Frontal decortication and adaptive changes in striatal cholinergic neurons in the rat

Silvana Consolo, Maria Sieklucka, Francesco Fiorentini, Gianluigi Forloni, Herbert Ladinsky

Research output: Contribution to journalArticlepeer-review

Abstract

Interruption of the corticostriatal pathway by undercutting the cortex resulted in a reduction of glutamate uptake by 55% and in a depression of acetylcholine (ACh) synthesis by 30% in striatum after two postlesion weeks without affecting the content of ACh and choline, the specific binding of [3H]dexetimide to muscarinic receptors, the activity of choline acetyltransferase and the levels of noradrenaline, serotonin, dopamine and 3,4-dihydroxyphenylacetic acid. The influence of this excitatory pathway on striatal cholinergic neuropharmacology was investigated. It was found that the effect of a number of agonists (R-apomorphine, bromocriptine, lisuride, quinpirole, JL-14389, 2-chloroadenosine, oxotremorine and methadone), capable of depressing cholinergic activity in the striatum through receptor-mediated responses - reflected as an increase in ACh content - is operative only when the corticostriatal pathway is intact. By contrast, antagonists capable of decreasing ACh content, i.e. the typical neuroleptics pimozide, haloperidol and the atypical ones clozapine, l-sulpiride, as well as the anti-muscarinic agent scopolamine, were not influenced by the lesion. The possibility that the lesion non-specifically damaged striatal cells on which the agonists, but not the antagonists acted was excluded by results showing, firstly, that the increase in striatal ACh elicited by the ACh precursor, choline, was not blocked by decortication, and secondly, that the degeneration of the corticostriatal neurons did not prevent the ACh-increasing effect of bromocriptine, a long-acting ergot alkaloid, when sufficient time was allowed for the drug to act. It was furthermore possible to restore the inhibitory action of apomorphine of cholinergic neurons either by short-term chemical lesion of the nigrostriatal dopaminergic input or by the administration of choline. The results suggest that the deafferentiated cholinergic neurons, being already inhibited by the loss of the excitatory input, cannot further be depressed by drugs that slow down their activity and their ACh turnover rate. Finally, some comments on the relationship between the dopaminergic, cholinergic and excitatory inputs in the striatum will be given.

Original languageEnglish
Pages (from-to)128-134
Number of pages7
JournalBrain Research
Volume363
Issue number1
DOIs
Publication statusPublished - Jan 15 1986

Keywords

  • acetylcholine
  • apomorphine
  • bromocriptine
  • choline
  • corticostriatal pathway
  • decortication
  • neuroleptic
  • nigrostriatal pathway
  • rat
  • striatum

ASJC Scopus subject areas

  • Developmental Biology
  • Molecular Biology
  • Clinical Neurology
  • Neuroscience(all)

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