Abstract

Contralateral turning was produced by unilateral injection of carbachol (0.5, 2.5, 5 μg) into the nucleus accumbens, but not into the dorsal or ventral striatum. This behaviour was inhibited by muscarinic M 1 acetylcholine receptor blockade in the nucleus accumbens, and less effectively by blockade of muscarinic M 2 and nicotinic acetylcholine receptors. Unilateral injection of a mixture of the dopamine D 1 receptor agonist 1-phenyl-2,3,4,5-tetrahydro-1 H-3-benzazepine-7,8-diol (SKF 38393, 5 μg) and the dopamine D 2 receptor agonist quinpirole (10 μg) also produced contralateral turning. The stepping pattern, however, completely differed from that induced by carbachol. The number of carbachol-induced turnings was reduced by dopamine D 1 or D 2 receptor blockade (8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1 H-3-benzazepine-7-ol (SCH 23390) and l-sulpiride, respectively) in the nucleus accumbens. However, the reduction was due to a change in the turning pattern. Blockade of muscarinic acetylcholine receptors in the nucleus accumbens did not change the contralateral turning induced by unilateral injection of dopamine receptor agonists into the nucleus accumbens. The results demonstrate that there is no functional interaction between the cholinergic and dopaminergic substrates involved, although blockade of the dopamine receptors elicited behavioural deficits that competed with the turning elicited by carbachol. The contralateral turning elicited by carbachol injection into the nucleus accumbens requires an intact dopamine activity at the level of dopamine D 1 and D 2 receptors in the ipsilateral, but not contralateral, ventrolateral striatum.

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