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.
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.
Synaptophysins and gyrins dampen synaptic strength selectively at low frequencies, hinting that synaptic transmission may play a frequency filtering role in biological computation that is more general than currently envisioned.
Behaviorally-driven expression of the immediate early gene transcription factor NPAS4 changes local circuit connectivity and short-term plasticity by selectively recruiting CCK basket cell synapses to pyramidal neuron somas.
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.