Saigusa T, Koshikawa N, Kitamura M, Mizutani K, Kobayashi M, Cools A R
Department of Pharmacology, Nihon University School of Dentistry, Tokyo, Japan.
Eur J Pharmacol. 1995 Feb 14;274(1-3):213-20. doi: 10.1016/0014-2999(94)00741-o.
Contralateral turning was produced by unilateral injection of carbachol (0.5, 2.5, 5 micrograms) into the nucleus accumbens, but not into the dorsal or ventral striatum. This behaviour was inhibited by muscarinic M1 acetylcholine receptor blockade in the nucleus accumbens, and less effectively by blockade of muscarinic M2 and nicotinic acetylcholine receptors. Unilateral injection of a mixture of the dopamine D1 receptor agonist 1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine-7,8-diol (SKF 38393, 5 micrograms) and the dopamine D2 receptor agonist quinpirole (10 micrograms) 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 D1 or D2 receptor blockade (8-chloro-2,3,4,5-tetrahydro-3-methyl-5-phenyl-1H-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 D1 and D2 receptors in the ipsilateral, but not contralateral, ventrolateral striatum.
向伏隔核单侧注射卡巴胆碱(0.5、2.5、5微克)可引起对侧转身,但向背侧或腹侧纹状体注射则不会。伏隔核中的毒蕈碱M1型乙酰胆碱受体阻断可抑制这种行为,而毒蕈碱M2型和烟碱型乙酰胆碱受体阻断的抑制效果则较差。向伏隔核单侧注射多巴胺D1受体激动剂1-苯基-2,3,4,5-四氢-1H-3-苯并氮杂卓-7,8-二醇(SKF 38393,5微克)和多巴胺D2受体激动剂喹吡罗(10微克)的混合物也可引起对侧转身。然而,其步行动作模式与卡巴胆碱诱导的完全不同。多巴胺D1或D2受体阻断(分别为8-氯-2,3,4,5-四氢-3-甲基-5-苯基-1H-3-苯并氮杂卓-7-醇(SCH 23390)和左旋舒必利)可减少伏隔核中卡巴胆碱诱导的转身次数。然而,减少是由于转身模式的改变。伏隔核中毒蕈碱型乙酰胆碱受体阻断不会改变向伏隔核单侧注射多巴胺受体激动剂所诱导的对侧转身。结果表明,尽管多巴胺受体阻断引发了与卡巴胆碱诱导的转身相竞争的行为缺陷,但所涉及的胆碱能和多巴胺能底物之间不存在功能相互作用。向伏隔核注射卡巴胆碱所引发的对侧转身需要同侧腹外侧纹状体中多巴胺D1和D2受体水平的多巴胺活性完整,但对侧则不需要。