Srijeda, 14. rujna 2017. u 11 sati profesori sa Leibniz Institute for Neurobiology (Magdeburg, Njemačka) održati će znanstvena predavanja
Dragi kolegice i kolege, dragi studenti, pozivamo vas na znanstvena predavanja koja će se održati
u četvrtak, 14. rujna 2017. u 11.00 sati
u seminarskoj dvorani u prizemlju Hrvatskog instituta za istraživanje mozga.
Predavanja će održati znanstvenici s Leibniz Institute for Neurobiology (Magdeburg, Njemačka):
11.00 – 11.45 Prof. Dirk Montag – A Gene-switch for memories: neuroplastin ablation causes retrograde amnesia and cognitive deterioration
11.45 – 12.30 Dr. Rodrigo Herrera-Molina – Past, Present and Future of the Cell adhesion molecule neuroplastin
Radujemo se vašem dolasku i diskusiji!
Sažeci predavanja
Dirk Montag, Leibniz Institute for Neurobiology, Magdeburg, Germany
A Gene-switch for memories: neuroplastin ablation causes retrograde amnesia and cognitive deterioration
Neuron-type-specific neuroplastin ablation empowers the investigation of circuit-coded learning and memory and its relation to cognitive deterioration. The inducible neuroplastin-deficient mouse model, achieving experimental induction of retrograde amnesia genetically, provides new means to analyze the molecular and cellular mechanisms underlying retrograde amnesia and memory.
Rodrigo Herrera-Molina, Leibniz Institute for Neurobiology, Magdeburg, Germany
Past, Present and Future of the Cell adhesion Molecule Neuroplastin
Thirty years ago, the two main isoforms of the cell adhesion molecule neuroplastin were characterized as abundant glycoproteins in synaptic membrane fractions derived from rodent brains. Since then, studies in our laboratories in Magdeburg have revealed that neuroplastins are of great importance for architecture and function of the brain as they are crucially involved in neuronal plasticity, balance of excitatory/inhibitory synapse ratio, GABAergic transmission, and circuit activity commanding particular behaviors. Further, the finding of a number of binding partners of neuroplastin including subunits of the GABAA receptor, Plasma Membrane Calcium ATPase, and the tumor necrosis factor receptor-associated factor 6 has opened the exploration of molecular mechanisms involved in formation and stabilization of synapses, synaptic transmission and plasticity as well as calcium homeostasis all of them fundamental for the physiology of different neuron types. We propose that alteration of neuroplastin-partners function could underlie severe neurological and neurodegenerative conditions.