Prof. Benedikt Berninger
Laboratory of Adult Neurogenesis and Cellular Reprogramming, Institute of Physiological Chemistry, University Medical Center Johannes Gutenberg University Mainz, Germany
Dr Benedikt Berninger is currently a professor of Physiological Chemistry at the University Medical Center of the University Mainz. Benedikt received his doctoral degree in 1996 at the Ludwig Maximilians University Munich for work on activity-dependent regulation of neurotrophin gene expression. He then joined the lab of Professor Mu-ming Poo as a postdoctoral fellow at the University of California San Diego to study fast actions of neurotrophins on synapses and growth cones. After a brief stay at the Karolinska Institute, Benedikt returned to Munich and eventually obtained a position as senior lecturer at the Ludwig Maximilians University Munich. In 2012 he received a call to the Johannes Gutenberg University of Mainz. The work of his laboratory focuses on lineage progression of adult neural stem cells, the functional integration of adult-generated neurons into pre-existing circuits, and on direct conversion of brain resident cells into induced neurons.
Ramón Bernabeu, PhD
Depto. de Fisiología e Instituto de Fisiología y Biofísica, Universidad de Buenos Aires, Argentina
Our laboratory study the mechanisms involved in the rewarding and relapsing properties of nicotine. We are particularly interested in understanding how nicotine, at individual and in social interactions, can modulate the reward systems to ultimately modify individual and/or group behavior. The focus of our research is to evaluate the behavioral effects of nicotine by using conditioned-place preference (CPP) task in zebrafish as a method to determine the rewarding properties of the drug. Using this behavioral task and a sensitization/tolerance model, we currently investigate, at pharmacological and neurochemical levels, the rewarding and relapsing effects of nicotine, as well as the individual vulnerability to the drug. Because the signals triggered by activation of second messengers cannot justify the maintenance of synaptic activity in long-term synaptic processes such as drug relapse, we focus our analysis in epigenetic factors involved in the rewarding and relapsing properties of nicotine, since recent studies showed evidence that the regulation of chromatin structure through posttranslational modifications of proteins that bind DNA and DNA methylation can mediate the long-term behavioral changes generated by drugs of abuse.
Veronica Bisagno, PhD
Instituto de Investigaciones Farmacológicas - ININFA .UBA-CONICET
Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Argentina
Our lab at the Instituto de Investigaciones Farmacologicas, ININFA, (CONICET-UBA), in Buenos Aires, Argentina, uses a wide variety of experimental approaches to understand how sensory and motor brain circuits in mammals adjust to drug intake, in particular psychostimulant drugs. We do this by integrating well-established behavioral models, with molecular and biochemical techniques and electrophysiological recordings. In the last few years, we have described various thalamocortical alterations induced by addictive (cocaine) and non-addictive (methylphenidate) psychostimulants in mice. In addition, we have also showed profound changes in areas of the meso-cortico-limbic system induced by other highly addictive psychostimulant (methamphetamine). Recently, we have described neuroprotective properties of another psychostimulant, modafinil, against methamphetamine-induced toxicity and cognitive deficits.
Hans Hofmann, PhD
Institute for Neuroscience, University of Texas at Austin, Austin, Texas, USA
Research in our laboratory seeks to answer these questions by utilizing a broad range of approaches to gain insight into the basic mechanisms underlying social and socially regulated behavior in a range of model systems, but most prominently in cichlid fishes. Our work has established an experimental and conceptual framework for understanding the molecular and neural basis of social behavior – and its evolution – in a naturalistic and organismal context. All animals continuously integrate their internal physiological state with environmental events and subsequently choose one action over another to increase their chances of survival and reproduction. These decisions are about obtaining and defending resources (such as food, shelter or mates) or evading danger (such as predator avoidance), and they often take place in a social context, such as dominance hierarchies, mate choice, and/or offspring care. Even though the survival value and evolution of behavioral decisions have been examined in great detail by behavioral ecologists, we are just now beginning to understand the neural and molecular mechanisms underlying these decision-making processes. As biologists have moved beyond the ultimately fruitless debates about the relative contributions of nature and nurture, we have come to understand that behavior – like all phenotypes – is the result of interactions between genetic, environmental, and developmental/epigenetic processes. At the same time, comparative studies have illuminated the behavioral, neural, and molecular underpinnings of behavior, suggesting that – similar to developmental and genetic systems – at least some of the mechanisms regulating behavior across multiple levels of biological organization are conserved in a wide range of species.
William Kristan, PhD
Section of Neurobiology, Division of Biological Sciences, La Jolla, USA
My colleagues and I determine how networks of nerve cells produce different behaviors, and how these neuronal networks are established during embryogenesis. We use physiological, anatomical, computational, and embryological techniques to characterize these circuits in the relatively tractable nervous system of the medicinal leech.
Rubèn López-Vales, PhD
Department of Cellular Biology, Physiology and Immunology, Institut de Neurociències Faculty of Medicine Universitat Autònoma de Barcelona, Barcelona, Spain
The overarching goal of his research is to study the contribution of inflammation to tissue damage after spinal cord injury, and to other neurological conditions such as multiple sclerosis and amyotrophic lateral sclerosis. In particular, the research lines they are currently working are: (l) To understand the molecular mechanisms that mediate the detrimental aspects of macrophage activation in the central nervous system. (ll) To assess the therapeutic effects of molecules that actively regulate the resolution programs of the inflammatory response in central nervous system disorders. (lll) To identify factors that could create an immune response that is conducive to both neuroprotection and regeneration after spinal cord injury
Antonia Marin-Burgin, PhD
Instituto de Investigación en Biomedicina de Buenos Aires-CONICET-Partner Institute of the Max Planck Society, Buenos Aires, Argentina
Our research group is interested in understanding how interactions among excitatory and inhibitory circuits leads to different patterns of activity associated with the representation of stimuli in the hippocampus.
The hippocampus is a brain area that is involved in a variety of functions. In particular, the formation of memory and the codification of space depend on the functioning of the hippocampus. Virtually all areas of the hippocampus, and of most parts of the brain, contain excitatory and inhibitory neurons that form individual microcircuits. It is in the interaction between excitatory and inhibitory circuits where appropriate functional responses arise. Also, the imbalance between excitation and inhibition has been associated with various pathologies from epilepsy to schizophrenia. While some patterns of connectivity between excitatory and inhibitory neurons are known, the functional dynamics of these connections is extremely important to understand how the same circuit can result in very different patterns of activity.
We use electrophysiology, anatomy, calcium imaging and optogenetics in order to study how information processing in hippocampal microcircuits leads to different patterns of activity associated with diverse cognitive processes, and evaluate the effects of the excitation / inhibition imbalance in the generation of pathologies.
Prof. Stéphane Oliet, PhD/em>
Physiopathologie de la plasticité neuronale, Neurocentre Magendie, INSERM, Université Bordeaux, Bordeaux, France
The focus of our research: Our group is investigating neuron-glia interactions with a particular interest for the tripartite synapse that considers astrocytes as active partners of chemical synapses. The ability of astrocytes to ensure neurotransmitter uptake and to release gliotransmitters and their impact on synaptic transmission and synaptic plasticity has raised a lot of attention, identifying astroglial cells as possible targets to generate new and effective therapeutic strategies for brain diseases. The general objective of our current research projects is to enhance our understanding of glial functions in healthy and diseased nervous system. We aim at characterize the impact of astrocytes on synaptic functions in physiological conditions as well as in the context of different pathologies like Alzheimer disease, multiple sclerosis, amyotrophic lateral sclerosis and addiction. To investigate glia-neurons interactions, we are using different physiological and pathological models in combination with the multidisciplinary approach available in our team like in vitro electrophysiology, morphological analysis, biochemical assays, state-of-the-art cell imaging and MRI. More specifically, we are interested in deciphering the cellular mechanisms underlying gliotrasmission from detecting synaptic
Alberto Pereda, MD, PhD
Dept. Neuroscience. Albert Einstein College of Medicine
New York, USA
Our laboratory is interested in the properties and dynamics of gap junction-mediated electrical transmission in the vertebrate brain. Because perhaps of the relative simplicity of transmission, electrical synapses are generally perceived as passive intercellular channels that lack dynamic control. While the study of plasticity of chemical synapses has long been an area of primary interest to neuroscientists, less is known about the modifiability of electrical synapses.
We investigate these dynamic properties in both mammalian and teleost (goldfish and larval zebrafish) electrical synapses. In contrast with mammalian electrical synapses that generally have limited experimental access, lower vertebrates have provided with advantageous experimental models in which basic properties of electrical transmission can be more easily study. This is the case of identifiable auditory afferents terminating on teleost Mauthner cells known as “Large Myelinated Club endings”. These endings are “mixed” (electrical and chemical) synaptic contacts that offer the rare opportunity to correlate physiological properties with molecular composition and specific ultrastructural features of individual synapses. Gap junctions at these model synapses undergo activity-dependent potentiation and are mediated by fish homologs of connexin 36, which is widely distributed across the mammalian brain.
Our current work focuses on the mechanisms underlying activity-dependent changes in electrical synapses by investigating: (l) Their functional relationship with glutamate receptors. (ll) Their interaction with the dopaminergic and endocannabinoid systems. (lll)The molecular mechanisms responsible for changes in the strength of electrical transmission, in particular the role of trafficking of gap junction channels and interactions with connexin-associated regulatory proteins. (lV) Interactions between intrinsic membrane properties and gap junctional conductance, as a mechanism for the control of the synaptic strength. Thus, while focusing in the properties of electrical synapses, the research of our laboratory explores the complexity of synaptic transmission and signaling mechanisms in general.