The Journal of Neuroscience, September 17, 2008, 28(38):9440-9450; doi:10.1523/JNEUROSCI.2226-08.2008
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Cellular/Molecular
Fidelity of Complex Spike-Mediated Synaptic Transmission between Inhibitory Interneurons
Michael T. Roberts,
Kevin J. Bender, and
Laurence O. Trussell
Vollum Institute and Oregon Hearing Research Center, Oregon Health & Science University, Portland, Oregon 97239
Correspondence should be addressed to Laurence O. Trussell, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, L335A, Portland, OR 97239. Email: trussell{at}ohsu.edu
Complex spikes are high-frequency bursts of Na+ spikes, often riding on a slower Ca2+-dependent waveform. Although complex spikes may propagate into axons, given their unusual shape it is not clear how reliably these bursts reach nerve terminals, whether their spikes are efficiently transmitted as a cluster of postsynaptic responses, or what function is served by such a concentrated postsynaptic signal. We examined these questions by recording from synaptically coupled pairs of cartwheel cells, neurons which fire complex spikes and form an inhibitory network in the dorsal cochlear nucleus. Complex spikes in the presynaptic soma were reliably propagated to nerve terminals and elicited powerful, temporally precise postsynaptic responses. Single presynaptic neurons could prevent their postsynaptic partner from firing complex but not simple spikes, dramatically reducing dendritic Ca2+ signals in the postsynaptic neuron. We suggest that rapid transmission of complex spikes may control the susceptibility of neighboring neurons to Ca2+-dependent plasticity.
Key words: complex spike; synaptic transmission; interneuron; cochlear nucleus; electrophysiology; calcium imaging
Received May 16, 2008;
revised July 15, 2008;
accepted Aug. 12, 2008.
Correspondence should be addressed to Laurence O. Trussell, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, L335A, Portland, OR 97239. Email: trussell{at}ohsu.edu
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