Calcium channel modulation as an all-purpose mechanism for short-term synaptic plasticity.
The paper by Mochida et al. in this issue of Neuron proposes that synaptic facilitation, depression, and augmentation all arise from calcium-dependent regulation of calcium channels in the presynaptic terminal. Their proposal provides a unifying explanation for several forms of short-term presynaptic plasticity.
Cheng
Qing
Q
Department of Neurobiology, Duke University Medical Center, Box 3209, Durham, NC 27710, USA.
Augustine
George J
GJ
D000818:Animals; D015220:Calcium Channels / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D013569:Synapses / Q000502:physiology*
D015220:Calcium Channels