Hearing research
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gamma-Aminobutyric acid (GABA), acting at GABA(A) receptors, mediates inhibition in inferior colliculus (IC) central nucleus (ICc) neurons and plays a prominent role in mediating acoustically evoked non-monotonicity, offset inhibition, and binaural inhibition, and is also important in tonic inhibition. The IC plays an important role in a number of pathophysiological conditions that involve hearing, including tinnitus, age-related hearing loss, and audiogenic seizures (AGS). AGS are a major form of rodent neurological disorder that can be genetically mediated and can also be readily induced in both young and mature animals. ⋯ AGS can be induced in normal animals by treatments that reduce the effectiveness of GABA in the IC. Glutamate-mediated excitation is a critical element of neurotransmission in IC neurons, and excessive activation of glutamate receptors in the IC is also strongly implicated as the other major mechanism in the pathophysiology of AGS. These neurotransmitter abnormalities result in excessive firing of ICc neurons that acts as the critical initiation mechanism for triggering seizures in response to intense acoustic stimuli.
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A model of the mammalian auditory-nerve neuron has been developed based on the classical work of Frankenhauser and Huxley [(1964) J. Physiol. 171, 302-315], modified by McNeal [(1976) IEEE Trans. Biomed. ⋯ Finally the results of the model are compared with behavioral data obtained from patients and monkeys implanted with cochlear prostheses. In the companion paper [(1987) Hear. Res. 31, 267-286] predictions of the model are quantitatively compared with single-neuron data from squirrel monkeys.