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A model of activity-dependent anatomical inhibitory plasticity applied to the mammalian auditory system

A model of activity-dependent anatomical inhibitory plasticity applied to the mammalian auditory system
A model of activity-dependent anatomical inhibitory plasticity applied to the mammalian auditory system
We construct a model of activity-dependent, anatomical inhibitory plasticity. We apply the model to the mammalian auditory system. Specifically, we model the activity-dependent topographic refinement of inhibitory projections in the auditory brain stem, and we construct an anatomically abstract model of binaural band formation in the primary auditory cortex involving the segregation of different populations of inhibitory and excitatory afferents. Issues raised and predictions made include the nature of interactions between excitatory and inhibitory afferents innervating the same population of target cells, and the possibility that pharmacological manipulations of the developing primary auditory cortex might induce a shift in the periodicity of binaural bands. Any model of inhibitory plasticity must confront the issue of postulating mechanisms underlying such plasticity. In order to attempt to understand, at least theoretically, what the mechanisms underlying inhibitory plasticity might be, we propose the existence of a new class of neurotrophic factors that promote neurite outgrowth from and mediate competitive interactions between inhibitory afferents. We suppose that such factors are up-regulated by hyperpolarisation and down-regulated by depolarisation. Furthermore, we suppose that their activity-dependent release from target cells depends on Cl- influx. Such factors are therefore assumed to be the physiological inverse of such factors as nerve growth factor and brain-derived neurotrophic factor, which are up-regulated by depolarisation and down-regulated by hyperpolarisation, with their activity-dependent release depending on Na+, and not Ca2+, influx.
0340-1200
455-464
Elliott, T.
b4262f0d-c295-4ea4-b5d8-3931470952f9
Shadbolt, N.R.
5c5acdf4-ad42-49b6-81fe-e9db58c2caf7
Elliott, T.
b4262f0d-c295-4ea4-b5d8-3931470952f9
Shadbolt, N.R.
5c5acdf4-ad42-49b6-81fe-e9db58c2caf7

Elliott, T. and Shadbolt, N.R. (1998) A model of activity-dependent anatomical inhibitory plasticity applied to the mammalian auditory system. Biological Cybernetics, 78 (6), 455-464. (doi:10.1007/s004220050449).

Record type: Article

Abstract

We construct a model of activity-dependent, anatomical inhibitory plasticity. We apply the model to the mammalian auditory system. Specifically, we model the activity-dependent topographic refinement of inhibitory projections in the auditory brain stem, and we construct an anatomically abstract model of binaural band formation in the primary auditory cortex involving the segregation of different populations of inhibitory and excitatory afferents. Issues raised and predictions made include the nature of interactions between excitatory and inhibitory afferents innervating the same population of target cells, and the possibility that pharmacological manipulations of the developing primary auditory cortex might induce a shift in the periodicity of binaural bands. Any model of inhibitory plasticity must confront the issue of postulating mechanisms underlying such plasticity. In order to attempt to understand, at least theoretically, what the mechanisms underlying inhibitory plasticity might be, we propose the existence of a new class of neurotrophic factors that promote neurite outgrowth from and mediate competitive interactions between inhibitory afferents. We suppose that such factors are up-regulated by hyperpolarisation and down-regulated by depolarisation. Furthermore, we suppose that their activity-dependent release from target cells depends on Cl- influx. Such factors are therefore assumed to be the physiological inverse of such factors as nerve growth factor and brain-derived neurotrophic factor, which are up-regulated by depolarisation and down-regulated by hyperpolarisation, with their activity-dependent release depending on Na+, and not Ca2+, influx.

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Published date: July 1998
Organisations: Web & Internet Science

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Local EPrints ID: 252285
URI: https://eprints.soton.ac.uk/id/eprint/252285
ISSN: 0340-1200
PURE UUID: 504541e0-16b8-47f5-a084-65fff3a88c94

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Date deposited: 21 Jan 2000
Last modified: 20 Dec 2018 17:32

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