New insights into the circuits of sight: Max Planck Florida study reveals cortical circuits that encode black and white

While some things may be ‘as simple as black and white’, this has not been the case for the circuits in the brain that make it possible for you to distinguish black from white. The patterns of light and dark that fall on the retina provide a wealth of information about the world around us, yet scientists still don’t understand how this information is encoded by neural circuits in the visual cortex—a part of the brain that plays a critical role in building the neural representations that are responsible for sight. But things just got a lot clearer with the discovery that the majority of neurons in visual cortex respond selectivity to light vs dark, and they combine this information with selectivity for other stimulus features to achieve a detailed representation of the visual scene.

Scientists have long known that neurons in the retina that provide information to higher centers in the brain respond selectively to light vs dark stimuli. ‘ON’ cells that respond selectively to light stimuli and ‘OFF’ cells that respond selectively to dark stimuli were known to form separate parallel channels relaying information to circuits in visual cortex. But here is where the picture got murky. Based on recording the responses of single cortical neurons with electrodes, it appeared that as soon as the ON and OFF channels entered the cortex, they converged onto single neurons, a convergence necessary for the emergence of a novel cortical response property: selectivity for the orientation of edges. Further stages in cortical processing were thought to lead to more and more mixing of the ON and OFF signals, so that individual neurons responded similarly to both dark and light stimuli. These results raised an obvious question: If the responses of single cortical neurons to dark and light are ambiguous, how is it that the brain allows us to perceive these differences?

Drs. Gordon Smith and David Whitney in David Fitzpatrick’s lab at Max Planck Florida Institute for Neuroscience decided it was time to revisit this question. Using new imaging technologies that make it possible for the first time to visualize the activity of hundreds of neurons simultaneously in the living brain, they quantified the responses of neurons in ferret visual cortex to light and dark stimulation.

The first surprise for the team happened when they looked at cortical responses to the presentation of uniform dark or light stimuli. Although previous studies had not observed responses to uniform luminance changes, Smith et al. were not only able to visualize neurons that responded to these stimuli, they discovered patches of neurons that responded preferentially to dark vs light stimulation. Even more surprising, they found that the cortical neurons that responded selectively to the orientation of edges or to the direction of stimulus motion also responded preferentially to dark vs light stimuli. In short, the Max Planck Florida scientists discovered that information about dark and light is preserved in the responses of most neurons in visual cortex, and it is an integral part of the neural code that cortical circuits use to represent our visual world.

The next challenge for Max Planck Florida scientists is to understand the precise patterns of synaptic connections that enable cortical circuits to construct this modular representation of black and white. Stay tuned for more exciting discoveries that promise to reshape our understanding of cortical function.


Modular Representation of Luminance Polarity in the Superficial Layers of Primary Visual Cortex

Gordon B. Smith1, David E. Whitney1, David Fitzpatrick
1Co-first author
DOI: http://dx.doi.org/10.1016/j.neuron.2015.10.019


Image: Abstraction of cortical neurons, responsive to both the polarity and orientation of edges, and not just orientation: A key feature of visual scenes is the polarity of local changes in luminance. Polarity signals are segregated in the activity of different populations of neurons as early as the retina and relayed into cortex. However, the fate of these polarity signals within the activity of cortex has remained uncertain. In this paper, we show that information about edge polarity and orientation are jointly encoded and preserved within the population activity of superficial layers of visual cortex. Illustration by Martha Iserman.


When the neuron’s doorman allows too much in

(Above Image) This is what a neuron from the hippocampus of a rat looks like. The cell and it’s extensive processes are visualised using a fluorescent dye, filled via a glass pipette. The glass pipette, with dye, is shown on the left of the cell body. (c) Photo: AG Heinz Beck/Uni Bonn

Researchers at the University of Bonn discover a new mechanism of epilepsy

Bonn, 16.11.2015. – In epilepsy, nerve cells lose their usual rhythm, and ion channels, which have a decisive influence on their excitability, are involved. A team of researchers under the direction of the University of Bonn has now discovered a new mechanism for influencing ion channels in epilepsy. They found that spermine inside neurons dampens the neuron’s excitability. In epilepsy, spermine levels decrease, causing hyperexcitability. The researchers hope that their findings can be exploited to develop new therapies for epilepsies. They are reporting their findings in The Journal of Neuroscience.

In Germany, approximately one out of a hundred people suffer from epilepsy and one out of twenty suffer a seizure at least once during their lifetime. Seizures occur when many nerve cells in the brain fire in synchrony. Scientists are searching for the causes leading to this simultaneous excitation of brain cells. Researchers at the Department of Epileptology, the Institute for Neuropathology and the Institute for Molecular Psychiatry, together with the Caesar Research Center and the Hebrew University (Israel) have discovered a mechanism which previously was not thought to be involved in the development of epilepsy.

“Doormen” determine how many sodium ions are allowed in

Neurons integrate many inputs together to then determine an appropriate output, and sodium channels play a key role in both processes. “They play an important role in the excitation of nerve cell axons and signal transfer between various cells,” says Prof. Dr. Heinz Beck, who conducts research in experimental epileptology at the Department of Epileptology, at the Life & Brain center and the German Center for Neurodegenerative Diseases (DZNE). Like a type of door, sodium channels allow sodium ions to flow into nerve cells through tiny pores. They consist of large protein complexes located in the membranes of nerve cells. The scientists found a large increase in a certain sodium influx which significantly increased the excitability of cells in the epileptic animal.

For this reason, scientists working with Prof. Beck initially compared the sodium channel proteins from the brains of epileptic rats to those of healthy animals. “However, this did not reveal any increased formation of sodium channel proteins, which could have explained the over-excitation of nerve cells.” reports the epilepsy researcher. After a long search, the team of researchers found a completely different group of substances: the polyamines. Spermine belongs to this group; it is produced in cells and plugs the pores of the sodium channels from within. Spermine then acts like a doorman, blocking entry to sodium ions and dampening the excitability of the nerve cells.

Over-excitation is attenuated through administration of spermine

The scientists investigated how much of the seizure-inhibiting substance is present in the nerve cells of rats suffering from epilepsy and compared the values to those of healthy animals. “The amount of spermine in the cells of the hippocampus was significantly reduced in diseased animals as compared to the healthy animals,” report the lead authors Dr. Michel Royeck and Dr. Thoralf Optiz from Dr. Beck’s team. “Furthermore, the reduced spermine in the nerve cell led to increased excitability; the cells were more sensitive to input and generated more output” said fellow lead author Dr. Tony Kelly. The investigators tested this important finding, compensating for the deficiency in the nerve cells of epileptic rats by adding spermine back into the cell. As a result, the increase in sodium currents was reversed and the excitability of the neuron returned to normal.

The lower level of spermine in the epileptic rat’s brain was evidently caused by an upregulation of spermidine/spermine-N(1)-acetyltransferase. This enzyme breaks down the spermine which is important in the control of sodium channels. According to the scientists, this result could be a potential starting point for novel epilepsy therapies. “If a substance was available to reduce the activity of acetyltransferase back to normal levels, the lack of spermine and thus the symptoms of epilepsy could be mitigated,” speculates Prof. Beck. However, concrete therapeutic applications are still a long way off.


 

Original publication

Royeck, M., Kelly, T., Opitz, T., Otte, D.M., Rennhack, A., Woitecki, A., Pitsch, J., Becker, A., Schoch, S., Kaupp, U.B., Yaari, Y., Zimmer, H. & Beck, H. “Downregulation of Spermine Augments Dendritic Persistent Sodium Currents and Synaptic Integration after Status Epilepticus” The Journal of Neuroscience 35, 15240-15253

D10.1523/JNEUROSCI.0493-15.2015

Contact
Prof. Dr. Heinz Beck
University Hospital for Epileptology, Life & Brain Center,
German Center for Neurodegenerative Diseases
Spokesperson for Collaborative Research Center 1089
Tel. ++49-228-6885215
E-Mail: Heinz.Beck@ukb.uni-bonn.de

Dr. Tony Kelly
University Hospital for Epileptology, Life & Brain Center,
Tel. ++49-228-6885276
E-Mail: tony.kelly@ukb.uni-bonn.de

 

http://www.general-anzeiger-bonn.de/bonn/wissenschaft/Wenn-der-Ionen-Tuersteher-zu-viel-durchlaesst-article1780424.html

Welcome to IMPRS for Brain and Behavior

There has never been a better time to obtain a Ph.D. in the neurosciences: new technologies allowing access to circuits within the whole brain are enabling researchers to address questions about brain circuitry and the underlying principles in behaving animals. The challenge now arises of how to best prepare the next generation of neuroscience students with the necessary skill sets to understand, use, and advance such technologies to answer questions of the brain.

The new International Max Planck Research School for Brain and Behavior is a fully funded graduate program jointly hosted between caesar, Bonn, Germany and the Max Planck Florida Institute for Neuro- science (MPFI), USA. In addition, IMPRS for Brain and Behavior is co-run by partner Universities: University of Bonn, Germany and Florida Atlantic University in the USA. The IMPRS for Brain and Behavior offers fully funded Ph.D. positions in Neuroscience.

Students will receive both theoretical and hands-on training in a large range of modern imaging, electro- physiological and molecular techniques. They will be exposed to a broad range of research areas based on how sensory information is encoded in neural circuits and how these circuits are activated during behavior. Students will take courses and attend scientific symposia at the partner institutions in Bonn and Florida – thereby being exposed to an exceptionally broad group of international scientists and provided the opportunity to earn a doctorate under outstanding research conditions.

Successful candidates will work in a young and dynamic international environment, embedded in the local scientific communities of caesar or MPFI. As both caesar and MPFI are part of a large cluster of Max Planck Institutes working in the neurosciences, students will have unparalleled insight into the broad range of outstanding research taking place in the Max Planck Society, Germany’s most successful research organization.

The Ph.D. program is open to highly qualified and motivated candidates from all over the world who hold an outstanding diploma or master degree. Please upload your application through the online application portal found at: www.imprs-brain-behavior.mpg.de

Application deadline is December 1, each year starting 2015.