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.
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.
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.
During learning, one climbing fiber input instructs plasticity that is expressed in the simple-spike responses of cerebellar Purkinje cells, and causes neural learning that may inhibit future climbing fiber instructions.
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.