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.
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.
Two classes of premotor inhibitory neurons have specific roles in controlling flexor-extensor behaviors in mice, which is the underlying neural mechanism for limb driven movements in terrestrial vertebrates.