Effects of Amplitude Modulation on the Coding of Interaural Time Differences of Low-Frequency Sounds in the Inferior Colliculus. II. Neural Mechanisms

Department of Neuroscience, University of Connecticut Health Center, Farmington, Connecticut 06030 Submitted 20 March 2003; accepted in final form 25 July 2003 In our companion paper, we reported on interaural time difference (ITD)-sensitive neurons that enhanced, suppressed, or did not change their...

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Veröffentlicht in:Journal of neurophysiology 2003-11, Vol.90 (5), p.2827-2836
Hauptverfasser: D'Angelo, W. R, Sterbing, S. J, Ostapoff, E.-M, Kuwada, S
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Sprache:eng
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Zusammenfassung:Department of Neuroscience, University of Connecticut Health Center, Farmington, Connecticut 06030 Submitted 20 March 2003; accepted in final form 25 July 2003 In our companion paper, we reported on interaural time difference (ITD)-sensitive neurons that enhanced, suppressed, or did not change their response when identical AM was added to both ears. Here, we first examined physical factors such as the difference in the interaural correlation, spectrum, or energy between the modulated and unmodulated signals. These were insufficient to explain the observed enhancement and suppression. We then examined neural mechanisms by selectively modulating the signal to each ear, varying modulation depth, and adding background noise to the unmodulated signal. These experiments implicated excitatory and inhibitory monaural inputs to the inferior colliculus (IC). These monaural inputs are postulated to adapt to an unmodulated signal and adapt less to a modulated signal. Thus enhancement or suppression is created by the convergence of these excitatory or inhibitory inputs with the inputs from the binaural comparators. Under modulation, the role of the monaural input is to shift the threshold of the IC neuron. Consistent with this role, background noise mimicked the effect of modulation. Functionally, enhancement and suppression may serve in detecting the degree of modulation in a sound source while preserving ITD information. Address for reprint requests and other correspondence: S. Kuwada Dept. of Neuroscience, University of Connecticut Health Center, 263 Farmington Ave., Farmington, CT 06030 (E-mail: shig{at}neuron.uchc.edu ).
ISSN:0022-3077
1522-1598
DOI:10.1152/jn.00269.2003