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Neuron. 2014 Jul 16;83(2):324-330. doi: 10.1016/j.neuron.2014.06.008. Epub 2014 Jul 4.

Control of interneuron firing by subthreshold synaptic potentials in principal cells of the dorsal cochlear nucleus.

Author information

1
Neuroscience Graduate Program, Oregon Health & Science University, Portland, OR 97239, USA; Vollum Institute & Oregon Hearing Research Center, Oregon Health & Science University, Portland, OR 97239, USA.
2
Vollum Institute & Oregon Hearing Research Center, Oregon Health & Science University, Portland, OR 97239, USA. Electronic address: trussell@ohsu.edu.

Abstract

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 Ih 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.

PMID:
25002229
PMCID:
PMC4185201
DOI:
10.1016/j.neuron.2014.06.008
[Indexed for MEDLINE]
Free PMC Article

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