularly those made “too early,” are expendable.

The practical consequence is that younger women entering science today still don’t see themselves in the field’s canonical history. They don’t know that microelectrodes were invented by a woman who worked in a hat factory until age twenty-one, who studied physiology from smuggled lecture notes, who founded a university department in Kansas. That erasure has costs – not just for historical accuracy, but for who believes they belong in science.

If you were speaking to a young woman today – someone facing obstacles in accessing education or recognition in science – what would you tell her?

I’d tell her that obstacles are real, that discrimination isn’t imagined, and that persistence isn’t always rewarded. I wouldn’t offer false comfort.

But I’d also tell her that science is worth pursuing – not because it will necessarily bring recognition, but because the work itself matters. Understanding how the world functions, contributing to knowledge that might improve lives, solving problems that no one else has solved – that has intrinsic value, regardless of whether your name is remembered.

And I’d tell her to build community. The women who supported me – the Association of Collegiate Alumnae who funded my fellowship, the colleagues who shared laboratory space, the students I mentored who went on to do their own work – that collective effort is what sustained me. Individual achievement matters, but so does creating structures that enable others to succeed. If she has the opportunity to mentor someone, to fund a scholarship, to advocate for institutional change – do it. That work compounds over generations.

Finally, I’d tell her to document her contributions. Publish your methods, even if they’re not yet fully developed. Claim your inventions, even if the field isn’t ready for them. Name your discoveries. Because if you don’t, someone else will, and the historical record will forget you were there first.

Dr Hyde, thank you. Your contributions – to physiology, to electrophysiology, to the inclusion of women in science – deserve to be remembered. This conversation is part of ensuring they are.

Thank you for asking the questions. History is written by those who take the time to listen.

Letters and emails

Since our conversation with Dr Ida Henrietta Hyde, we’ve received an overwhelming response from readers across continents – scientists, students, historians, and advocates – all eager to continue the dialogue. We’ve selected five letters and emails from our growing community who want to ask her more about her life, her work, and what she might say to those following similar paths in science today.

Zuri Mwangi (28, PhD Candidate in Biomedical Engineering, Nairobi, Kenya):
Dr Hyde, if you had access to today’s microfabrication techniques and modern electronics, how would you redesign the microelectrode to improve its sensitivity or versatility for single-cell studies?

What a marvellous question, Miss Mwangi. I’ve spent considerable time since our conversation reading about contemporary microfabrication – photolithography, silicon etching, the extraordinary precision of modern glass-pulling apparatus – and I confess it makes me envious. The tools available now would have transformed what I could accomplish in 1921.

If I were redesigning the microelectrode today, my first priority would be addressing the fundamental limitation of my mercury-filled device: electrode impedance. Mercury is conductive, certainly, but the resistance at the tip – where the bore narrows to three or four micrometres – was substantial enough that I couldn’t make stable recordings of membrane potential. I could stimulate cells, I could inject fluids, but I couldn’t reliably measure the voltage changes that Alan Hodgkin and Andrew Huxley later demonstrated in the squid giant axon. That required amplifiers with input impedances in the hundreds of megohms, which simply didn’t exist in the 1920s.

With modern electronics, I’d fill the micropipettes with potassium chloride solution rather than mercury – precisely as Ralph Gerard and Gilbert Ling did in the 1940s. Potassium chloride provides excellent conductivity, doesn’t oxidise, and maintains ionic continuity with the intracellular environment, which reduces junction potentials. I’d pair those electrodes with high-impedance amplifiers capable of measuring millivolt-scale changes without drawing significant current from the cell. That combination would enable intracellular recording from cells far smaller than the squid axon – mammalian neurons, cardiac myocytes, even individual smooth muscle fibres.

The second improvement would be tip geometry and fabrication precision. In 1921, I drew out glass capillaries by hand over a Bunsen flame, which meant every electrode was slightly different. The tips weren’t uniform, the taper wasn’t controlled, and I couldn’t reliably reproduce dimensions. Modern micropipette pullers – I’ve read about programmable devices that heat glass tubing with platinum filaments and pull with computer-controlled force – can produce tips with sub-micrometre precision. That consistency matters enormously when you’re trying to penetrate a cell membrane without rupturing it, or when you’re comparing measurements across multiple experiments.

I’d also want to explore dual-barrel electrodes – micropipettes with two separate channels running parallel through the same glass shaft. One barrel could be used for recording membrane potential whilst the other injects current, allowing you to measure a cell’s input resistance and time constant directly. Or you could use one barrel to apply pharmacological agents – neurotransmitters, ion channel blockers, metabolic inhibitors – whilst simultaneously recording how the cell’s electrical behaviour changes. That would enable experiments I could only dream about in Kansas: asking not just whether a substance affects cellular excitability, but how rapidly, at what concentration, and through what mechanism.

The third redesign would address spatial resolution. My 1921 device could interact with individual cells, but it couldn’t target subcellular structures. If I had access to modern micromanipulators – piezoelectric positioners with nanometre-scale precision – and high-resolution microscopy, I could position electrode tips against specific regions of a cell: the axon hillock where action potentials initiate, dendritic spines where synaptic inputs arrive, even individual mitochondria. That spatial control would allow you to map electrical gradients within cells, to understand how voltage changes propagate through complex cellular geometries.

Finally, I’d want to integrate my microelectrodes with optical methods. I’ve read about voltage-sensitive dyes and genetically encoded calcium indicators that allow researchers to visualise electrical activity across entire populations of cells simultaneously. Combining those optical techniques with targeted microelectrode recordings would give you the best of both approaches: broad spatial coverage to identify interesting phenomena, and precise intracellular measurements to characterise mechanisms.

What stands out to me most about your question, Miss Mwangi, is that the fundamental principle remains unchanged: you need a fine-tipped conduit that can interact with individual cells without destroying them, that can deliver or measure electrical signals, that can be positioned precisely. The materials and precision have improved spectacularly – silicon instead of glass, computer-controlled fabrication instead of hand-pulling over flames, picoampere-resolution amplifiers instead of galvanometers – but the core concept I described in Biological Bulletin in 1921 is still the foundation. That gives me some satisfaction, even if my name wasn’t attached to the later refinements.

Esteban Vargas (24, Undergraduate in Neuroscience, Bogotá, Colombia):
If another scientist had published a competing method for intracellular recording at the same time, what experiments would you have run to prove the unique advantages of your mercury-filled microelectrode device?

Mr Vargas, that’s precisely the sort of question that keeps a researcher awake at night – or ought to, if she’s honest about the competitive nature of scientific priority. If I’d faced a competing method in 1921, I would have needed to demonstrate not just that my microelectrode worked, but that it offered measurable advantages over alternative approaches.

The first experiment I’d design would be a direct comparison of cellular penetration and recovery. My mercury-filled micropipette had tips fine enough – three to four micrometres in diameter – to interact with individual cells without causing irreversible damage. I demonstrated this with Vorticella, showing that the contractile stalk would respond to electrical stimulation and then resume normal function afterward. If a competitor claimed their method could do the same, I’d challenge them to a side-by-side test: insert your electrode and mine into identical Vorticella specimens, deliver comparable stimuli, and then observe which cells recover normal contractile behaviour and which ones show signs of trauma – membrane rupture, loss of turgor, cessation of ciliary beating. The electrode that causes less damage whilst still delivering effective stimulation would be demonstrably superior for long-term physiological studies.

The second experiment would test versatility – specifically, whether the device could perform multiple functions without withdrawing from the cell. My microelectrode wasn’t merely a stimulating electrode; it could inject fluids, withdraw cellular contents, and deliver electrical current, all through the same instrument. The mercury meniscus moved in response to current flow, which meant I could expel a small volume of saline into a cell to test how it responded to osmotic changes, then immediately follow with an electrical stimulus to measure excitability under those altered conditions.

To prove that advantage, I’d design an experiment using frog muscle fibres – larger than Vorticella, easier to observe under magnification, and well-characterised in the physiological literature. I’d penetrate a fibre with my microelectrode, inject a known quantity of potassium chloride solution to locally depolarise the membrane, and then measure the resulting change in contractile threshold by applying graded electrical stimuli through the same pipette. A competing device that could only stimulate, or only inject, would require multiple penetrations of the same fibre, each one increasing the risk of damage and making it impossible to attribute observed changes to your experimental manipulation rather than to trauma.

The third experiment would address temporal precision and reproducibility. My device allowed me to demonstrate that Vorticella contractions were graded rather than all-or-none – that stronger stimuli produced stronger responses. That finding required precise control over stimulus intensity and timing. I’d design a protocol where I delivered a series of electrical pulses at varying intensities – measured in microamperes if I had sufficiently sensitive galvanometers – to a population of Vorticella specimens, recording the degree of stalk contraction for each stimulus strength. Then I’d plot stimulus intensity against contraction magnitude and show a continuous, graded relationship rather than a binary threshold response.

If a competitor’s device produced inconsistent results – perhaps because their electrode tips varied in size, or because their delivery mechanism wasn’t reproducible – my data would show tighter error bars, more reliable dose-response curves, and better agreement across replicate experiments. Reproducibility is everything in physiology; if you can’t reliably produce the same result under identical conditions, your method isn’t scientifically useful.

The fourth experiment would be a practical demonstration of applications beyond simple stimulation. I’d use the microelectrode to extract a small sample of cytoplasm from a large protozoan – perhaps an amoeba or a paramecium – and analyse its chemical composition. Could I demonstrate the presence of particular ions, proteins, or metabolites that differed from the surrounding medium? That would prove the device’s utility for biochemical studies, not merely electrophysiological ones. A competitor whose method couldn’t perform extraction would have a narrower range of applications.

Finally, I’d run an experiment specifically designed to expose the limitations of my competitor’s approach. If their method required large cells – say, the squid giant axon that Hodgkin and Huxley later used – I’d demonstrate that my microelectrode could work on much smaller specimens: individual cardiac muscle cells from a frog heart, neurons from a molluscan ganglion, perhaps even plant cells. Size versatility matters: the vast majority of cells in nature aren’t giant axons, and a tool that only functions on exceptionally large specimens is of limited general utility.

Now, would these experiments have secured my priority if someone else had published simultaneously? Possibly. But I suspect the real determinant wouldn’t have been the quality of my experiments – it would have been whether I had the institutional resources, the professional networks, and the visibility to ensure those experiments were seen, cited, and remembered. A man at Harvard or Hopkins publishing the same work I did at Kansas would have had advantages I couldn’t overcome through superior data alone. That’s the uncomfortable truth I’ve come to accept.

Nora Fischer (37, Clinical Physiologist, Munich, Germany):
Thinking about your cardiovascular research, what lessons do you believe still apply for investigating heart tissue function today, especially as data now comes from imaging and molecular methods that weren’t available previously?

Dr Fischer, your question goes to the heart – if you’ll pardon the expression – of what defines good physiological research. The tools change, the resolution improves, the speed of data acquisition accelerates, but certain fundamental principles about how we investigate living systems remain constant.

The first lesson from my cardiovascular work is this: always account for the mechanical constraints of the system you’re studying. When I investigated the effect of ventricular distention on coronary blood flow in 1898, I wasn’t merely measuring pressures and volumes abstractly. I was asking: how does the physical architecture of the heart – the arrangement of coronary vessels within the muscular wall, the compression of those vessels during systole, the timing of diastolic relaxation – shape what’s physiologically possible?

That principle holds today, even with your extraordinary imaging methods. You can visualise coronary vessels in three dimensions using computed tomography, you can track blood flow velocity with Doppler ultrasound, you can measure myocardial perfusion with positron emission tomography – but you still need to understand that the heart is a pump working against resistance, that it must perfuse itself whilst simultaneously ejecting blood, and that excessive wall tension compromises its own blood supply. The Starling mechanism – the relationship between ventricular filling and contractile force that Ernest Starling described after my work – is still taught in medical schools because it describes a mechanical reality that doesn’t change regardless of how you measure it.

Modern molecular methods can tell you which genes are expressed in failing heart tissue, which proteins are upregulated or downregulated, which signalling pathways are activated. That’s invaluable information. But it doesn’t replace the need to understand how those molecular changes translate into altered mechanical function – how a mutation affecting calcium handling proteins changes the force-frequency relationship of cardiac muscle, how fibrosis stiffens the ventricular wall and impairs diastolic filling. My generation worked from mechanics toward chemistry; yours works from chemistry toward mechanics. Both directions are necessary.

The second lesson is the importance of controlled experimentation. When I studied coronary flow, I used isolated, perfused hearts – removed from the body, supplied with oxygenated saline at controlled pressure, freed from nervous and hormonal influences. That reductionist approach was criticised at the time by some who felt it was too artificial, that an isolated heart couldn’t tell you about the living organism.

But isolation allowed me to manipulate one variable whilst holding others constant. I could increase ventricular pressure without simultaneously changing heart rate, blood chemistry, or sympathetic tone. That control revealed causal relationships: distention caused reduced coronary flow, not merely correlated with it.

Your modern methods – molecular biology, genetic manipulation, advanced imaging – offer even greater control. You can knock out a single gene, express a fluorescent protein in specific cell types, stimulate individual neurons with light. But the logic is identical: isolate the variable you’re interested in, change it whilst holding everything else constant, measure the effect, and infer causation. I used mechanical isolation; you use genetic and optical tools. The principle still holds.

The third lesson concerns the integration of multiple levels of organisation. The heart isn’t merely a collection of individual myocytes; it’s a coordinated organ where electrical activation propagates in specific sequences, where mechanical contraction is coupled to metabolism, where local autoregulation responds to changing demands. My 1898 paper examined tissue-level phenomena – how wall tension affects vascular resistance – but I was always aware that those phenomena emerged from cellular and molecular processes I couldn’t directly observe.

Today, you can observe those underlying processes: calcium transients in individual myocytes, mitochondrial membrane potential, the opening and closing of ion channels. But you still need to integrate that cellular data back up to tissue and organ function. A mutation that affects a single calcium channel might be interesting molecularly, but its clinical relevance depends on whether it alters contractility enough to cause heart failure, arrhythmia, or sudden death. That requires thinking across scales – precisely what my generation attempted with cruder tools.

The fourth lesson, perhaps less obvious, is about the value of comparative physiology. I studied hearts from dogs, cats, rabbits, frogs – whatever was available and appropriate for the question I was asking. Different species revealed different aspects of cardiac function. Frog hearts, which lack coronary vessels and are perfused directly through the endocardium, taught me about myocardial oxygen requirements. Mammalian hearts, with their coronary circulations, taught me about autoregulation.

Modern medicine focuses heavily on human disease, which is understandable. But comparative approaches still yield insights: zebrafish for studying heart regeneration, which mammals can’t do; mice for genetic manipulation; large mammals whose cardiovascular physiology more closely resembles our own. The principle my generation understood – that nature has conducted evolutionary experiments revealing the range of possible solutions to physiological problems – remains valid.

Finally, there’s a lesson about patience and iteration. My cardiovascular work didn’t produce dramatic breakthroughs; it contributed incremental pieces to a larger puzzle that others were also assembling. I measured pressures, quantified flows, documented relationships. That foundational work enabled later researchers to ask more sophisticated questions.

Your molecular and imaging tools generate vast quantities of data very rapidly. That’s powerful, but it can also be overwhelming. The discipline of careful experimental design, of asking focused questions, of building knowledge incrementally – those habits my generation developed out of necessity, because we couldn’t generate data quickly – remain valuable even when you can.

Derek Thompson (41, History Teacher, Toronto, Canada):
Do you ever wonder how your life and scientific legacy might have changed if the timing had been different – say, if you’d started your research career amidst greater institutional acceptance or technological advancement?

Mr Thompson, that is a question which stirs a peculiar kind of melancholy, and every so often I will admit to indulging a spell of what the poets used to call “if only.” The sciences, you see, are not immune to the vagaries of fate – born as much on tides of circumstance as on efforts of hands and mind.

If I had begun my training in an era when women could attend lectures openly – say, amongst the golden laboratories of Cambridge or Leipzig, rather than burgling Kühne’s lecture notes like a thief in my own department – I suspect my road would have wound differently. I might have gained fluency in technical procedures not second-hand, but as part of the lively fray. There’s a clarity to learning directly at the bench, watching the shimmer of a filament lamp, the twitch of a frog’s leg, the hum of a galvanometer, unmarred by embarrassment or the anxiety of concealment.

Institutional acceptance would have secured me colleagues – peers with whom to debate and refine ideas, to share the satisfaction of a result, or to commiserate a botched trial. The camaraderie that develops in scientific circles is not a trivial matter; it fosters new directions, strengthens one’s resolve, and multiplies progress. As it was, I often felt as if peering into a window from outside, passing observations in hopes that someone would reply.

Technological advancement colours the picture in a different tint. The first electrical amplifiers and cathode ray oscillographs – had they been available to me alongside my mercury microelectrode – I believe my study of cellular behaviour would have leapt ahead a generation. Imagine: instead of simple contraction or relaxation recorded by eye, intracellular voltages measured as crisp waves of light on a screen. My Vorticella experiments could have yielded quantitative records with a permanence and detail that my hand-drawn graphs could not rival. In fact, with proper amplification, I could have charted the fine gradations of neural and muscular activity at a degree of precision that became routine for Hodgkin, Huxley, and their heirs.

Would greater recognition have followed? Perhaps. Scientific credit often lands where visibility is greatest, and I confess that a position at Harvard or the Rockefeller Institute would have brought more invitations to speak, more correspondence, more citations in the literature. The American Physiological Society, into which I entered as a lone woman in 1902, may have seemed less forbidding had I joined later – or perhaps I would have been one amongst many, not a singular curiosity.

Yet I am wary of giving the impression that fate alone governs legacy. I did what I could: taught hundreds of students, wrote my essays and textbooks, founded scholarships for women who might outpace me with less friction. I built what communities I could, sent out my findings into the world for others to use or abandon as they saw fit.

Would a different era have made me into a name found in every textbook, etched onto an instrument’s label? That I cannot say. But I do know that longing for another world does little to alter the one in front of us. I am proud of the work, and if credit followed the quality of effort rather than the currents of history, my place – perhaps – would be surer. Still, as my grandfather used to say, “There’s honour in work done for its own sake.” My hope is that those who read this today, especially the women and men forging new paths amidst their own adversities, might take comfort in knowing the value of their endeavours is not always set by when or where they begin.

Fatima Khan (32, Science Policy Advisor, Lahore, Pakistan):
In your career, you often gave time and support to other women scientists. Facing institutional resistance, how did you maintain hope and purpose, and what reflections might you share about the costs and benefits of building solidarity in science?

Miss Khan, your question reaches into territory I don’t often discuss publicly, because it reveals vulnerabilities that women of my generation were taught to conceal. We were expected to be twice as competent, never complain, and certainly never admit to doubt or exhaustion. But I’ll be candid with you: maintaining hope was not always possible, and there were years when purpose felt like a coat I wore out of habit rather than warmth.

The institutional resistance wasn’t merely frustrating – it was designed to break you. When Wilhelm Kühne barred me from his lectures, when Harvard permitted me to research but not to belong, when I sat alone at Physiological Society meetings for eleven years as the only woman in a room of fifty men – each instance was a reminder that I was tolerated, not welcomed. That takes a toll on the spirit. You begin to question whether your contributions matter, whether the effort is worth the cost, whether you’re foolish for persisting when the world has made its position abundantly clear.

What sustained me, when it did, was the practical work of helping others. After I earned my doctorate at Heidelberg in 1896, I received letters from young women asking how they might pursue similar paths. Some were teachers saving money for university, as I had been. Others were recent graduates uncertain whether German or Swiss universities would admit them, or whether the Naples Zoological Station would grant them laboratory space. I answered every letter, shared what I knew about fellowships and sympathetic professors, and in 1897 I helped establish the Naples Table Association specifically to fund American women’s research there.

That work gave me a sense of agency when my own research felt stalled or undervalued. I couldn’t control whether the American Physiological Society would elect more women members, but I could ensure that talented women had the financial means to conduct research. I couldn’t force Harvard to offer me a faculty position, but I could endow scholarships at Kansas and Cornell so that the next generation wouldn’t need to spend seven years in a millinery shop before entering university.

The cost, though, was real. Time spent writing letters of recommendation, organising fellowships, serving on scholarship committees – that was time not spent at the laboratory bench. Men of my generation had wives who managed their correspondence, households that ran without their involvement, secretaries who handled administrative tasks. I had none of that. Every hour devoted to service work was an hour subtracted from research, and research is what generates publications, citations, and recognition.

There’s a bitter arithmetic to it: women are expected to perform service work because we understand, viscerally, what it means to be excluded, and we can’t in good conscience refuse to help others when we know how desperately assistance is needed. But that service work is invisible in the historical record. Nobody wins a Nobel Prize for establishing scholarships or mentoring students. The men who focused single-mindedly on their own research – who declined committee service, who didn’t answer letters from struggling students, who prioritised their careers above collective advancement – those men often achieved greater individual recognition.

So when you ask about the benefits of building solidarity, I must be honest: the benefits are diffuse and long-term, whilst the costs are immediate and personal. The Ida H. Hyde Woman’s International Fellowship, which I endowed through the American Association of University Women, supported over one hundred women scientists in the decades after I established it. Some of those women went on to distinguished careers; others left science due to marriage or institutional barriers. But each of them had an opportunity she might not otherwise have had, and collectively they expanded what was possible for women in science.

That collective benefit is what I hold onto when I consider the trade-offs. My individual legacy may be smaller than it would have been had I devoted myself solely to research, but the aggregate impact – counting not just my own publications but the work enabled by the women I supported – is perhaps larger. It’s difficult to measure, and scientific history doesn’t account for it properly, but it matters nonetheless.

As for maintaining hope: I won’t romanticise this. There were years, particularly after I retired from Kansas in 1920 and found myself isolated in California without institutional affiliation, when I felt adrift. The microelectrode I’d published in 1921 generated little immediate interest. My cardiovascular research, though cited occasionally, didn’t lead to the kinds of breakthroughs that secure one’s name in textbooks. I watched younger researchers – men, invariably – build careers on foundations I’d helped lay, without acknowledgment.

What kept me engaged, finally, was the conviction that the work itself had value independent of recognition. Understanding how hearts function, how cells respond to stimuli, how physiological systems maintain homeostasis – that knowledge improves lives, informs medical practice, advances human understanding. Whether my name was attached to it became, in time, less important than whether the knowledge existed.

And solidarity, Miss Khan, is its own reward in ways that are hard to articulate but impossible to dismiss. When Mabel Purefoy FitzGerald was elected to the American Physiological Society in 1913, ending my eleven-year isolation, I felt an enormous relief – not because my status changed, but because I was no longer alone. We exchanged letters, discussed research, shared frustrations. That connection, modest as it was, made the work bearable.

If you’re asking whether I’d make the same choices again – whether I’d devote so much energy to supporting others rather than advancing my own career – I honestly don’t know. But I do know that the women who came after me faced fewer obstacles because of that work, and that has to count for something.

Reflection

Ida Henrietta Hyde died on 22nd August 1945 in Berkeley, California, at the age of eighty-seven. She had spent the final quarter-century of her life conducting independent research without institutional affiliation, publishing occasionally, corresponding with colleagues, and watching from the periphery as the field of electrophysiology – which she had helped establish – accelerated towards discoveries that would define mid-century neuroscience. By the time of her death, the microelectrode she had invented in 1921 was being independently rediscovered by researchers who had no knowledge of her precedent, and her name had begun its slow fade from the scientific record.

Speaking with Dr Hyde across the span of history reveals themes that resonate with uncomfortable persistence: the fragility of scientific credit, the invisibility of women’s contributions, and the cruel arithmetic of timing. Her story is not one of triumphant barrier-breaking, though she broke more barriers than most scientists ever encounter. Rather, it is a story about what happens when innovation arrives too early, when the infrastructure needed to prove a discovery’s worth doesn’t yet exist, and when the person making that discovery lacks the institutional power to ensure it is remembered.

The microelectrode stands as the clearest example of this tragedy. Hyde’s 1921 device – a mercury-filled glass micropipette fine enough to penetrate individual cells, capable of electrical stimulation, fluid injection, and recording cellular responses – represented a conceptual leap that the technology of her era couldn’t fully exploit. Without high-impedance amplifiers, drift-free circuitry, or sophisticated oscillographs, she could demonstrate the principle but not the transformative applications. By the time those technologies emerged in the 1940s and 1950s, enabling Ralph Gerard, Gilbert Ling, and others to make intracellular recordings that would revolutionise neurophysiology, Hyde’s 1921 paper in Biological Bulletin had been forgotten. Gerard received Nobel consideration for work Hyde had pioneered three decades earlier, and when Alan Hodgkin and Andrew Huxley used microelectrodes to elucidate the ionic basis of action potentials – winning the 1963 Nobel Prize – Hyde’s name did not appear in the historical accounts.

This pattern of independent rediscovery and subsequent erasure extends beyond the microelectrode. Hyde’s cardiovascular research, published in the inaugural issue of the American Journal of Physiology in 1898, contributed foundational knowledge about coronary circulation and ventricular mechanics. Yet her work is rarely cited in historical narratives about cardiac physiology, overshadowed by the contributions of Ernest Starling, Otto Frank, and other male contemporaries whose names became attached to laws and mechanisms. Her role in founding the Department of Physiology at the University of Kansas, her twenty-two years as chair, her textbook Laboratory Outlines of Physiology – these accomplishments are documented but not celebrated, remembered as “firsts” rather than as substantive intellectual contributions.

Throughout our conversation, Hyde spoke with a clarity and candour that complicates the sanitised historical record. Where official accounts emphasise her barrier-breaking achievements – first woman at Heidelberg, first woman at Harvard, first woman in the American Physiological Society – Hyde herself insisted on naming the costs: the humiliation of studying from smuggled lecture notes because Kühne forbade her from attending lectures, the isolation of being the sole woman in a professional society for eleven years, the exhaustion of performing unpaid service work whilst male colleagues focused single-mindedly on research. Her perspective diverges from the triumphalist narratives often imposed on pioneering women, refusing to frame discrimination as merely an obstacle she overcame rather than a structural force that fundamentally shaped what she could accomplish.

Hyde was also remarkably frank about the trade-offs inherent in her advocacy work. The scholarships and fellowships she established – supporting over one hundred women scientists – represent an extraordinary collective impact, but she acknowledged that the time devoted to that work was time subtracted from her own research. Scientific history privileges individual discoveries over infrastructural support, and whilst Hyde’s endowed fellowships enabled generations of women to pursue careers in science, that contribution doesn’t generate Nobel Prizes or eponymous techniques. The men who declined service work and focused exclusively on their own advancement often achieved greater individual recognition, even as their collective impact remained narrower.

There are gaps and uncertainties in the historical record that merit acknowledgment. Hyde’s 1921 microelectrode paper is brief – only a few pages – and lacks the extensive follow-up studies that would typically establish priority for such a significant methodological advance. Why she published only this single paper on the device remains unclear. In our conversation, Hyde suggested that she didn’t fully realise the microelectrode’s revolutionary potential, that she retired before she could develop it further, and that she lacked the institutional resources to pursue extended investigations. But the historical record doesn’t provide definitive answers, and other interpretations are possible: perhaps the device was more limited than Hyde suggested, perhaps reviewers or colleagues dismissed it as insufficiently novel, or perhaps the demands of teaching and administration at Kansas left insufficient time for sustained methodological development.

Similarly, whilst Hyde’s essay “Before Women Were Human Beings” (1938) documents explicit discrimination she faced at Heidelberg and elsewhere, the full extent of her experiences remains partially obscured. What conversations occurred behind closed doors when faculty debated whether to grant her a degree? What informal exclusions – invitations not extended, collaborations not offered, citations not made – shaped her career in ways that left no documentary trace? Hyde’s willingness to name institutional barriers was unusual for her era, but even her candour has limits imposed by what could be articulated, what was remembered, and what evidence survived.

The afterlife of Hyde’s work reveals both belated recognition and continued erasure. In 2017, the Journal of General Physiology published a comprehensive history of the glass micropipette electrode, crediting Hyde as an early pioneer and noting that her 1921 device predated the microelectrodes developed by Gerard and others by more than two decades. That acknowledgment, appearing ninety-six years after her original publication, represents a corrective to the historical record but also underscores how long erasure persisted. Modern neuroscience textbooks rarely mention Hyde, and when microelectrode techniques are taught, the canonical narrative begins with Hodgkin and Huxley in the 1940s, skipping over the conceptual groundwork laid a generation earlier.

Yet Hyde’s influence persists in ways both direct and diffuse. Every intracellular recording made in contemporary neuroscience laboratories, every patch-clamp experiment characterising ion channels, every microelectrode-guided deep brain stimulation surgery for Parkinson’s disease – these techniques trace their lineage to the principle Hyde established in 1921. The Ida H. Hyde Woman’s International Fellowship continues to support women scientists, extending her legacy of institutional advocacy across more than a century. And her 1938 essay remains a powerful reminder to the barriers women faced in accessing higher education, cited by historians documenting gender discrimination in science.

Connecting Hyde’s story to contemporary challenges in science reveals both progress and persistent inequities. Women now constitute roughly half of biology PhD recipients, a transformation Hyde could scarcely have imagined when she was the sole woman in the American Physiological Society. Universities no longer forbid women from attending lectures or require them to study from smuggled notes. Legal and policy frameworks mandate gender equity in education and employment, at least nominally.

Yet the patterns Hyde identified persist in subtler forms. Women in science still perform disproportionate service work – mentoring, committee service, outreach – that is essential but undervalued in tenure and promotion decisions. Women’s contributions are still cited less frequently than men’s, their co-authored papers still attributed primarily to male colleagues, and their priority claims still more readily dismissed. The “leaky pipeline” that sees women leave academic science at higher rates than men reflects structural barriers – caregiving responsibilities, hostile work environments, lack of mentorship – that differ in degree but not in kind from those Hyde faced. And methodological innovations, particularly those made by women or scientists at non-elite institutions, remain vulnerable to being overlooked and later rediscovered by researchers with greater visibility and institutional support.

Hyde’s life offers no simple lessons, no reassuring narrative of inevitable progress. She was extraordinarily accomplished – a doctorate from Heidelberg, groundbreaking research in cardiovascular physiology and electrophysiology, twenty-two years chairing a university department, over one hundred women supported through her scholarships – and yet she died largely forgotten, her most significant invention credited to others. That injustice cannot be undone, and attempting to frame it as redemptive would dishonour her experience.

What Hyde’s story does provide is an unflinching account of what it costs to persist when institutions are designed to exclude you, and what it means to choose collective advancement over individual recognition. Her insistence that obstacles were real, that discrimination wasn’t imagined, that persistence isn’t always rewarded – this refusal to offer false comfort is perhaps her most valuable legacy for young women entering science today. Visibility matters, mentorship matters, solidarity matters, but they do not guarantee justice. The work of building equity is ongoing, incomplete, and carried forward by those who understand that their contributions may not be recognised in their lifetimes.

If there is a spark to carry forward from Hyde’s life, it is this: the value of scientific work does not depend on whether it is remembered, and the act of enabling others to succeed can be as significant as individual achievement. Hyde invented a tool that transformed neuroscience, even though others received credit. She supported over one hundred women scientists, even though that work diverted time from her own research. She documented the discrimination she faced, even though doing so risked professional consequences. And she did this knowing that recognition might never arrive, that justice might remain deferred, that history might forget her name.

We remember her now not to claim belated triumph, but to ensure that her contributions – and the contributions of countless other women whose work was erased – are restored to the record. And we carry forward her conviction that science belongs to everyone willing to pursue it, regardless of whether the institutions of their era are ready to welcome them.

Who have we missed?

This series is all about recovering the voices history left behind – and I’d love your help finding the next one. If there’s a woman in STEM you think deserves to be interviewed in this way – whether a forgotten inventor, unsung technician, or overlooked researcher – please share her story.

Email me at voxmeditantis@gmail.com or leave a comment below with your suggestion – even just a name is a great start. Let’s keep uncovering the women who shaped science and innovation, one conversation at a time.

Editorial Note: This interview with Ida Henrietta Hyde is a dramatised reconstruction created for educational and commemorative purposes. Whilst Dr Hyde’s scientific contributions, biographical details, and institutional experiences are drawn from historical records – including her published research, autobiographical essay “Before Women Were Human Beings” (1938), university archives, and contemporary accounts – the conversational exchanges presented here are fictional. We have aimed to represent her voice, perspective, and technical expertise as faithfully as possible, grounding her responses in documented facts about her life and work. However, the specific phrasing, reflections, and personal anecdotes she shares in this interview are imagined interpretations based on available evidence, not verbatim transcripts. Similarly, the supplementary questions from readers represent the kinds of inquiries modern audiences might pose, rather than actual correspondence. Our aim is to honour Hyde’s legacy by bringing her story to life in an accessible format whilst acknowledging the inherent limitations of reconstructing historical voices. Readers interested in primary sources are encouraged to consult Hyde’s original publications and the growing body of scholarship documenting women’s contributions to early physiology and neuroscience.

Bob Lynn | © 2025 Vox Meditantis. All rights reserved.