The synaptomatrix: a solid though dynamic contact disconnecting transmissions from exocytotic events.

The vesicular hypothesis originally introduced to explain the quantal nature of presynaptic neurotransmitter (NT) release has been initially confirmed by the presence of NT within presynaptic vesicles and by an exo-endocytotic traffic associated with intense synaptic activity. Since then, an increasing number of synaptic transmission properties cannot be readily incorporated into the now popular model in which each quantal NT packet is prepared in a vesicle and is released by diffusion across the synaptic cleft when this vesicle fuses transiently or definitively with the plasma membrane. Interestingly, presynaptic exocytosis exhibits the characteristics of the ubiquitous secretory pathway by which all eukaryotic cells interact with their immediate environment, not just externalizing soluble products, but principally delivering at particular location of the cell surface specific glycoconjugates constituting the extracellular matrix (ECM) that mediates intercellular adhesion, recognition and signaling.

SV2 frustrating exocytosis at the semi-diffusor synapse.

Presynaptic exocytosis is the mechanism commonly believed to release transmitters by diffusion through a pore opening during vesicular membrane fusion with the plasmalemma, but evidence suggesting that exocytosis and transmitter release are two separate steps of synaptic transmission is accumulating. Vesicular glycoconjugates such as Synaptic Vesicle Protein 2 (SV2) proteoglycans and gangliosides retain transmitters in a nondiffusible form and are transported to the synaptic cleft where they contribute forming a dense synaptomatrix. Transmitters are permanently present in synaptic clefts and readily releasable transmitter is easily accessible from the outer side of the presynaptic membrane suggesting that synaptomatrix glycoconjugates prevent immediate release after PKC-dependent exocytosis.

Ocsyn and mitochondrial-canalicular complexes in vestibular hair cells.

Ocsyn, a syntaxin-interacting protein characterized by Safieddine et al. [Safieddine, S., Ly, C.

Presynaptic quantal plasticity: Katz's original hypothesis revisited.

Changes in the amplitudes of signals conveyed at synaptic contacts between neurons underlie many brain functions and pathologies. Here we review the possible determinants of the amplitude and plasticity of the elementary postsynaptic signal, the miniature. In the absence of a definite understanding of the molecular mechanism releasing transmitters, we investigated a possible alternative interpretation.