Cavefish Secrets Revealed: What These Stress-Free Fish Can Teach Us About Neural Adaptation
- Erik Duboue
- 1 day ago
- 18 min read
Astyanax mexicanus, the Mexican tetra, lives a double life, split between the bright, predator-rich rivers of northeastern Mexico and the perpetual darkness of its subterranean caves. It’s the same species, yet two radically different worlds. Surface fish dart through shimmering waters, constantly alert to threats. Their cave-dwelling cousins float unhurried in a silent blackness, their eyes sealed by evolution and their colors faded to bone-white. These fish raise a compelling question for neuroscientists and evolutionary biologists alike: how does a brain reinvent itself when it no longer answers to light or to fear?
Life in the cave stripped away much of what drives stress in the surface world. No predators. Little environmental variation. Time flows differently where the sun never rises. Yet rather than simply becoming a slower, quieter version of their surface ancestors, cave populations of A. mexicanus exhibit profound rewiring of behavior and physiology. They sleep less, forage more efficiently, and show blunted stress responses. Somehow, evolution dialed down the circuitry of alarm while fine-tuning the machinery of survival, turning these fish into a living study of how the brain adapts to constant calm amid chronic scarcity.
But this “stress-free” world is also unforgiving. Food arrives unpredictably, often in brief pulses of organic matter washing in from the surface, and the baseline state is energetic poverty. The environment is stable and predictable in its darkness, yet harsher in its chronic scarcity, forcing fish to stretch limited calories across growth, reproduction, and survival. Under these conditions, cavefish have evolved to forage more efficiently and invest heavily in energy acquisition and storage, turning their bodies and brains into tight economies tuned for survival in a world where the threat is not being eaten, but slowly starving.
The Origin Story of Astyanax
Astyanax is a name drawn directly from Greek mythology, where Astyanax is the infant son of Hector and Andromache in the Iliad, a child associated with a royal household and, tragically, with the fall of Troy. Taxonomists often borrowed such mythological names for genera, and in this case the name was likely chosen because the type species bears large, gleaming silver scales that evoke a kind of armored nobility, loosely echoing the martial world surrounding Hector. For Astyanax mexicanus, the name is inherited from that genus-level choice, giving these small tetras a surprisingly epic, Homeric pedigree despite their humble river and cave habitats.
The tale becomes intriguing when zooming out to consider that there isn’t just one cavefish but many. Astyanax mexicanus has colonized more than 30 caves across Mexico, evolving into distinct populations that independently adapted to the dark. Each lineage represents its own natural experiment in rapid evolution, a parallel test case conducted by nature itself. This replication makes A. mexicanus extraordinary - a biological library of solutions to the same set of challenges: how to find food without sight, navigate without reference points, and reproduce in an energy-poor world. My old advisor used to say that this is a million-year-old experiment that has been replicated at least 30 times. Some caves produced fish that forage obsessively; others harbor populations that evolved strikingly different social behaviors or stress responses. Each adaptation reveals another facet of how the brain and body negotiate life when typical sensory and emotional anchors are gone. In their quiet darkness, these fish illuminate one of biology’s oldest questions: what happens when evolution rewires the mind to fit a world without fear, but also without light?
Astyanax in the Lab
Astyanax mexicanus is a powerful lab model because it couples classic teleost tractability with dramatic, naturally evolved divergence in morphology, behavior, and physiology within a single species. Surface and cave forms remain fully interfertile, yet differ sharply in eyes, pigmentation, craniofacial structure, brain organization, metabolism, and sleep, so many of the questions usually asked across species can be addressed with controlled crosses and hybrids. This makes it possible to treat evolution itself as an experiment, while still enjoying the practical advantages of a small, fecund, externally developing fish.
A. mexicanus has become a flagship evo‑devo system for understanding both regressive and constructive trait evolution. Multiple independent cave populations have repeatedly evolved eye loss, albinism, and craniofacial remodeling alongside expansion and reorganization of nonvisual sensory systems and brain regions. Because the embryos are transparent, develop externally, and can be produced in large, synchronized clutches, standard embryological tools such as whole‑mount in situ hybridization, immunostaining, live imaging, and now transgenesis and CRISPR can be used to dissect when and how these traits diverge during development. Interfertility between surface and cave morphs allows QTL mapping and hybrid analyses that link specific genomic regions and developmental pathways to evolved phenotypes, making the system unusually well suited for mechanistic studies of pleiotropy, modularity, and constraint.
A. mexicanus can also be used as a model for disease exploration. John Bland Sutton once wrote, “and in many instances we shall find conditions which we regard as abnormal in man presenting themselves as normal states in other animals.” What Sutton was suggesting here is that some animals may have phenotypes which we consider maladaptive, but which they use in adaptive ways. These models can be used as a system for disease exploration. Cave populations routinely exhibit obesity‑like fat stores, hyperphagia, elevated blood glucose, are perpetually diabetic, and shortened sleep durations, yet do not show the classical downstream pathologies familiar from mammalian models. Comparative metabolomics and physiological assays across independent cave populations reveal convergent reprogramming of sugar and lipid utilization, starvation resistance, and muscular endurance, suggesting that evolution has found stable, non‑pathological solutions to chronic nutrient stress and low‑resource environments. Because these traits segregate in crosses with surface fish and can be probed with modern genomic tools, the system offers a rare window into how vertebrate tissues and circuits can be rewired to tolerate “disease‑like” states.
Taken together, these perspectives underscore why A. mexicanus is such a strong lab model: it unites the strengths of a traditional developmental genetic system with the richness of a replicated natural experiment in evolution, metabolism, and behavior. Researchers can move fluidly from field‑relevant questions about ecological adaptation to high‑resolution mechanistic work in the lab, all within a single, experimentally accessible vertebrate species.
Sleep in a dark cave
One of the earliest hints that Astyanax mexicanus was doing something extraordinary came from a behavior so universal we barely think about it: sleep. This was the focus of my graduate work – I had realized that the system was poised to understand how morphological traits differ, but the same tools could be applied the behavior or the brain. I chose to look at sleep because it seemed important to humans, appeared relevant for a cavefish (and my insomnia) and was just interesting. I remember the first night I watched videos of cavefish and surface fish sleeping – a 2 am trip to the lab in 2009 had me sleepless for the rest of the day.
When we first compared how much the surface-dwelling fish slept versus their cave-dwelling relatives, the results were startling. Surface fish slept robustly, showing clear day–night cycles. Cavefish across multiple independent populations had all but abandoned the behavior – cavefish slept, but the amount of time they spent in sleep states was minimal. Some populations slept 80 percent less, and others were barely ever still. Yet they weren’t sick, stunted, or stressed. They were perfectly healthy. In 2011, this became one of the landmark discoveries in the field (and my PhD thesis): sleep, a behavior deeply conserved across animals, had been dramatically eroded not once, but repeatedly, in separate cavefish lineages.
This immediately raised a crucial question: how do you lose sleep without breaking the brain? Sleep isn’t just rest, it’s tied to metabolism, immunity, and neural development. Something fundamental must have shifted in cavefish biology. Early follow-ups showed that the sleep-like inactivity that did occur still met key physiological criteria: increased arousal thresholds and sleep rebound after deprivation. Cavefish still had a sleep system; they were just using it differently.
From here, the search turned to genetics. Hybrid studies between surface fish and Pachón cavefish showed that reduced sleep behaved as a dominant trait, driven by only a small number of genetic loci. That meant sleep loss wasn’t polygenic drift over millions of years; it was likely controlled by a focused mechanism. Me, Masato Yoshizawa and Alex Keene then compared sleep and another cave-specific trait: enhanced vibration attraction behavior (VAB), a lateral-line–driven prey-seeking behavior. VAB and sleep were both heightened in cavefish, but we (2015) revealed something surprising: the genetic architecture underlying these traits was entirely independent. Cavefish didn’t lose sleep because they gained mechanosensory foraging. Sleep loss was its own evolutionary target.
The next leap came from looking directly into the cavefish brain. A clue emerged from a region long known to regulate wakefulness across vertebrates: the hypothalamus, home of the neuropeptide hypocretin (also called orexin). In mammals, deficiencies in hypocretin signaling cause narcolepsy. In zebrafish, hypocretin neurons promote arousal and locomotion. If cavefish were chronically awake, perhaps their hypocretin system had been dialed up. That hypothesis was spot-on. In a 2018 study, Alex and I, led by James Jaggard, discovered that cavefish possess significantly more hypocretin-producing neurons, and those neurons express more hypocretin at both the RNA and protein level. This wasn’t subtle modulation; it was a wholesale amplification of a wake-promoting circuit. When researchers pharmacologically blocked hypocretin receptors, cavefish, for the first time, slept more like surface fish. When they genetically knocked down hypocretin signaling, the same thing happened. Cavefish sleep loss was not a mysterious whole-brain phenomenon; it was traceable to a specific neurochemical pathway.
But the story went deeper. Two ecological factors uniquely relevant to cave life, viz. food scarcity and lateral line hypersensitivity, also modulated this system. Starvation (a natural feature of cave environments) decreased hypocretin levels in cavefish but not in surface fish. Ablating the lateral line (the sensory system that detects water vibrations) similarly reduced hypocretin expression only in cavefish. This meant that the hypocretin system had become functionally rewired: in surface fish it played a stable role in sleep-wake regulation, but in cavefish it evolved into a sensorimotor integrator, combining information about food availability, environmental stress, and mechanosensory cues.
What began as a simple behavioral observation, “cavefish barely sleep,” ultimately uncovered a precise, evolutionarily modified neurocircuit that combines ecological pressures and sensory experience into a single physiological output: stay awake and search for food. Sleep was not discarded; it was strategically suppressed via a known vertebrate arousal system tuned for a new environment.
This sleep phenotype became the prototype for cavefish neuroscience as a whole. It demonstrated that if you dig deep enough into a dramatic behavioral change, you can uncover a clear mechanistic origin: one neuron type, one neuropeptide, one circuit. And it showed that evolution does not need to build new machinery to reshape behavior. Sometimes, it just turns the dial on a circuit that already exists.
Stress: How Cavefish Evolved Calm Minds in a Predator-Free World
If sleep reveals how cavefish rewired their brains for efficiency, their stress response illustrates something even more striking: evolution didn’t just change how these fish act. It changed how they feel. In the quiet darkness of Mexican caves, where predators are absent and the environment is remarkably stable, cavefish appear to have shed large portions of their neuroendocrine stress response. What emerges is a picture of animals that are, comparatively speaking, almost anxiety-proof.
The story began with a simple behavioral test. When placed into an unfamiliar tank, surface fish do what most fish (and humans) do when they are overwhelmed: they freeze, they hug the bottom, and they cautiously explore only after many minutes. This “novel tank diving” behavior is a classic vertebrate stress readout. But when researchers ran the same test on adult Pachón cavefish, the result was unmistakable. Cavefish barely hesitated. They began exploring the entire tank within minutes, spent more time near the top, and showed significantly less immobility - behavior directly opposite to the stress-associated bottom dwelling in surface fish.
Even more compelling was the fact that this wasn’t a one-off anomaly. In the 2018 Jacqueline chin and I showed that adults from multiple independently evolved cave populations (Pachón, Tinaja, and Molino) showed the same reduced-stress profile, demonstrating convergent evolution toward calm behavior in the novel tank assay. The data show this clearly: surface fish remain rooted to the bottom, while cavefish consistently swim near the top, move more, and freeze less. In other words, what stress looks like in surface fish barely registers in cavefish.
Of course, behavioral readouts are only one window into stress. To test whether these differences reflected true physiological changes, we probed the neuroendocrine stress axis, the fish equivalent of the mammalian HPA (hypothalamic–pituitary–adrenal) system. In a follow-up study focusing on larvae, we delivered mild electric shocks to surface and Pachón fry and measured stress-induced freezing and cortisol release. Surface larvae responded robustly: they froze significantly more after stimulation, and their cortisol levels spiked fifteen minutes later, showing normal activation of the glucocorticoid pathway. Cavefish larvae, in contrast, barely changed their behavior, and their cortisol levels hardly increased at all.
This wasn’t because cavefish lacked the machinery to produce cortisol. Instead, they appeared to regulate the system differently. Gene expression analyses showed that larvae from Pachón cavefish had significantly elevated levels of the glucocorticoid receptor (GR / nr3c1), the receptor that receives cortisol’s “stress signal” and also acts as the primary negative feedback regulator of the stress axis. In other words, the cavefish stress system is tuned to shut itself down quickly. Elevated GR expression dampens cortisol responses by enhancing feedback inhibition. This fits perfectly with what behavioral and physiological assays showed: surface fish mount a strong stress response; cavefish suppress it rapidly.
This pattern of reduced behavioral stress, muted hormonal response, elevated GR appears in some cave populations at both larval and adult stages (Pachón, Tinaja). Others show reduced stress only in adults, not larvae (e.g., Molino), suggesting that evolution acted on stress circuitry in multiple ways, fine-tuning how each population coped with its unique environment. But across populations, the overall direction was the same: stress got dialed down. That convergence is striking, because it suggests that in the absence of predators, chronic stress—and the metabolic costs associated with it—became unnecessary. Pharmacology confirmed all of this. Treating surface fish with the anxiolytic drug buspirone made them behave indistinguishably from cavefish in the novel tank: they swam more, froze less, and explored the top half freely. Treating cavefish did almost nothing, because their baseline state already resembled an anxiolytic-treated fish.
Taken together, these results suggest that cavefish didn’t simply “lose” stress, they evolved a fundamentally different tuning of the entire neuroendocrine cascade. What surface fish interpret as threatening, cavefish treat as routine. Their brains, operating in a predator-free world, prioritize exploration and energy efficiency over anxiety and vigilance. The result is a naturally evolved, repeatedly derived model of stress resistance, one that offers insights into how genes, environment, and neural circuits shape vulnerability to stress-related disorders.
In a sense, cavefish reveal a remarkable truth: stress isn’t just a reaction to the outside world. It is shaped by evolution, sculpted by ecology, and encoded in circuitry that can be rewired when the environment no longer requires vigilance. In the deep stillness of their caves, these fish became calm not by accident, but by adaptation
From Behavior to Brain-Wide Circuits: How Cavefish Let Us See Evolution at the Neuronal Level
Evolution sculpts the brain at the level of regions, circuits, and even individual cell types. Many model organisms let us probe neural circuits with exquisite precision, but few offer a naturally occurring evolutionary experiment with replicated populations, deep ecological contrast, and full genetic compatibility between morphs. Cavefish do all of this at once. Their dramatic changes in sleep, stress, sociality, escape behavior, and light responses serve as entry points into understanding how vertebrate neural circuits adapt to novel environments. Each behavior acts like a signpost that guides us toward the specific neural substrates that evolution modified.
The first major step in connecting behavior to brain came through the development of complete three-dimensional brain atlases for surface fish and multiple cave populations. These atlases, produced through high-resolution imaging and automated segmentation, revealed a remarkably consistent pattern across independently evolved cavefish: dorsal sensory structures, especially the optic tectum, contract, while ventral regions such as the hypothalamus expand. This dovetails easily with what we see behaviorally—cavefish rely less on vision and more on internal-state regulation, feeding circuits, and homeostatic mechanisms. Convergent expansion of the hypothalamus, as well as changes in neuromodulatory cell numbers, align neatly with sleep loss, hyperphagia, altered stress responses, and the reorganization of sensory priorities. In this way, the brain-wide atlas work provides a neuroanatomical framework that links evolved behaviors to the broader architecture of the cavefish brain.
Because cavefish and surface fish can interbreed to produce viable hybrids, researchers can go even further, directly mapping naturally occurring genetic variation to brain-wide anatomical differences. Analyses of F1 and F2 hybrid brains show that the volumetric and shape differences between surface and cavefish are heritable and modular. Some regions show surface-dominant inheritance, others cave-dominant, and many intermediates reveal developmental trade-offs that affect the entire dorsal–ventral axis. These patterns suggest that brain evolution in Astyanax is not random drift but is structured by developmental constraints and coordinated changes across related brain areas. The hybrid data are especially compelling because they allow neuroanatomical evolution to be treated like any other quantitative trait, making it possible to dissect how many genetic loci influence regional growth and to identify the developmental modules that underlie convergent anatomical change.
Once anatomical differences were resolved, the next step was to understand how these changes influence neural activity. Whole-brain MAP-mapping using pERK staining revealed that not only do cavefish brains look different—they activate differently. Surface fish increase neural activity in visually driven regions such as the optic tectum during lights-on transitions, whereas cavefish show enhanced activity in the pineal and hypothalamic regions instead. Activity patterns during sleep, feeding, and light responses diverge strongly across forms, reinforcing the idea that evolution has altered not just the hardware of the brain but also how that hardware is dynamically engaged.
To understand how evolution reshapes behavior, we need to do more than document what animals do - we need to watch their brains in action. For decades, neuroscientists relied on traditional electrophysiology to record the electrical activity of individual neurons. While precise, these methods are inherently limited: you can measure a handful of cells at once, but not the coordinated patterns across thousands of neurons that drive behavior. Calcium imaging transformed this landscape. Instead of inserting electrodes, researchers engineer neurons to produce a fluorescent signal whenever they become active. Because neural firing triggers a rapid influx of calcium ions, these fluorescent calcium indicators act like tiny lanterns, lighting up each time a neuron fires. This allows scientists to visualize the dynamics of large neural populations simultaneously, producing a movie of the brain “thinking” in real time.
In small, transparent organisms like zebrafish calcium imaging opens the extraordinary possibility of reading brain-wide activity patterns as an animal responds to sensory stimuli, explores its environment, or executes a learned behavior. When paired with genetically encoded calcium indicators like GCaMP, which fill entire neurons with light-responsive molecules, researchers can record thousands of active cells across deep brain regions at millisecond resolution. This approach bridges the gap between structure, which brain atlases give us, and function, which calcium imaging reveals. The technique allows us to see not just where brain differences exist, but how those differences shape the moment-to-moment computations that underlie evolved behaviors. We therefore made genetically modified surface and cavefish, which express the calcium indicator, GCaMP in all neurons
The emergence of stable, pan-neuronal GCaMP lines in Astyanax represents a turning point for the field. For the first time, we could look directly at whole-brain activity in both surface and cave morphs, comparing how the same stimulus engages different neural circuits. This pushes the research beyond anatomy and gene expression into the realm of circuit logic: Which neurons respond? When do they fire? How do activity patterns propagate across the brain? And crucially, do the brains of cavefish and surface fish represent the same sensory world in fundamentally different ways? Calcium imaging gives us the resolution to answer these questions—something no other evolutionary model system has ever offered at this scale.
One of the first things we did with these fish is look at the optic tectum, a large visual area that comprises about 25-30% of the fish brain. Clearly, eyeless cavefish have smaller optic tectum, but it’s not absent. Using GCaMP, we can show that presentation of light causes neural depolarizations in the tectum of surface fish – but what about cavefish? Surprisingly, when we delivered the same light stimulus to cavefish, the optic tectum still responded. Despite millions of years without eyes, and despite a dramatic reduction in tectal size, the underlying circuitry remains functional enough to detect and process changes in illumination. This was unexpected: the cavefish brain had retained at least part of a visual processing pathway despite the complete loss of vision itself.
That finding became a critical clue. If the tectum could still respond to light, then cavefish must be using non-visual photoreceptors to detect illumination, and those signals must be traveling through conserved central pathways. Suddenly, a simple behavioral readout - how fish move when the lights turn on or off - became a powerful tool to trace the sensory circuits that evolution had modified. Light responses were no longer just a vestigial reflex; they were an entry point into understanding how a blind brain repurposes ancient circuits to navigate a world without vision.
Classic studies in zebrafish have shown that when fish are placed in a lighted arena, and the lights are suddenly turned off, fish begin swimming in hyperactive circling patterns. You can place a small light dot on an otherwise dark background, and they will continue to swim until hitting the light. Hyperactivity in darkness is a light searching behavior. What makes this response remarkable is not just its strength, but its evolutionary reach: virtually all sighted teleost fishes spanning more than 200 million years of divergence show the same fundamental pattern. Whether it is medaka, goldfish, killifish, sticklebacks, or zebrafish, sudden darkness triggers an immediate spike in locomotion as animals try to reorient toward illumination. Across this radiation of species, dark-induced hyperactivity appears to be a deeply conserved ancestral reflex, one that relies on a core sensorimotor program linking illumination loss to rapid exploration.
What do cavefish do when illumination changes – nothing, well kind of. Cavefish do become hyperactive, but when lights are turned on, not off. If hyperactivity in darkness for sighted fish is a light searching behavior, it’s fun to think of hyperactivity in cavefish as a light searching behavior.
To understand which circuits might drive these opposing behaviors, Robert Kozol and I used whole-brain activity mapping to identify regions whose activity changed when illumination shifted. This analysis pointed toward the caudal posterior tuberculum, a dopaminergic-rich midbrain region long known to integrate motivational and sensorimotor signals. In surface fish, this region became active during darkness, consistent with the idea that dark-search behavior relies on a dopaminergic arousal circuit. In cavefish, however, the same region showed increased activity during light exposure. Anatomically, the structure was conserved. Functionally, it had been repurposed.
The true breakthrough came when the team leveraged newly generated Astyanax lines expressing pan-neuronal GCaMP, allowing them to watch neural activity unfold during light transitions in real time. Calcium imaging revealed that within the caudal posterior tuberculum, a specific subpopulation of neurons that is dark-sensitive in surface fish becomes light-sensitive in cavefish. This was not a global shift in brain activity but a precise tuning change in a small, identifiable group of dopaminergic neurons. Their sensory preference had switched polarity. That simple inversion - dark excites the circuit in surface fish, light excites the circuit in cavefish - perfectly mirrored the behavioral inversion observed at the whole-organism level.
To test causality, Rob manipulated dopamine signaling pharmacologically. Blocking dopaminergic transmission disrupted the evolved light-on hyperactivity in cavefish, showing that this single neuromodulatory system is required for the behavior. Importantly, cavefish did not evolve an entirely new circuit; they retained the ancestral dopaminergic architecture but shifted its functional input. This demonstrated that evolution’s most powerful lever is often not to add or remove brain regions, but to change what drives the neurons that are already there. The study concluded that a conserved dopaminergic module—shared across vertebrates from fish to mammals—can be adaptively reprogrammed by natural selection to support a new behavioral meaning.
In sum, our study showed that a deeply rooted teleost behavior (dark-induced searching) can be completely inverted through a targeted modification of sensory tuning in a specific dopamine circuit. The discovery offers one of the clearest examples in vertebrate neuroscience of circuit-level evolutionary change: behavior, brain activity, and cellular physiology all shift together through a simple, elegant mechanism. It marks a turning point in our understanding of how natural selection shapes neural systems, not by redesigning the brain from scratch, but by flipping the polarity of a single, well-defined neuronal population.
Conclusion: What Cavefish Teach Us About Evolving Minds
If there is a single lesson that Astyanax mexicanus offers, it is that evolution does not simply sculpt bodies, it sculpts brains. And it does so in ways that are far more elegant, targeted, and adaptable than we might have imagined. Across thirty independent cave populations, we see the same story written again and again: alter the environment, and the nervous system rewires itself to meet new demands. Strip away light, and vision collapses while other senses bloom. Remove predators, and stress circuits quiet. Impose chronic starvation, and metabolic pathways reorganize to preserve energy and fuel relentless foraging. Cavefish survive not by adding complexity, but by tuning, trimming, and repurposing neural circuits that vertebrates have carried for hundreds of millions of years.
What makes this system so powerful is that the adaptations are both dramatic and mechanistically accessible. Reduced sleep maps onto a specific hypothalamic neuropeptide. Blunted stress maps onto shifts in glucocorticoid receptor expression and endocrine feedback regulation. Altered social and escape behaviors trace to predictable shifts in sensory processing and thalamic integration. And in perhaps the clearest example, a centuries-old light-search behavior found across the teleost lineage is inverted through a single dopamine circuit whose tuning has been flipped by natural selection. In cavefish, evolution is not rewriting the brain from scratch; it is revising it; editing ancient circuits until they produce entirely new interpretations of the world.
These discoveries remind us that neural evolution is not mystical or opaque. It is tractable. It is modular. And in the right system, it can be watched as it happens. Astyanax mexicanus gives us that vantage point. It lets us start with a behavior such as sleep loss, anxiety reduction, hyperactivity in light and follow it all the way down to the neurons, the receptors, the genes, and the ecological pressures that shaped them. Few vertebrate models offer this level of resolution and evolutionary replication.
And perhaps most importantly, cavefish challenge our assumptions about what is “adaptive,” what is “pathological,” and what is possible within the architecture of a brain. Behaviors we might consider maladaptive-insomnia, perpetual hyperphagia, chronic hyperglycemia—become advantageous in the caves. Circuits that in humans support anxiety or arousal are retuned toward calm exploration. Systems we think of as fixed like stress responsivity or wake-promoting neuromodulators turn out to be flexible, evolvable levers shaped by context. Evolution does not care about the norms of mammals; it cares about survival under specific constraints.
In the silent darkness of the caves of northeastern Mexico, Astyanax has reinvented itself dozens of times. Each reinvention offers a window into how vertebrate brains change, how behaviors evolve, and how flexible the neural code truly is. These fish are not just curiosities of natural history, they are living laboratories for understanding the principles that govern all brains, including our own. They show us that the nervous system is not a static organ but a dynamic, evolving machine, continually adapting to the demands of the environment.
In revealing their secrets, cavefish offer something even more profound: a reminder that hidden worlds often hold the clearest answers. All we have to do is look in the dark.