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The striatonigral fibres and the feedback control of dopamine metabolism1

  • I. F. Tulloch (a1), G. W. Arbuthnott (a1), A. K. Wright (a1), M. Garcia-Munoz (a1) and N. M. Nicolaou (a1)...
Synopsis

It proved possible to make lesions which interrupted the striatonigral GABA-containing pathway in the rat brain without causing concomitant damage to the nigrostriatal dopamine containing system. Estimations of striatal concentrations of dopamine (DA), dihydroxyphenyl-acetic acid (DOPAC) and homovanillic acid (HVA) indicated that these lesions had no influence either on normal striatal DA turnover or on the enhancement of DA turnover induced by neuroleptics. Behavioural experiments suggested a motor output function for the striatonigral pathway.

Copyright
COPYRIGHT: © Cambridge University Press 1978
Corresponding author
2Address for correspondence: Dr G. W. Arbuthnott, MRC Brain Metabolism Unit, 1 George Square, Edinburgh.
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1

This presentation is based largely on preliminary work already published as chapter 3 in Psychobiology of the Striatum which is edited by A. R. Cools, A. H. M. Lohman and J. H. L. Van Den Bercken, and published in 1977 by Elsevier/North Holland Biochemical Press to whom we are grateful for permission to reproduce the material. Since then, further work (to be published) has done nothing to modify the interpretation of the results, and recent experiments with kainic acid, which causes the destruction of cell bodies in the striatum without damage to the DA-containing terminals, led others to similar conclusions (Di Chiara et al. 1977).

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