Intraperitoneal injection of 1.0 mg/kg (-)-scopolamine hydrobromide had no effect upon the firing rate of caudate-putamen neurones recorded in immobilized, locally anaesthetized rats, although the pattern of their spike trains over time was somewhat altered. Pretreatment of animals with this same dose of scopolamine, but not with 1.0 mg/kg (-)-scopolamine methyl bromide, transformed the normally biphasic response of caudate-putamen neurones to 2.5 mg/kg (+)-amphetamine into a response consisting of only a depression of firing rate. A less common response of caudateputamen neurones to amphetamine, a prolonged increase in firing rate, was unaffected by scopolamine pretreatment. The transient initial potentiation of activity seen in most caudate-putamen neurones to precede the amphetamine-induced depression of unit activity therefore appears to require the activity of a central muscarinic receptor. The results are discussed in relation to the interaction of dopaminergic and cholinergic systems in the striatum.
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience