The 2026 Nobel Prize for Medicine or Physiology, announced today, honors Karl Deisseroth, Peter Hegemann and Georg Nagel—three pioneers of optogenetics, a groundbreaking technique in basic neuroscience research.
Hegemann, professor of neuroscience at Humboldt University of Berlin, and Nagel, professor of molecular plant physiology at the University of Würzburg, discovered light-sensitive channelrhodopsin proteins in single-cell algae in the early 2000s. Deisseroth, professor of bioengineering, psychiatry and behavioral sciences at Stanford University, leveraged these proteins to control neuronal activity with flashes of light. This optogenetics approach—described in a 2005 Nature Neuroscience paper that has been cited more than 4,700 times, according to the journal—has enabled researchers to precisely manipulate circuits in the brain in an unprecedented manner.
“I’m obviously incredibly honored and proud of everyone who worked on this,” Deisseroth says. “Like all science these days, particularly for big interdisciplinary work like this, it takes a lot of people to make this work well.” (At the time of this article’s publication, Hegemann and Nagel had not replied to an emailed request for an interview.)
The researchers had previously won prestigious awards for their work, including the 2013 Brain Prize (awarded to all three Nobel winners and others) and the 2021 Albert Lasker Basic Medical Research Award (awarded to Deisseroth, Hegemann and another scientist), so the Nobel was a long time coming, says Hillel Adesnik, associate professor of neuroscience at the University of California, Berkeley. “This was inevitable, given that optogenetics has radically transformed much of neuroscience,” he says. “So it was really just a matter of when, not a matter of if.”
Optogenetics advances ranked among the most transformative new neuroscience tools and technologies in a survey for The Transmitter’s 2025 State of Neuroscience report. Neuroscientists have leveraged it for a wide range of research, from studying the role of sleep and the formation of long-term memories to the neural mechanisms underlying emotion. Deisseroth and others have continued to iterate, developing techniques such as two-photon holographic optogenetics, which mimics natural neuronal activity and offers greater target specificity.
Optogenetics “allows us to ask which cell types are governing a particular stage in perception or cognition or action,” Deisseroth says. In the future, optogenetics might be used in therapies and to locate cell types responsible for psychiatric and neurological symptoms, he adds. “That opens the door to any kind of treatment; it could be medication designed to target that causal cell.”
Here is how optogenetics has transformed neuroscience and defined researchers’ career trajectories, according to eight neuroscientists.
These responses have been lightly edited for length and clarity.
“The initial paper in Nature Neuroscience from Deisseroth came out in 2005. I was a graduate student, and at the time, there were really only two or three places in the brain where you could actually do electrical stimulation and really interpret your results, because those structures were highly layered: the hippocampus, the cerebellum and the retina. Anywhere else you couldn’t access. At the time, the cerebral cortex had basically not been studied at the circuit level at all, because you can’t just put a microelectrode in the cortex and really know what you’re stimulating, because axons are going everywhere. So when optogenetics came out, I was like, ‘Yeah, this is the answer.’ We can target optogenetic proteins to specific cell types in the cerebral cortex. That’s what I do now, and we can really dissect the cerebral cortex, which had been really just a big black box. It’s almost inarguable to say optogenetics has transformed really every aspect of systems neuroscience, whether it be perception or motor action; these have been entirely transformed from C. elegans all the way up into nonhuman primates.” —Hillel Adesnik, associate professor of neuroscience, University of California, Berkeley
“Optogenetics has had such a big impact on neuroscience over the past decade and a half. It has really been enabling for how we dissect how circuits function at a mechanistic level and how we think about the involvement, or not, of different neurons in complex behavior. The most exciting thing is it’s also an example of something that started out as basic biology influencing work in everything from insects to mammals and everything in between … Optogenetics, particularly red-shifted variants of channelrhodopsin—including from the lab of another pioneer in the field, Edward Boyden—have allowed us to screen for the involvement of specific cell types in a wide range of behaviors by selective activation and silencing. It has allowed us to test plasticity rules and models of attractor dynamics in navigational circuits by selectively perturbing subsets of a cell type using two-photon laser scanning in vivo. And it has allowed us to precisely control how we appetitively reward hungry flies in learning tasks by activating their sugar receptors rather than actually feeding them. The flies stay hungry, and you can get many trials that way. But even more than that, what has been underlying a lot of the use cases is that cell types are just so important in understanding how a neural circuit works.” —Vivek Jayaraman, senior group leader, Janelia Research Campus, Howard Hughes Medical Institute
“I see science as two phases: the dark ages—where we could do a lot of things; we could do drugs; we could do lesions; we could do electrical stimulation—but nothing was specific. And then came optogenetics. We welcomed in the light, the new age. We’re now really only limited by our imagination. For memory research and my own research, it has allowed us to manipulate specific cells. So rather than manipulating the entire lateral amygdala or the entire hippocampus—people have done that before, and those studies have been really important, but it’s not specific—what we can do now is manipulate specific cells that make up one specific memory. So rather than manipulating all memories, we can manipulate a specific memory. We can activate those cells and have a mouse seemingly recall a memory, or we can silence those cells and have a mouse not be able to recall a memory. So it has really been just a game changer.” —Sheena Josselyn, senior scientist, Hospital for Sick Children
“Optogenetics has been a transformative approach in neuroscience. The ability to precisely control neural activity—up and down, with millisecond precision, in cells defined by genetic markers, projections to other brain areas or combinations thereof—is incredibly powerful for disentangling cause and effect. Karl has even extended this beyond the nervous system—for example, using optogenetics to probe interactions between the cardiac and nervous systems. In my own research on dopamine, we’ve seen how much precision matters. For example, we have experiments where we train mice to respond for reward on a random interval schedule, meaning they perform a lot of responses just to get one that’s rewarded. Dopamine goes up on rewarded responses and down on unrewarded responses. But what do those ups and downs really mean? We’ve seen that optogenetic inhibition of dopamine terminals on rewarded responses does what you might expect—increases learning and the persistence of reward-seeking. But surprisingly, the same optogenetic inhibition on unrewarded responses can increase persistence in reward-seeking. Without optogenetics, we would have had no way of differentiating these opposite effects! By allowing experiments like this one, optogenetics has enabled scientists to really probe the algorithms of the brain and make some surprising discoveries. In my opinion, this type of circuit neuroscience is going to be a key way forward for precision psychiatry. It’s very exciting!” —Talia Newcombe Lerner, senior scientist and scientific director of preclinical neuroscience, Centre for Addiction and Mental Health; and associate professor of psychiatry, University of Toronto
“It is exciting to see this prize awarded for optogenetics. This has been a revolutionary approach for the neuroscience field and has transformed what we can do in the lab. For example, my lab studies the vagus nerve, and optogenetics has provided an amazing and essential tool for us, enabling us to control autonomic physiology with light. Prior to optogenetics, people used whole vagal nerve stimulation or cut the nerve—very coarse approaches that don’t lend themselves to cell-specific manipulations. We observed that there were a couple dozen molecularly distinct neuron types in the vagus nerve, and then by using optogenetics, we revealed what different neurons were doing. We observed a surprising division of labor, with different vagal sensory neurons controlling breathing, heart rate, blood pressure, digestion and other reflexes. None of this would have been possible without the foundational invention of optogenetics. I am very excited to see that this approach received appropriate recognition by winning the Nobel Prize. It is a terrific day for the field!” —Stephen Liberles, professor of cell biology, Harvard University
“This is long overdue and so exciting. I was a senior postdoc, and later a research associate, in Karl’s lab, and I was the first to apply optogenetic tools to control seizures in real time. Optogenetics really changed what we can do in the epilepsy field, because detecting seizures and understanding which cells are sufficient to perturb in order to stop seizures without side effects, that’s something that really could not have been addressed before these tools were developed. It’s very exciting. Before, it was very, very hard to know which cells matter, which connections in the brain matter, to cause seizures, and how to disrupt them without causing side effects like sleep disruption, for example. Optogenetic tools allowed us to specifically interrogate, ‘OK, does this cell type matter in this region?’ to find what I call ‘choke points’ for seizures.” —Jeanne Paz, senior investigator, Gladstone Institutes; and professor of neurology, University of California, San Francisco
“From various indirect experiments in genetics and disease conditions, we knew that dopamine neurons in the middle of the brain had roles both in learning and in movement. But in Parkinson’s disease, dopamine neurons die, ultimately causing severe movement disorders. Optogenetics allowed the field to directly show the role of dopamine neurons in driving synaptic plasticity, in driving learning, the relationship of dopamine-dependent changes in synapses and learning, and also their effects on movement in different circuits. There were a lot of unintended discoveries. So, for example, we discovered that channelrhodopsin goes into axons. Now you could study connections between neurons across all length scales in the brain, and a few discovered that Dale’s law isn’t quite what it was made out to be. Many neurons actually release multiple neurotransmitters. More generally, in the context of systems neuroscience, there’s this problem of causality, right? Systems neuroscience tends to still be a science that relies heavily on very sophisticated correlational approaches. So if there’s something that happens in neurons in one brain region that correlates with the behavior, now you can go in and manipulate the activity using optogenetics in different kinds of ways, even in ways that the brain never produces.” —Karel Svoboda, executive vice president and director, Allen Institute for Neural Dynamics
“Within each part of the brain is a very complex circuit in itself that has dozens of different types of neurons. Understanding what each population, or each cell type, does requires a technique that can target them selectively and allow you to switch them on or off. This is something that people had been trying to do, but until channelrhodopsin came around, it was very hard to actually implement. Hegemann and Nagel’s contribution was that they actually discovered this light-gated ion channel, which was the first of its kind. Until then, we knew about other kinds of light-activated proteins, but none of them allowed the kind of millisecond control that channelrhodopsin allows. When I was a postdoc in Deisseroth’s lab, we collaborated extensively with Hegemann, and we made new variants of channelrhodopsin. We created slow and fast variants of channelrhodopsin. We actually made the first red-shifted channelrhodopsin, which responds to yellow light, which allowed dual channel control. We started expanding the toolbox beyond the original channelrhodopsin, and today this toolbox has dozens of different tools. The downstream effect is not necessarily activating the neurons; it could be silencing the neurons; it could be silencing their axon terminals to prevent the release of neurotransmitters—it became a very versatile toolbox that, if you use it properly, you can ask a lot of different questions about what the neurons do and how they work and how they contribute to cognition and behavior.” —Ofer Yizhar, principal investigator, Weizmann Institute of Science
