Strömbom U, Svensson T H
J Neural Transm. 1980;47(1):29-39. doi: 10.1007/BF01256637.
Administration of clonidine, 0.05 mg/kg i.p. to mice 30 min before trial significantly depressed the exploration of a Y-maze. This effect was completely antagonized by 1-amphetamine, 0.75 mg/kg i.p., given 10 min before trial, which by itself did not change the behaviour studied. The clonidine-induced behavioural depression also appeared reduced after pretreatment with desipramine (10 mg/kg i.p., 30 min before clonidine) which, like l-amphetamine, by itself was inactive. The above treatment with clonidine significantly reduced the accumulation of dopa after inhibition of central aromatic L-amino acid decarboxylase both in the noradrenaline (NA) rich neocortex and the dopamine-rich neocortex and the dopamine-rich corpus striatum, whereas the dopa accumulation in the limbic brain regions was not significantly affected. l-Amphetamine, 0.75 mg/kg i.p., did not by itself significantly affect the dopa accumulation, but reduced the clonidine-induced effects. The results are compatible with the notion that the depression of exploratory behaviour by clonidine is related to impaired central NA-neurotransmission and rule out the possibility that it is due to activation of central post-synaptic NA-(alpha-)-receptors.
在试验前30分钟给小鼠腹腔注射0.05毫克/千克可乐定，显著抑制了其在Y迷宫中的探索行为。在试验前10分钟腹腔注射0.75毫克/千克的1-苯丙胺可完全拮抗这种作用，而1-苯丙胺本身并未改变所研究的行为。在用去甲丙咪嗪（在注射可乐定前30分钟腹腔注射10毫克/千克）预处理后，可乐定诱导的行为抑制也似乎有所减轻，去甲丙咪嗪与1-苯丙胺一样，本身没有活性。上述可乐定处理显著降低了在抑制中枢芳香族L-氨基酸脱羧酶后，去甲肾上腺素（NA）丰富的新皮层、多巴胺丰富的新皮层以及多巴胺丰富的纹状体中多巴的积累，而边缘脑区中多巴的积累未受到显著影响。腹腔注射0.75毫克/千克的1-苯丙胺本身并未显著影响多巴的积累，但减轻了可乐定诱导的效应。这些结果与以下观点一致，即可乐定对探索行为的抑制与中枢NA神经传递受损有关，并排除了其是由于中枢突触后NA-α受体激活所致的可能性。
