Scientists use lasers to control mouse brain switchboard

Ever wonder why it’s hard to focus after a bad night’s sleep? Using mice and flashes of light, scientists show that just a few nerve cells in the brain may control the switch between internal thoughts and external distractions. The study, partly funded by the National Institutes of Health, may be a breakthrough in understanding how a critical part of the brain, called the thalamic reticular nucleus (TRN), influences consciousness.

“Now we may have a handle on how this tiny part of the brain exerts tremendous control over our thoughts and perceptions,” said Michael Halassa, M.D., Ph.D., assistant professor at New York University’s Langone Medical Center and a lead investigator of the study. “These results may be a gateway into understanding the circuitry that underlies neuropsychiatric disorders.”

The TRN is a thin layer of nerve cells on the surface of the thalamus, a center located deep inside the brain that relays information from the body to the cerebral cortex. The cortex is the outer, multi-folded layer of the brain that controls numerous functions, including one’s thoughts, movements, language, emotions, memories, and visual perceptions. TRN cells are thought to act as switchboard operators that control the flow of information relayed from the thalamus to the cortex.

“The future of brain research is in studying circuits that are critical for brain health and these results may take us a step further,” said James Gnadt, Ph.D., program director at NIH’s National Institute Neurological Disorders and Stroke (NINDS), which helped fund the study. “Understanding brain circuits at the level of detail attained in this study is a goal of the President’s Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative.”

To study the circuits, the researchers identified TRN cells that send inhibitory signals to parts of the thalamus known to relay visual information to the cortex. Using a technique known as multi-electrode recordings, they showed that sleep and concentration affected these cells in opposite ways.

They fired often when the mice were asleep, especially during short bursts of simultaneous brain cell activity called sleep spindles. These activity bursts briefly widen electrical brain wave traces making them look like spindles, the straight spikes with rounded bottoms used to make yarn. In contrast, the cells fired infrequently when the mice were tasked with using visual cues to find food. The results suggested that these cells blocked visual information from reaching the cortex during sleep and allowed its transmission when the mice were awake and attentive.

For Dr. Halassa, a practicing psychiatrist who treats schizophrenia, these surprising results may provide fundamental insights into how the brain controls information transmission, a process that is disrupted in patients with neuropsychiatric disorders. Previous studies suggested that people who experienced more spindles while sleeping were less susceptible to being disturbed by outside noises. Moreover, people with schizophrenia and autism spectrum disorder may experience fewer spindles.

“Spindles may be peepholes into the mysteries of these disorders,” said Dr. Halassa.

To test this idea, the researchers used optogenetics, a technique that introduces light-sensitive molecules into nerve cells. This allowed them to precisely control the firing patterns of visual TRN cells with flashes of laser light. The experiments were performed in well-rested as well as sleep-deprived mice. Similar to what is seen in humans, sleep deprivation can disrupt the ability of mice to focus and block out external distractions.

Well-rested mice needed just a second or two to find the food whereas sleep-deprived mice took longer, suggesting that lack of sleep had detrimental effects on their ability to focus. When the researchers used flashes of laser light to inhibit the firing of optogenetically engineered visual TRN cells in sleep-deprived mice, the mice found the food faster. In contrast, if they used optogenetics to induce sleep-like firing patterns in well-rested mice, then the mice took longer to find food.

“It’s as if with a flick of a switch we could alter the mental states of the mice and either mimic or cure their drowsiness,” said Dr. Halassa.

In a parallel set of experiments the researchers found neighbors of the visual TRN cells had very different characteristics. These neighboring cells control the flow of information to the cortex from limbic brain regions, which are involved with memory formation, emotions and arousal. The cells fired very little during sleep and instead were active when the mice were awake. Dr. Halassa thinks that their firing pattern may be important for the strengthening of new memories that often occurs during sleep. Combined, the results suggest that the TRN is divided into sub-networks that oversee discrete mental states. The researchers think understanding the sub-networks is an initial step in thoroughly exploring the role of the TRN in brain disorders.

Discovery of new pathways controlling the serotonergic system

With the aid of new methods, a research team at Karolinska Institutet have developed a detailed map of the networks of the brain that control the neurotransmitter serotonin. The study, published in the scientific journal Neuron, may lead to new knowledge on a number of psychiatric conditions and the development of new pharmaceuticals.

The neurotransmitter serotonin controls impulsivity, mood and our cognitive functions, among other things, and comes from the serotonergic neurons – the neurons that produce serotonin. So that we have good mental health and normal behaviour, it is important that there is correctly regulated activity among these neurons. The activity is governed by other neurons from different regions of the brain via direct links, known as synapses, on the serotonergic neurons. Imbalance in the serotonergic system can lead to depression, Parkinson’s disease, schizophrenia and autism, among other things.

So far it has been impossible to study in detail how different types of nerve cells are interlinked and how the brain’s networks control behaviour. Consequently, there has also been a lack of knowledge of which nerve cells control the activity of the serotonergic neurons. But with the help of new methods, researchers at Karolinska Institutet can now investigate how the various networks of the brain are organised and how they work. The research team, led by Konstantinos Meletis of the Department of Neuroscience, has established which networks of the brain control the serotonergic neurons.

“We have been able to create a new type of map of the neurons’ contacts and discovered new pathways that control the serotonergic system. These networks were previously unknown and are very interesting in terms of how they help us to understand how the serotonergic system works, which could also help us to understand certain mental illnesses,” Konstantinos Meletis explains.

In order to map out which neurons have direct contact with serotonergic neurons, the researchers established a method in which these cells were marked with a rabies virus which produced a fluorescent marker. Via genetic manipulation, the rabies virus was then spread to all of the neurons directly linked to the serotonergic neurons. The researchers thereby gained a very detailed, three-dimensional image of the networks of the brain that control serotonin. Using optogenetics, a method in which light is used to control the activity of neurons, the researchers were then able to manipulate select networks and thus study their effect on the serotonergic neurons.

Via mapping, the researchers discovered a network in the frontal lobe which is associated with cognition and well-being and which controls the serotonergic neurons. Researchers also found that serotonin can be controlled from new types of neurons in the basal ganglia, an area of the cerebrum which among other things controls movement, well-being and decision-making; a discovery which may have significance for conditions such as Parkinson’s disease.

“We are very optimistic that the revolution we are now seeing in brain research could also lead to entirely new and effective medicine in the field of psychiatry,” Konstantinos Meletis explains.

Division of labour in the fish brain

For a fish to swim forward, the nerve cells, or neurons, in its brain and spine have to control the swishing movements of its tail with very close coordination. However, the posture of the tail, which determines swimming direction somewhat like a rudder, also needs to be fine-tuned by the brain’s activity. Using the innovative method of optogenetics, scientists from the Max Planck Institute of Neurobiology in Martinsried have now identified a group of only about 15 nerve cells which steer the movements of the tail fin. Movements of the human body are also controlled via nerve pathways in the same region of the brain, which may therefore use processing mechanisms similar to those in fish.

For a long time, neurobiologists have been trying to find out how neuronal networks control both animal and human behaviour. In this context, there is controversy as to whether the brain’s organisation is decentralised as opposed to modular. In decentralised organisation, the interaction of a large number of neurons produces a specific behaviour pattern. If this is the case, individual neurons cannot be assigned an exact function. On the other hand, if the brain has a modular structure, individual regions might possess certain competencies, each making a specific contribution to behaviour. These types of neuronal circuit modules could be combined in many ways and influence a broad range of different behavioural responses.

Switches in the fish brain?

Researchers in Herwig Baier’s Group at the Max Planck Institute of Neurobiology want to get to the bottom of the brain’s organisational structure with the aid of zebrafish larvae. A network known as the descending reticular formation is located in the brainstem of these animals. The neurons of that region are optimally suited for studying the organisation of the brain: the cells are in direct contact with motor neurons in the spinal cord of the fish and can thus directly influence tail movements. “The reticular formation is a like a ‘cockpit’ for the fish, and we asked ourselves whether there are individual ‘switches’ or ‘joysticks‘, which are used to control the movements of the tail”, is how Herwig Baier summarises this challenge.

In their search for these switches, the researchers concentrated on a small brain nucleus (nMLF) within the reticular formation. But how can the influence of individual nMLF neurons on tail movements be studied? It is only recently that such investigations even became a possibility. Using the new method of optogenetics, the activity of nerve cells can be influenced with light. Since a zebrafish larva – including its brain – is transparent, scientists can very accurately “switch on” small sets of genetically modified cells by exposing the larva to blue light. Consequently, tail movements that are induced in this way can be attributed to identified neurons.

Neurons and tillers

The first series of tests showed that the cells of the nMLF region seem to be involved in a variety of movements – from forward propulsion to rotational motion. A second experimental series using optogenetic stimulation, however, suggested that the cells control the deflection of the tail in particular. Are the nMLF cells thus part of a multifunctional centre or are they truly specialised to perform certain functions? To resolve this question, the neurobiologists performed another set of trials in which they very specifically removed small sets of nMLF cells from the circuit. “This experiment gave us our breakthrough”, recalls Tod Thiele, lead author of the now published study.

The results show that, while nMLF cells are active in many aspects of swimming, a subset of these neurons contribute to only one part of the movement: they determine swimming direction through the posture of the tail. Thus, this population of neurons in the nMLF region are more akin to a specialised module within a decentralised control system of the swimming apparatus. Herwig Baier explains it like this: “We can compare the whole setup with the propulsion of a motorboat”. The boat’s engine, which drives the propeller, determines the thrust, whereas the tiller steers the boat. It seems that the tasks in the brain are divided up in a very similar way.

Some time ago, Herwig Baier’s team discovered a small region in the hindbrain, which acts like an engine and propels the fish forwards. “With the nMLF cells, we have now also found the tiller in the fish brain”, says Herwig Baier. In the human brain, movements are also controlled by a multitude of nuclei in the reticular formation. The study therefore suggests that the allocation of tasks in our brain could be similar to that of the zebrafish.

Noninvasive brain control

Optogenetics, a technology that allows scientists to control brain activity by shining light on neurons, relies on light-sensitive proteins that can suppress or stimulate electrical signals within cells. This technique requires a light source to be implanted in the brain, where it can reach the cells to be controlled.

MIT engineers have now developed the first light-sensitive molecule that enables neurons to be silenced noninvasively, using a light source outside the skull. This makes it possible to do long-term studies without an implanted light source. The protein, known as Jaws, also allows a larger volume of tissue to be influenced at once.

This noninvasive approach could pave the way to using optogenetics in human patients to treat epilepsy and other neurological disorders, the researchers say, although much more testing and development is needed. Led by Ed Boyden, an associate professor of biological engineering and brain and cognitive sciences at MIT, the researchers described the protein in the June 29 issue of Nature Neuroscience.

Optogenetics, a technique developed over the past 15 years, has become a common laboratory tool for shutting off or stimulating specific types of neurons in the brain, allowing neuroscientists to learn much more about their functions.

The neurons to be studied must be genetically engineered to produce light-sensitive proteins known as opsins, which are channels or pumps that influence electrical activity by controlling the flow of ions in or out of cells. Researchers then insert a light source, such as an optical fiber, into the brain to control the selected neurons.

Such implants can be difficult to insert, however, and can be incompatible with many kinds of experiments, such as studies of development, during which the brain changes size, or of neurodegenerative disorders, during which the implant can interact with brain physiology. In addition, it is difficult to perform long-term studies of chronic diseases with these implants.

Mining nature’s diversity

To find a better alternative, Boyden, graduate student Amy Chuong, and colleagues turned to the natural world. Many microbes and other organisms use opsins to detect light and react to their environment. Most of the natural opsins now used for optogenetics respond best to blue or green light.

Boyden’s team had previously identified two light-sensitive chloride ion pumps that respond to red light, which can penetrate deeper into living tissue. However, these molecules, found in the bacteria Haloarcula marismortui and Haloarcula vallismortis, did not induce a strong enough photocurrent — an electric current in response to light — to be useful in controlling neuron activity.

Chuong set out to improve the photocurrent by looking for relatives of these proteins and testing their electrical activity. She then engineered one of these relatives by making many different mutants. The result of this screen, Jaws, retained its red-light sensitivity but had a much stronger photocurrent — enough to shut down neural activity.

“This exemplifies how the genomic diversity of the natural world can yield powerful reagents that can be of use in biology and neuroscience,” says Boyden, who is a member of MIT’s Media Lab and the McGovern Institute for Brain Research.

Using this opsin, the researchers were able to shut down neuronal activity in the mouse brain with a light source outside the animal’s head. The suppression occurred as deep as 3 millimeters in the brain, and was just as effective as that of existing silencers that rely on other colors of light delivered via conventional invasive illumination.

A key advantage to this opsin is that it could enable optogenetic studies of animals with larger brains, says Garret Stuber, an assistant professor of psychiatry and cell biology and physiology at the University of North Carolina at Chapel Hill.

“In animals with larger brains, people have had difficulty getting behavior effects with optogenetics, and one possible reason is that not enough of the tissue is being inhibited,” he says. “This could potentially alleviate that.”

Restoring vision

Working with researchers at the Friedrich Miescher Institute for Biomedical Research in Switzerland, the MIT team also tested Jaws’s ability to restore the light sensitivity of retinal cells called cones. In people with a disease called retinitis pigmentosa, cones slowly atrophy, eventually causing blindness.

Friedrich Miescher Institute scientists Botond Roska and Volker Busskamp have previously shown that some vision can be restored in mice by engineering those cone cells to express light-sensitive proteins. In the new paper, Roska and Busskamp tested the Jaws protein in the mouse retina and found that it more closely resembled the eye’s natural opsins and offered a greater range of light sensitivity, making it potentially more useful for treating retinitis pigmentosa.

This type of noninvasive approach to optogenetics could also represent a step toward developing optogenetic treatments for diseases such as epilepsy, which could be controlled by shutting off misfiring neurons that cause seizures, Boyden says. “Since these molecules come from species other than humans, many studies must be done to evaluate their safety and efficacy in the context of treatment,” he says.

Boyden’s lab is working with many other research groups to further test the Jaws opsin for other applications. The team is also seeking new light-sensitive proteins and is working on high-throughput screening approaches that could speed up the development of such proteins.

Controlling movement with light

For the first time, MIT neuroscientists have shown they can control muscle movement by applying optogenetics — a technique that allows scientists to control neurons’ electrical impulses with light — to the spinal cords of animals that are awake and alert.  

Led by MIT Institute Professor Emilio Bizzi, the researchers studied mice in which a light-sensitive protein that promotes neural activity was inserted into a subset of spinal neurons. When the researchers shone blue light on the animals’ spinal cords, their hind legs were completely but reversibly immobilized. The findings, described in the June 25 issue of PLoS One, offer a new approach to studying the complex spinal circuits that coordinate movement and sensory processing, the researchers say.

In this study, Bizzi and Vittorio Caggiano, a postdoc at MIT’s McGovern Institute for Brain Research, used optogenetics to explore the function of inhibitory interneurons, which form circuits with many other neurons in the spinal cord. These circuits execute commands from the brain, with additional input from sensory information from the limbs.

Previously, neuroscientists have used electrical stimulation or pharmacological intervention to control neurons’ activity and try to tease out their function. Those approaches have revealed a great deal of information about spinal control, but they do not offer precise enough control to study specific subsets of neurons.

Optogenetics, on the other hand, allows scientists to control specific types of neurons by genetically programming them to express light-sensitive proteins. These proteins, called opsins, act as ion channels or pumps that regulate neurons’ electrical activity. Some opsins suppress activity when light shines on them, while others stimulate it.

“With optogenetics, you are attacking a system of cells that have certain characteristics similar to each other. It’s a big shift in terms of our ability to understand how the system works,” says Bizzi, who is a member of MIT’s McGovern Institute.

Muscle control

Inhibitory neurons in the spinal cord suppress muscle contractions, which is critical for maintaining balance and for coordinating movement. For example, when you raise an apple to your mouth, the biceps contract while the triceps relax. Inhibitory neurons are also thought to be involved in the state of muscle inhibition that occurs during the rapid eye movement (REM) stage of sleep.

To study the function of inhibitory neurons in more detail, the researchers used mice developed by Guoping Feng, the Poitras Professor of Neuroscience at MIT, in which all inhibitory spinal neurons were engineered to express an opsin called channelrhodopsin 2. This opsin stimulates neural activity when exposed to blue light. They then shone light at different points along the spine to observe the effects of neuron activation.

When inhibitory neurons in a small section of the thoracic spine were activated in freely moving mice, all hind-leg movement ceased. This suggests that inhibitory neurons in the thoracic spine relay the inhibition all the way to the end of the spine, Caggiano says. The researchers also found that activating inhibitory neurons had no effect on the transmission of sensory information from the limbs to the brain, or on normal reflexes.

“The spinal location where we found this complete suppression was completely new,” Caggiano says. “It has not been shown by any other scientists that there is this front-to-back suppression that affects only motor behavior without affecting sensory behavior.”

“It’s a compelling use of optogenetics that raises a lot of very interesting questions,” says Simon Giszter, a professor of neurobiology and anatomy at Drexel University who was not part of the research team. Among those questions is whether this mechanism behaves as a global “kill switch,” or if the inhibitory neurons form modules that allow for more selective suppression of movement patterns.

Now that they have demonstrated the usefulness of optogenetics for this type of study, the MIT team hopes to explore the roles of other types of spinal cord neurons. They also plan to investigate how input from the brain influences these spinal circuits.

“There’s huge interest in trying to extend these studies and dissect these circuits because we tackled only the inhibitory system in a very global way,” Caggiano says. “Further studies will highlight the contribution of single populations of neurons in the spinal cord for the control of limbs and control of movement.”

(Image caption: In this artist’s representation of the adult subependymal neurogenic niche (viewed from underneath the ependyma), electrical signals generated by the ChAT+ neuron give rise to newborn migrating neuroblasts, seen moving over the underside of ependymal cells. Credit: Illustration by O’Reilly Science Art.)

Neuron Tells Stem Cells to Grow New Neurons

Duke researchers have found a new type of neuron in the adult brain that is capable of telling stem cells to make more new neurons. Though the experiments are in their early stages, the finding opens the tantalizing possibility that the brain may be able to repair itself from within.

Neuroscientists have suspected for some time that the brain has some capacity to direct the manufacturing of new neurons, but it was difficult to determine where these instructions are coming from, explains Chay Kuo, M.D. Ph.D., an assistant professor of cell biology, neurobiology and pediatrics.

In a study with mice, his team found a previously unknown population of neurons within the subventricular zone (SVZ) neurogenic niche of the adult brain, adjacent to the striatum. These neurons expressed the choline acetyltransferase (ChAT) enzyme, which is required to make the neurotransmitter acetylcholine. With optogenetic tools that allowed the team to tune the firing frequency of these ChAT+ neurons up and down with laser light, they were able to see clear changes in neural stem cell proliferation in the brain.

The findings appeared as an advance online publication June 1 in the journal Nature Neuroscience.

The mature ChAT+ neuron population is just one part of an undescribed neural circuit that apparently talks to stem cells and tells them to increase new neuron production, Kuo said. Researchers don’t know all the parts of the circuit yet, nor the code it’s using, but by controlling ChAT+ neurons’ signals Kuo and his Duke colleagues have established that these neurons are necessary and sufficient to control the production of new neurons from the SVZ niche.

"We have been working to determine how neurogenesis is sustained in the adult brain. It is very unexpected and exciting to uncover this hidden gateway, a neural circuit that can directly instruct the stem cells to make more immature neurons," said Kuo, who is also the George W. Brumley, Jr. M.D. assistant professor of developmental biology and a member of the Duke Institute for Brain Sciences. "It has been this fascinating treasure hunt that appeared to dead-end on multiple occasions!"

Kuo said this project was initiated more than five years ago when lead author Patricia Paez-Gonzalez, a postdoctoral fellow, came across neuronal processes contacting neural stem cells while studying how the SVZ niche was assembled.

The young neurons produced by these signals were destined for the olfactory bulb in rodents, as the mouse has a large amount of its brain devoted to process the sense of smell and needs these new neurons to support learning. But in humans, with a much less impressive olfactory bulb, Kuo said it’s possible new neurons are produced for other brain regions. One such region may be the striatum, which mediates motor and cognitive controls between the cortex and the complex basal ganglia.

"The brain gives up prime real estate around the lateral ventricles for the SVZ niche housing these stem cells," Kuo said. "Is it some kind of factory taking orders?" Postdoctoral fellow Brent Asrican made a key observation that orders from the novel ChAT+ neurons were heard clearly by SVZ stem cells.

Studies of stroke injury in rodents have noted SVZ cells apparently migrating into the neighboring striatum. And just last month in the journal Cell, a Swedish team observed newly made control neurons called interneurons in the human striatum for the first time. They reported that interestingly in Huntington’s disease patients, this area seems to lack the newborn interneurons.

"This is a very important and relevant cell population that is controlling those stem cells," said Sally Temple, director of the Neural Stem Cell Institute of Rensselaer, NY, who was not involved in this research. "It’s really interesting to see how innervations are coming into play now in the subventricular zone."

Kuo’s team found this system by following cholinergic signaling, but other groups are arriving in the same niche by following dopaminergic and serotonergic signals, Temple said. “It’s a really hot area because it’s a beautiful stem cell niche to study. It’s this gorgeous niche where you can observe cell-to-cell interactions.”

These emerging threads have Kuo hopeful researchers will eventually be able to find the way to “engage certain circuits of the brain to lead to a hardware upgrade. Wouldn’t it be nice if you could upgrade the brain hardware to keep up with the new software?” He said perhaps there will be a way to combine behavioral therapy and stem cell treatments after a brain injury to rebuild some of the damage.

The questions ahead are both upstream from the new ChAT+ neurons and downstream, Kuo says. Upstream, what brain signals tell ChAT+ neurons to start asking the stem cells for more young neurons? Downstream, what’s the logic governing the response of the stem cells to different frequencies of ChAT+ electrical activity?

There’s also the big issue of somehow being able to introduce new components into an existing neuronal circuit, a practice that parts of the brain might normally resist. “I think that some neural circuits welcome new members, and some don’t,” Kuo said.

How to Erase a Memory – And Restore It

Researchers at the University of California, San Diego School of Medicine have erased and reactivated memories in rats, profoundly altering the animals’ reaction to past events.

The study, published in the June 1 advanced online issue of the journal Nature, is the first to show the ability to selectively remove a memory and predictably reactivate it by stimulating nerves in the brain at frequencies that are known to weaken and strengthen the connections between nerve cells, called synapses.

“We can form a memory, erase that memory and we can reactivate it, at will, by applying a stimulus that selectively strengthens or weakens synaptic connections,” said Roberto Malinow, MD, PhD, professor of neurosciences and senior author of the study.

Scientists optically stimulated a group of nerves in a rat’s brain that had been genetically modified to make them sensitive to light, and simultaneously delivered an electrical shock to the animal’s foot. The rats soon learned to associate the optical nerve stimulation with pain and displayed fear behaviors when these nerves were stimulated.

Analyses showed chemical changes within the optically stimulated nerve synapses, indicative of synaptic strengthening.

In the next stage of the experiment, the research team demonstrated the ability to weaken this circuitry by stimulating the same nerves with a memory-erasing, low-frequency train of optical pulses. These rats subsequently no longer responded to the original nerve stimulation with fear, suggesting the pain-association memory had been erased.

In what may be the study’s most startlingly discovery, scientists found they could re-activate the lost memory by re-stimulating the same nerves with a memory-forming, high-frequency train of optical pulses. These re-conditioned rats once again responded to the original stimulation with fear, even though they had not had their feet re-shocked.

“We can cause an animal to have fear and then not have fear and then to have fear again by stimulating the nerves at frequencies that strengthen or weaken the synapses,” said Sadegh Nabavi, a postdoctoral researcher in the Malinow lab and the study’s lead author.

In terms of potential clinical applications, Malinow, who holds the Shiley Endowed Chair in Alzheimer’s Disease Research in Honor of Dr. Leon Thal, noted that the beta amyloid peptide that accumulates in the brains of people with Alzheimer’s disease weakens synaptic connections in much the same way that low-frequency stimulation erased memories in the rats. “Since our work shows we can reverse the processes that weaken synapses, we could potentially counteract some of the beta amyloid’s effects in Alzheimer’s patients,” he said.

Staying focused: Cortico-thalamic pathway filters relevant sensory cues from perceptual input

On the one hand, the nervous has limited computational capability – but at the same time, the sensory environment contains an immense amount of information. In this demanding situation, the brain somehow manages to selectively focus attention on relevant stimuli. Recently, scientists at Technische Universität München, Munich and Ruhr University Bochum, Bochum investigated thalamic tactile sensory relay by employing optogenetics (the use of light to control neurons which have been genetically sensitized to light) to control specific cortical input to the thalamus. They show that the deepest cortical layer (known as layer six, or simply L6) plays a key role in controlling thalamic signal transformation (specifically, by controlling adaptive responses of thalamic neurons) and thalamic gating of dynamic sensory input patterns by changing the firing mode.

Dr. Rebecca A. Mease and Dr. Alexander Groh discussed the paper they and Prof. Patrik Krieger published in Proceedings of the National Academy of Sciences. In this study they investigated how the brain actively controls and gates information reaching higher stages of cortical processing by using optogenetics to turn on specific cortical input to the thalamus and measure how this impacts the processing of sensory signals in the thalamus.

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