PROTEINS FUNCTIONING IN SYNAPTIC TRANSMISSION AT THE SENSORY TO MOTORSYNAPSE OF APLYSIA

Over expression of Aplysia synaptotagmin in acutely dissected choliner gic neurons from the buccal ganglia, or in primary co-cultures of glut aminergic sensory neurons and motor neurons, causes a reduction synapt ic transmission. Anti-sense oligonucleotide treatment of similar cultu res produced an enhancement of synaptic transmission. The interaction between Aplysia VAMP/synaptobrevin and syntaxin is reconstructed using the yeast two hybrid system, and used to identify amino acid residues of VAMP/synaptobrevin that are required for this interaction. Point m utations around residue 50, close to the site of cleavage by botulinum toxins specifically disrupt the interaction with syntaxin. An additio nal VAMP/synaptobrevin binding protein, VAP33, is identified using the yeast two hybrid system. Intracellular injection of VAP33 specific an tisera inhibits synaptic transmission in sensory-motor neuron co-cultu res.