The mobilization or silencing of two heterogeneous pools of synaptic vesicles via different frequencies probably enables granule cell to Purkinje cell synapses to better discriminate between the high-rate code of sensory information and background noise.
Synaptic defects previously attributed to loss of kinesin function are found to be mediated by the Wnd/DLK axonal injury signaling pathway, which restrains the total levels of presynaptic proteins in response to their accumulation.
Discovery of the structural basis for recognition and uptake of a human precursor for body odour production reveals an important role for bacterial peptide transport and novel routes to prevent its production in humans.
A novel region in the CaV2.1 α1 subunit regulates coupling of synaptic vesicles to CaV2.1 calcium channels, synaptic vesicle release and docking, and the size of the fast and total releasable pools of synaptic vesicles.
In central synapses, the mobility and supply of synaptic vesicles are determined by two independent biological factors: the morphological and structural organization of nerve terminals and the molecular signature of vesicles.