{"id":25270,"date":"2025-01-30T15:23:51","date_gmt":"2025-01-30T14:23:51","guid":{"rendered":"https:\/\/idibell.cat\/en\/?post_type=agenda&p=25270"},"modified":"2025-01-30T15:23:51","modified_gmt":"2025-01-30T14:23:51","slug":"facultyseminar-the-presynaptic-dimension-of-brain-pathologies-munc13-1-and-complexin-and-their-control-over-synaptic-dysfunction","status":"publish","type":"agenda","link":"https:\/\/idibell.cat\/en\/agenda\/facultyseminar-the-presynaptic-dimension-of-brain-pathologies-munc13-1-and-complexin-and-their-control-over-synaptic-dysfunction\/","title":{"rendered":"#Facultyseminar: The presynaptic dimension of brain pathologies: Munc13-1 and Complexin and their control over synaptic (dys)function"},"content":{"rendered":"

The proper functioning of the nervous system relies on fast and efficient neurotransmission at synapses, the communication junctions between nerve cells. Synapses control brain demands by modulating their strength and plasticity, a process that hinges on the specific molecular composition and regulation of the neurotransmitter release and reception machinery. These specialized properties vary between synapses and play a critical role in defining their unique functions. Understanding the distinct molecular mechanisms underlying synapse-specific machinery is essential for uncovering the roots of synaptopathies\u2014neurodevelopmental syndromes that arise from dysfunctions in particular synapse populations.<\/p>\n

Our research focuses on two key proteins: complexin-1 and Munc13-1, both integral components of the core neurotransmitter release machinery. We investigate how specific synapses in the hippocampus, cerebellum, and brainstem respond to critical mutations or knockouts of these proteins. By studying the resulting presynaptic dysfunctions, we aim to uncover their impact on brain microcircuit activity and provide insights into the mechanisms driving synaptopathy.<\/p>\n

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