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.