A MATHEMATICAL-MODEL OF ACTIVITY-DEPENDENT, ANATOMICAL SEGREGATION INDUCED BY COMPETITION FOR NEUROTROPHIC SUPPORT

Citation
T. Elliott et Nr. Shadbolt, A MATHEMATICAL-MODEL OF ACTIVITY-DEPENDENT, ANATOMICAL SEGREGATION INDUCED BY COMPETITION FOR NEUROTROPHIC SUPPORT, Biological cybernetics, 75(6), 1996, pp. 463-470
Citations number
68
Categorie Soggetti
Computer Science Cybernetics",Neurosciences
Journal title
ISSN journal
03401200
Volume
75
Issue
6
Year of publication
1996
Pages
463 - 470
Database
ISI
SICI code
0340-1200(1996)75:6<463:AMOAAS>2.0.ZU;2-7
Abstract
Mathematical or computational models of activity-dependent neural comp etition typically impose competition in anatomically fixed networks by the use of synaptic normalisation, for which there is very little exp erimental support. Recent experimental evidence, however, strongly imp licates neurotrophic factors in neural plasticity and competition, in addition to their well-known potent effects on neurite outgrowth and s ynaptogenesis. We therefore present a simple, mathematical model of an atomical segregation induced by activity-dependent competition for a l imited supply of a neurotrophic factor provided by target cells to aff erents. We extract the behaviour of the model in various regimes, in w hich the neurotrophic factor is either in critical supply or in abunda nt supply, by a combination of analytical and numerical methods, and s tudy the effects of correlations in afferent inputs on competition. We apply the model to three different systems: ocular dominance column f ormation; elimination of polyneuronal innervation at the vertebrate ne uromuscular junction; trigeminal brain stem whisker-related structure formation. Several classes of related predictions emerge, including th e prediction that kittens reared with strabismus should require a high er concentration of neurotrophic factor infusion into their primary vi sual cortex than normally reared cats in order to induce the anatomica l desegregation of ocular dominance columns. We also speculate on the mechanisms of support of inhibitory rather than excitatory neurons, an d suggest the existence of a separate, Cl--mediated activity-dependent pathway for their neurotrophic support.