Nature Neuroscience7, 719 - 725 (2004)
Published online: 20 June 2004; | doi:10.1038/nn1272
Cell-specific, spike timing−dependent plasticities in the dorsal cochlear nucleus
Thanos Tzounopoulos1, Yuil Kim1, Donata Oertel2
& Laurence O Trussell1
1
Oregon Hearing Research Center and Vollum Institute, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, Oregon 97239, USA.
2
Department of Physiology, University of Wisconsin Medical School, 1300 University Ave., Madison, Wisconsin 53706, USA.
Correspondence should be addressed to Thanos Tzounopoulos tzounopo@ohsu.edu
In the dorsal cochlear nucleus, long-term synaptic plasticity can be induced at the parallel fiber inputs that synapse onto both fusiform principal neurons and cartwheel feedforward inhibitory interneurons. Here we report that in mouse fusiform cells, spikes evoked 5 ms after parallel-fiber excitatory postsynaptic potentials (EPSPs) led to long-term potentiation (LTP), whereas spikes evoked 5 ms before EPSPs led to long-term depression (LTD) of the synapse. The EPSP-spike protocol led to LTD in cartwheel cells, but no synaptic changes resulted from the reverse sequence (spike-EPSP). Plasticity in fusiform and cartwheel cells therefore followed Hebbian and anti-Hebbian learning rules, respectively. Similarly, spikes generated by summing EPSPs from different groups of parallel fibers produced LTP in fusiform cells, and LTD in cartwheel cells. LTD could also be induced in glutamatergic inputs of cartwheel cells by pairing parallel-fiber EPSPs with depolarizing glycinergic PSPs from neighboring cartwheel cells. Thus, synaptic learning rules vary with the postsynaptic cell, and may require the interaction of different transmitter systems.
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