TY - JOUR
T1 - Control of interneuron firing by subthreshold synaptic potentials in principal cells of the dorsal cochlear nucleus
AU - Apostolides, Pierre F.
AU - Trussell, Laurence O.
N1 - Funding Information:
We thank Michael Bateschell and Ruby Larisch for help with mouse colony management and Delia Chiu, Brett Carter, and members of the Trussell Lab for helpful discussions during the course of these experiments. Funding was provided by NIH grants R01DC004450 and R01NS28901 (L.O.T.) and 1F31DC012222 (P.F.A.)
PY - 2014/7/16
Y1 - 2014/7/16
N2 - 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 synapsesactivate 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.
AB - 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 synapsesactivate 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.
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U2 - 10.1016/j.neuron.2014.06.008
DO - 10.1016/j.neuron.2014.06.008
M3 - Article
C2 - 25002229
AN - SCOPUS:84902340609
SN - 0896-6273
VL - 83
SP - 324
EP - 330
JO - Neuron
JF - Neuron
IS - 2
ER -