期刊
NEURON
卷 83, 期 2, 页码 324-330出版社
CELL PRESS
DOI: 10.1016/j.neuron.2014.06.008
关键词
-
资金
- NIH [R01DC004450, R01NS28901, 1F31DC012222]
Voltage-gated ion channels amplify, compartmentalize, and normalize synaptic signals received by neurons. We show that voltage-gated channels activated during subthreshold glutamatergic synaptic potentials in a principal cell generate an excitatory -> inhibitory synaptic sequence that excites electrically coupled interneurons. In fusiform cells of the dorsal cochlear nucleus, excitatory synapses activate a TTX-sensitive Na+ conductance and deactivate a resting I-h conductance, leading to a striking reshaping of the synaptic potential. Subthreshold voltage changes resulting from activation/deactivation of these channels subsequently propagate through gap junctions, causing slow excitation followed by inhibition in GABAergic stellate interneurons. Gap-junction-mediated transmission of voltage-gated signals accounts for the majority of glutamatergic signaling to interneurons, such that subthreshold synaptic events from a single principal cell are sufficient to drive spikes in coupled interneurons. Thus, the interaction between a principal cell's synaptic and voltage-gated channels may determine the spike activity of networks without firing a single action potential.
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