Molecular mechanisms in neurosecretion

Molecular mechanisms of exocytosis in a neuroendocrine model: the involvement of cytoskeleton and SNARE complex proteins:
Adrenomedullary chromaffin cells have been used as an excellent experimental model to study the exocytosis and therefore the molecular mechanisms of neurotransmission. It is now clear that the proteins involved in the processes of vesicle docking, membrane fusion and neurotransmitter release are common to many cellular systems (SNARE hypothesis). Our research interest is focused in two different aspects of the molecular mechanisms of neurotransmission: Implication of molecular motors such myosin-actin in vesicle transport during neurosecretion and the determination of essential aminoacids of synaptobrevin or SNAP-25 implicated in the process of membrane fusion. We coined the term “Molecular cytoarchitecture of exocytosis” to define the interaction between SNARE proteins, calcium channel and lately nicotinic receptors (integrating Dr. Criado main line) and the cohesive F-actin cortical network in order to improve secretory efficiency.
Experimental approaches involve strategies using antibodies, sequence peptide design and protein overexpression that demonstrate the participation of specific protein domains in exocytosis. In addition, the role of these proteins on the secretory stages have been studied using amperometry, technique that resolves single fusion events, and high resolution fluorescence microscopy. Lately, the description of the mechanisms used by signaling lipids to increase SNARE activity has allowed us to gain insights into the possible design of strategies for the treatment of excitotoxic neurodegenerative syndromes.