Genetic and electrophysiological experiments define how homeostatic signaling stabilizes both the gain and short-term dynamic properties of neurotransmitter release, ensuring that synaptic information transfer remains robust to external perturbation.
Genetic and electrophysiology experiments provide the first direct evidence that protein kinase C is a calcium-sensing protein in post-tetanic potentiation, a form of synaptic plasticity that supports short-term memory.
Heterogeneous distances between vesicles and Ca2+-channels make synapses prone to short-term depression, however, Ca2+-dependent increases in the number of release-ready vesicles supports facilitation even with broadly distributed vesicle:Ca2+-channel distances.
MCTP is a novel presynaptic calcium sensor, resident within the endoplasmic reticulum, that is required for normal baseline neurotransmission, short-term synaptic plasticity and presynaptic homeostatic plasticity.
A characterization of LGN-V1 synaptic transmission properties demonstrates thalamocortical synapses in vivo are weak and unreliable, but biologically constrained models show they efficiently drive cortex.
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.
Modulation of the energy barrier for membrane fusion is a common mechanism by which sensors in the synapse produce supralinear calcium dependence of vesicle release and short-term synaptic potentiation.