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J Neurosci. 1990 Jun;10(6):1762-8.

Delayed, frequency-specific inhibition in the cochlear nuclei of mice: a mechanism for monaural echo suppression.

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Department of Neurophysiology, University of Wisconsin-Madison 53706.


To understand how auditory information is processed in the cochlear nuclei, it is crucial to know what circuitry exists and how it functions. Previous anatomical experiments have shown that neurons in the deep layer of the dorsal cochlear nucleus (DCN) project topographically to the anteroventral cochlear nucleus (AVCN) (Wickesberg and Oertel, 1988). Because interneurons in the DCN and their targets in AVCN are excited by the same group of auditory nerve fibers, the projection is frequency-specific. Here we report that microinjections of glutamate in the DCN evoke trains of IPSPs in individual, impaled AVCN neurons in brain slices of the cochlear nuclear complex. Only injections along a rostrocaudal band in the DCN, matching the anatomical projection of tuberculoventral neurons, evoke IPSPs; elsewhere, there were no responses to the glutamate. The inhibition is blocked by 0.5 microM strychnine. Both bushy and stellate cells are targets of the inhibitory projection. Inhibition in the AVCN is delayed by an additional synaptic delay with respect to the excitation. Delayed, frequency-specific inhibition allows the first wavefront to be transmitted to higher auditory centers by bushy and stellate cells, while following inputs encoding signals of similar frequencies are attenuated at least for the duration of an IPSP. These findings are consistent with results from psychoacoustic experiments and suggest that this circuit provides a source of monaural echo suppression.

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