All events, 2018

Learning probabilistic representations in randomly connected neural circuits

Lecture
Date:
Wednesday, August 29, 2018
Hour: 10:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Ori Maoz (PhD Thesis Defense)
|
Elad Schneidman Lab, Dept of Neurobiology, WIS

The brain represents and reasons probabilistically about complex stimuli and motor actions using a noisy, spike-based neural code. A key building block for such neural computations, as well as the basis for supervised and unsupervised learning, is the ability to estimate the surprise or likelihood of incoming high-dimensional neural activity patterns. Despite progress in statistical modeling of neural responses and deep learning, current approaches either do not scale to large neural populations or cannot be implemented using biologically realistic mechanisms. Inspired by the sparse and random connectivity of real neuronal circuits, we present a new model for neural codes that accurately estimates the likelihood of individual spiking patterns from the joint activities of actual populations of cortical neurons. The model has a straightforward, scalable, efficiently learnable, and realistic neural implementation as either a randomly connected neural circuit or as single neuron with a random dendritic tree. In the corresponding implementation, a neuron can take advantage of random connectivity leading to it in order to autonomously learn the respond with the surprise of its input patterns based on the previous observed patterns. Importantly, it can be achieved using a local learning rule that utilizes noise intrinsic to neural circuits. Slower, structural changes in random connectivity, consistent with rewiring and pruning processes occurring on developmental time scales, can further improve the efficiency and sparseness of the resulting neural representations. Our results merge insights from neuroanatomy, machine learning, and theoretical neuroscience to suggest random sparse connectivity as a key design principle for neuronal computation.

Catecholamines in the hippocampal formation

Lecture
Date:
Monday, August 13, 2018
Hour: 10:00 - 11:15
Location:
Gerhard M.J. Schmidt Lecture Hall
Sima Verbitsky (PhD Thesis Defense)
|
Menahem Segal Lab, Dept of Neurobiology, WIS

Monoaminergic (noradrenergic, dopaminergic and serotonergic) modulation of hippocampal activity is assumed to play a major role in neuronal plasticity, learning and memory. Understanding the locus of action of these neuromodulators at the cellular level will expand our knowledge of their nature and allow us to identify issues related to their dysfunction. In the present work I study the effects of norepinephrine (NE) and dopamine (DA) on spontaneous and evoked activity in patch-clamped neurons of hippocampal slices. Both DA and NE induced a significant decrease in the amplitude of the evoked PSCs recorded from CA1 pyramidal neurons in response to stimulation of the Schaffer collaterals, accompanied by a small decrease in the cell input resistance, and a small hyperpolarization. While decreasing the evoked PSCs, NE promoted an overall increase in spontaneous synaptic activity. Pharmacological assessment of these results indicated an α1 adrenergic receptor involvement in both the decrease of the amplitude of evoked PSCs as well as the increase in spontaneous activity. Surprisingly, the effect of NE on evoked PSCs was partially antagonized by D1 dopaminergic receptor antagonist SCH23390, which suggests that NE activates dopamine receptors. The effect of DA on evoked PSCs was blocked by α1 adrenergic receptor antagonist prazosin, which suggests that DA, in turn, is activating adrenergic receptors. Noradrenergic system is highly affected by stress; in particular, the differences between NE effects in dorsal and ventral hippocampus (DH and VH, respectively) have been shown to change in stressed animals. In this work I used two types of stress protocols – Prenatal Stress (PS) and Acute Stress (AS) – to study the effect of stress on monoamine responses in slices of DH and VH. In non-stressed rats, NE effect on the evoked PSCs is larger in DH than in VH. PS and AS rats increased NE effect in VH, thus abolishing the difference between DH and VH. Pharmacological data suggests that these differences result from differential efficiencies of α1 and D1 receptors between DH and VH of both control and PS rats. Acute stress reversed the difference between PS and control rats; in the AS slices the PSC reduction was significantly different between DH and VH of PS rats, and not in control rats. I conclude that stress increases the NE modulation in VH, but not in DH, thus increasing the role of emotional processing associated with the VH.

Regulation of the blood-cerebrospinal fluid barrier as a gateway for leukocyte trafficking in physiology and pathology

Lecture
Date:
Sunday, August 12, 2018
Hour: 15:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Alexander Kertser (PhD Thesis Defense)
|
Michal Schwartz Lab, Dept of Neurobiology, WIS

The role of TrpC2 channel in mediating social behavior of male mice within a group

Lecture
Date:
Wednesday, August 1, 2018
Hour: 14:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Yefim Pen (PhD Thesis Defense)
|
Tali Kimchi Lab, Dept of Neurobiology, WIS

Neural circuits for skilled forelimb movement

Lecture
Date:
Thursday, July 26, 2018
Hour: 11:00
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Eiman Azim
|
Molecular Neurobiology Laboratory Salk Institute for Biological Studies, La Jolla, CA

Movement shapes our interactions with the world, providing a means to translate intent into action. Among the wide repertoire of mammalian motor behaviors, the precise coordination of limb muscles to propel arms, hands and digits through space with speed and precision represents one of the more impressive achievements of the motor system. Skilled forelimb movements emerge from interactions between feedforward command pathways that induce muscle contraction and feedback systems that report and refine movement. Two broad classes of feedback modify motor output: one that originates in the periphery, and a second that is generated within the central nervous system itself. Yet the mechanisms by which these feedback pathways influence forelimb movement remain poorly understood. We take advantage of the genetic tractability of mice to examine the organization of motor circuits and define the ways in which these pathways enable dexterous behaviors. First, I will discuss recent studies that explore the transmission of proprioceptive and cutaneous signals from the forelimb into the spinal cord and brainstem, describing neural circuits that modulate the strength of this peripheral feedback and the implications of this sensory gain control for limb movement. Second, I will describe work exploring a diverse class of spinal interneurons that we hypothesize convey copies of forelimb motor commands as internal feedback to the cerebellum, enabling online predictions of motor outcome and reducing dependence on delayed sensory information. Through a complementary set of molecular, anatomical, electrophysiological and behavioral approaches, these findings are yielding insight into the organizational and functional logic of peripheral and internal feedback, and revealing how the circuits that convey feedback information help to orchestrate skilled behavior.

Human physiological and behavioral responses to olfactory stimuli in health and disease

Lecture
Date:
Tuesday, July 17, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Liron Rozenkrantz (PhD Thesis Defense)
|
Noam Sobel Lab, Dept of Neurobiology, WIS

In my PhD I led three projects probing human behavioral and physiological responses to olfactory stimuli in health and disease. In these projects I used every-day olfactory occurrences in order to infer on biological underpinnings of human behavior. In my main project I tested olfactory processing in autism, using the sniff response, a ten-minute non-verbal measure of respiratory response to odors. I found this objective measure to be profoundly altered in children with autism, and furthermore, to be highly correlated with autism severity. Using computational methods, I demonstrated 81% correct ASD classification based on differences in olfactory processing alone. These results provide proof-of-concept for a potential biomarker for autism (Rozenkrantz et al, Curr Bio, 2015). In a second and soon-to-be-submitted project, I investigated olfactory social communication in recurrent pregnancy loss (RPL), resting on a phenomenon in rodents in which females miscarry following exposure to bodily odors of non-stud males. I found that women with RPL display heightened social olfactory abilities, which were significantly correlated with number of miscarriages. Additionally, women with RPL showed significantly altered hormonal, physiological and neural responses to body odors of unfamiliar men. This project provides novel evidence for altered olfactory processing in human recurrent miscarriages. The third project is also my first foothold in placebo effect research, which I will pursue in my postdoc. Taking advantage of the non-invasive nature of olfactory stimuli, I used an odor as the placebo carrier, and tested two groups of subjects for different creativity tests. Both groups smelled the odor, but only the placebo group was told that it increases creativity (placebo manipulation). I found that following this simple manipulation, the placebo group displayed significantly enhanced creativity (Rozenkrantz et al., PLoS one, 2017). Taken together, these projects convey my deep interest in the interplay between human behavior and physiology.

Sensory processing across behavioral and neuromodulatory states

Lecture
Date:
Tuesday, July 3, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Dr. Yuval Nir
|
Sagol School of Neuroscience & Sackler School of Medicine Tel-Aviv University

"Sensory disconnection" – conditions when the same sensory stimulus does not reliably affect behavior or subjective experience - is a defining feature of sleep, and similar processes may occur during light anesthesia or during cognitive lapses in wakefulness. What are the changes in brain activity that mediate sensory disconnection? In a series of studies in humans and rodents, we investigate how "disconnected" states affect sensory processing. The first set of studies reveals differences in neuronal responses to identical sensory stimuli across states. We find that in humans, cognitive lapses after sleep deprivation involve attenuated and delayed single-neuron responses in MTL co-occurring with local slow/theta waves. In the auditory domain, we show in both rodents and humans that responses in sleep and light anesthesia are preserved up to A1, challenging the classic "thalamic gating" notion, but robust attenuation occurs later in high-level cortical regions. In addition, sleep affects more strongly responses that require integration over long time intervals, and responses to high-frequency content. The second set of studies investigates the underlying mechanisms, testing the potential role of locus coeruleus-noradrenaline (LC-NE) neuromodulation. In rats, we test how NE signaling affects the probability to wake up from sleep in response to sounds. We establish a new approach for selective in-vivo LC optogenetics by showing effects on spiking activity, evoked sleep-wake transitions, and pupil dilation. Combined LC and auditory stimulation synergistically increases the probability of awakenings beyond independent effects of sound and laser alone, supporting a role for LC-NE activity in mediating sensory responses. We also tested the effects of NE levels on sensory perception and sensory-evoked activity (EEG, fMRI) in awake humans. Pharmacologically manipulating NE levels in double-blind placebo-controlled experiments, we found that NE modulates sensitivity and accuracy of visual perception without significant effects on decision bias (criterion). In addition, NE increased the fidelity of late EEG visual responses, and selectively modulated BOLD fMRI responses in high-order visual cortex, suggesting that NE plays an enabling causal role in visual awareness by affecting late visual processing.

Neural networks mapping actions to their sensory consequences

Lecture
Date:
Tuesday, June 26, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Roy Mukamel
|
School of Psychological Sciences and Sagol School of Neuroscience Tel-Aviv University

A specific motor action can lead to different sensory consequences, and a particular sensory consequence can be achieved by different motor actions. This non-unique mapping between actions and sensory consequences is context dependent and requires learning in order to optimize behavior. During my talk, I will describe behavioral and neuroimaging studies in humans, in which we examined how actions modulate perception and how perception can lead to motor skill learning even in the absence of voluntary movement. Manipulating the link between actions and their sensory consequences by using virtual reality, we explore various training techniques to facilitate learning in healthy subjects and rehabilitation in patients with hemiparesis due to neurological origin.

What the nose tells the brain

Lecture
Date:
Thursday, June 21, 2018
Hour: 12:30 - 13:30
Location:
Prof. Dmitry Rinberg
|
Dept of Neuroscience & Physiology NYU Neuroscience Institute

All living organisms extract chemical information from the surrounding world. We know a lot about the genetic, cellular, and anatomical organization of our sense of smell, which has similar organization from insects to mammals. However, we still do not know basic principles of odor coding, organization of the odor parameter space, and how odors are represented in the brain. In humans, odors are sensed by millions of receptor cells using ~350 types of receptor cells. Flies have 60 and mice ~1000 receptor types. An odor evokes a concentration-dependent spatial-temporal pattern of receptor cell activity. We are presented with an immensely complex combinatorial computation. And the central question of my research is to understand how these patterns are read by the brain. In this talk I will present our recent results on testing a novel model for concentration-invariant odor coding based on temporal ranking of receptor. And then I will discuss our attempt to build a theory of odor space representation in the brain based on this model.

Mechanisms of sparse coding in the dentate gyrus

Lecture
Date:
Tuesday, June 19, 2018
Hour: 12:30 - 13:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Dr. Heinz Beck
|
Institute of Experimental Epileptology and Cognition Research Life and Brain Center, University of Bonn Medical Center

Pages

All events, 2018

Learning probabilistic representations in randomly connected neural circuits

Lecture
Date:
Wednesday, August 29, 2018
Hour: 10:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Ori Maoz (PhD Thesis Defense)
|
Elad Schneidman Lab, Dept of Neurobiology, WIS

The brain represents and reasons probabilistically about complex stimuli and motor actions using a noisy, spike-based neural code. A key building block for such neural computations, as well as the basis for supervised and unsupervised learning, is the ability to estimate the surprise or likelihood of incoming high-dimensional neural activity patterns. Despite progress in statistical modeling of neural responses and deep learning, current approaches either do not scale to large neural populations or cannot be implemented using biologically realistic mechanisms. Inspired by the sparse and random connectivity of real neuronal circuits, we present a new model for neural codes that accurately estimates the likelihood of individual spiking patterns from the joint activities of actual populations of cortical neurons. The model has a straightforward, scalable, efficiently learnable, and realistic neural implementation as either a randomly connected neural circuit or as single neuron with a random dendritic tree. In the corresponding implementation, a neuron can take advantage of random connectivity leading to it in order to autonomously learn the respond with the surprise of its input patterns based on the previous observed patterns. Importantly, it can be achieved using a local learning rule that utilizes noise intrinsic to neural circuits. Slower, structural changes in random connectivity, consistent with rewiring and pruning processes occurring on developmental time scales, can further improve the efficiency and sparseness of the resulting neural representations. Our results merge insights from neuroanatomy, machine learning, and theoretical neuroscience to suggest random sparse connectivity as a key design principle for neuronal computation.

Catecholamines in the hippocampal formation

Lecture
Date:
Monday, August 13, 2018
Hour: 10:00 - 11:15
Location:
Gerhard M.J. Schmidt Lecture Hall
Sima Verbitsky (PhD Thesis Defense)
|
Menahem Segal Lab, Dept of Neurobiology, WIS

Monoaminergic (noradrenergic, dopaminergic and serotonergic) modulation of hippocampal activity is assumed to play a major role in neuronal plasticity, learning and memory. Understanding the locus of action of these neuromodulators at the cellular level will expand our knowledge of their nature and allow us to identify issues related to their dysfunction. In the present work I study the effects of norepinephrine (NE) and dopamine (DA) on spontaneous and evoked activity in patch-clamped neurons of hippocampal slices. Both DA and NE induced a significant decrease in the amplitude of the evoked PSCs recorded from CA1 pyramidal neurons in response to stimulation of the Schaffer collaterals, accompanied by a small decrease in the cell input resistance, and a small hyperpolarization. While decreasing the evoked PSCs, NE promoted an overall increase in spontaneous synaptic activity. Pharmacological assessment of these results indicated an α1 adrenergic receptor involvement in both the decrease of the amplitude of evoked PSCs as well as the increase in spontaneous activity. Surprisingly, the effect of NE on evoked PSCs was partially antagonized by D1 dopaminergic receptor antagonist SCH23390, which suggests that NE activates dopamine receptors. The effect of DA on evoked PSCs was blocked by α1 adrenergic receptor antagonist prazosin, which suggests that DA, in turn, is activating adrenergic receptors. Noradrenergic system is highly affected by stress; in particular, the differences between NE effects in dorsal and ventral hippocampus (DH and VH, respectively) have been shown to change in stressed animals. In this work I used two types of stress protocols – Prenatal Stress (PS) and Acute Stress (AS) – to study the effect of stress on monoamine responses in slices of DH and VH. In non-stressed rats, NE effect on the evoked PSCs is larger in DH than in VH. PS and AS rats increased NE effect in VH, thus abolishing the difference between DH and VH. Pharmacological data suggests that these differences result from differential efficiencies of α1 and D1 receptors between DH and VH of both control and PS rats. Acute stress reversed the difference between PS and control rats; in the AS slices the PSC reduction was significantly different between DH and VH of PS rats, and not in control rats. I conclude that stress increases the NE modulation in VH, but not in DH, thus increasing the role of emotional processing associated with the VH.

Regulation of the blood-cerebrospinal fluid barrier as a gateway for leukocyte trafficking in physiology and pathology

Lecture
Date:
Sunday, August 12, 2018
Hour: 15:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Alexander Kertser (PhD Thesis Defense)
|
Michal Schwartz Lab, Dept of Neurobiology, WIS

The role of TrpC2 channel in mediating social behavior of male mice within a group

Lecture
Date:
Wednesday, August 1, 2018
Hour: 14:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Yefim Pen (PhD Thesis Defense)
|
Tali Kimchi Lab, Dept of Neurobiology, WIS

Neural circuits for skilled forelimb movement

Lecture
Date:
Thursday, July 26, 2018
Hour: 11:00
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Eiman Azim
|
Molecular Neurobiology Laboratory Salk Institute for Biological Studies, La Jolla, CA

Movement shapes our interactions with the world, providing a means to translate intent into action. Among the wide repertoire of mammalian motor behaviors, the precise coordination of limb muscles to propel arms, hands and digits through space with speed and precision represents one of the more impressive achievements of the motor system. Skilled forelimb movements emerge from interactions between feedforward command pathways that induce muscle contraction and feedback systems that report and refine movement. Two broad classes of feedback modify motor output: one that originates in the periphery, and a second that is generated within the central nervous system itself. Yet the mechanisms by which these feedback pathways influence forelimb movement remain poorly understood. We take advantage of the genetic tractability of mice to examine the organization of motor circuits and define the ways in which these pathways enable dexterous behaviors. First, I will discuss recent studies that explore the transmission of proprioceptive and cutaneous signals from the forelimb into the spinal cord and brainstem, describing neural circuits that modulate the strength of this peripheral feedback and the implications of this sensory gain control for limb movement. Second, I will describe work exploring a diverse class of spinal interneurons that we hypothesize convey copies of forelimb motor commands as internal feedback to the cerebellum, enabling online predictions of motor outcome and reducing dependence on delayed sensory information. Through a complementary set of molecular, anatomical, electrophysiological and behavioral approaches, these findings are yielding insight into the organizational and functional logic of peripheral and internal feedback, and revealing how the circuits that convey feedback information help to orchestrate skilled behavior.

Human physiological and behavioral responses to olfactory stimuli in health and disease

Lecture
Date:
Tuesday, July 17, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Liron Rozenkrantz (PhD Thesis Defense)
|
Noam Sobel Lab, Dept of Neurobiology, WIS

In my PhD I led three projects probing human behavioral and physiological responses to olfactory stimuli in health and disease. In these projects I used every-day olfactory occurrences in order to infer on biological underpinnings of human behavior. In my main project I tested olfactory processing in autism, using the sniff response, a ten-minute non-verbal measure of respiratory response to odors. I found this objective measure to be profoundly altered in children with autism, and furthermore, to be highly correlated with autism severity. Using computational methods, I demonstrated 81% correct ASD classification based on differences in olfactory processing alone. These results provide proof-of-concept for a potential biomarker for autism (Rozenkrantz et al, Curr Bio, 2015). In a second and soon-to-be-submitted project, I investigated olfactory social communication in recurrent pregnancy loss (RPL), resting on a phenomenon in rodents in which females miscarry following exposure to bodily odors of non-stud males. I found that women with RPL display heightened social olfactory abilities, which were significantly correlated with number of miscarriages. Additionally, women with RPL showed significantly altered hormonal, physiological and neural responses to body odors of unfamiliar men. This project provides novel evidence for altered olfactory processing in human recurrent miscarriages. The third project is also my first foothold in placebo effect research, which I will pursue in my postdoc. Taking advantage of the non-invasive nature of olfactory stimuli, I used an odor as the placebo carrier, and tested two groups of subjects for different creativity tests. Both groups smelled the odor, but only the placebo group was told that it increases creativity (placebo manipulation). I found that following this simple manipulation, the placebo group displayed significantly enhanced creativity (Rozenkrantz et al., PLoS one, 2017). Taken together, these projects convey my deep interest in the interplay between human behavior and physiology.

Sensory processing across behavioral and neuromodulatory states

Lecture
Date:
Tuesday, July 3, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Dr. Yuval Nir
|
Sagol School of Neuroscience & Sackler School of Medicine Tel-Aviv University

"Sensory disconnection" – conditions when the same sensory stimulus does not reliably affect behavior or subjective experience - is a defining feature of sleep, and similar processes may occur during light anesthesia or during cognitive lapses in wakefulness. What are the changes in brain activity that mediate sensory disconnection? In a series of studies in humans and rodents, we investigate how "disconnected" states affect sensory processing. The first set of studies reveals differences in neuronal responses to identical sensory stimuli across states. We find that in humans, cognitive lapses after sleep deprivation involve attenuated and delayed single-neuron responses in MTL co-occurring with local slow/theta waves. In the auditory domain, we show in both rodents and humans that responses in sleep and light anesthesia are preserved up to A1, challenging the classic "thalamic gating" notion, but robust attenuation occurs later in high-level cortical regions. In addition, sleep affects more strongly responses that require integration over long time intervals, and responses to high-frequency content. The second set of studies investigates the underlying mechanisms, testing the potential role of locus coeruleus-noradrenaline (LC-NE) neuromodulation. In rats, we test how NE signaling affects the probability to wake up from sleep in response to sounds. We establish a new approach for selective in-vivo LC optogenetics by showing effects on spiking activity, evoked sleep-wake transitions, and pupil dilation. Combined LC and auditory stimulation synergistically increases the probability of awakenings beyond independent effects of sound and laser alone, supporting a role for LC-NE activity in mediating sensory responses. We also tested the effects of NE levels on sensory perception and sensory-evoked activity (EEG, fMRI) in awake humans. Pharmacologically manipulating NE levels in double-blind placebo-controlled experiments, we found that NE modulates sensitivity and accuracy of visual perception without significant effects on decision bias (criterion). In addition, NE increased the fidelity of late EEG visual responses, and selectively modulated BOLD fMRI responses in high-order visual cortex, suggesting that NE plays an enabling causal role in visual awareness by affecting late visual processing.

Neural networks mapping actions to their sensory consequences

Lecture
Date:
Tuesday, June 26, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Roy Mukamel
|
School of Psychological Sciences and Sagol School of Neuroscience Tel-Aviv University

A specific motor action can lead to different sensory consequences, and a particular sensory consequence can be achieved by different motor actions. This non-unique mapping between actions and sensory consequences is context dependent and requires learning in order to optimize behavior. During my talk, I will describe behavioral and neuroimaging studies in humans, in which we examined how actions modulate perception and how perception can lead to motor skill learning even in the absence of voluntary movement. Manipulating the link between actions and their sensory consequences by using virtual reality, we explore various training techniques to facilitate learning in healthy subjects and rehabilitation in patients with hemiparesis due to neurological origin.

What the nose tells the brain

Lecture
Date:
Thursday, June 21, 2018
Hour: 12:30 - 13:30
Location:
Prof. Dmitry Rinberg
|
Dept of Neuroscience & Physiology NYU Neuroscience Institute

All living organisms extract chemical information from the surrounding world. We know a lot about the genetic, cellular, and anatomical organization of our sense of smell, which has similar organization from insects to mammals. However, we still do not know basic principles of odor coding, organization of the odor parameter space, and how odors are represented in the brain. In humans, odors are sensed by millions of receptor cells using ~350 types of receptor cells. Flies have 60 and mice ~1000 receptor types. An odor evokes a concentration-dependent spatial-temporal pattern of receptor cell activity. We are presented with an immensely complex combinatorial computation. And the central question of my research is to understand how these patterns are read by the brain. In this talk I will present our recent results on testing a novel model for concentration-invariant odor coding based on temporal ranking of receptor. And then I will discuss our attempt to build a theory of odor space representation in the brain based on this model.

Mechanisms of sparse coding in the dentate gyrus

Lecture
Date:
Tuesday, June 19, 2018
Hour: 12:30 - 13:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Dr. Heinz Beck
|
Institute of Experimental Epileptology and Cognition Research Life and Brain Center, University of Bonn Medical Center

Pages

All events, 2018

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All events, 2018

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