Mason S T, Roberts D C, Fibiger H C
Psychopharmacology (Berl). 1978 Dec 15;60(1):53-7. doi: 10.1007/BF00429179.
Widespread depletion of forebrain noradrenaline, produced by the intracerebral injection of 4 microgram of 6-hydroxydopamine into the fibres of the dorsal noradrenergic bundle, potentiated the catalepsy induced by 20 mg/kg of morphine and severely attenuated the catalepsy induced by two separate cholinergic agonists, arecoline and pilocarpine. It did not, however, affect haloperidol catalepsy at any of the four doses tested. These results suggest that cholinergic catalepsy may be critically dependent on an intact noradrenergic substrate, perhaps through cholinergic receptors located either presynaptically on noradrenergic terminals or on the cell bodies of origin in the locus coeruleus. Noradrenaline appears to play a modulatory role in morphine catalepsy, although other sites of action must also be involved. Ascending noradrenergic systems do not appear to influence haloperidol catalepsy.
通过向去甲肾上腺素能背束纤维脑内注射4微克6-羟基多巴胺所产生的前脑去甲肾上腺素广泛耗竭,增强了20毫克/千克吗啡诱导的僵住症,并严重减弱了两种不同胆碱能激动剂槟榔碱和毛果芸香碱诱导的僵住症。然而,在所测试的四个剂量中的任何一个剂量下,它都不影响氟哌啶醇诱导的僵住症。这些结果表明,胆碱能僵住症可能严重依赖于完整的去甲肾上腺素能底物,可能是通过位于去甲肾上腺素能终末突触前或蓝斑核起源细胞体上的胆碱能受体。去甲肾上腺素似乎在吗啡诱导的僵住症中起调节作用,尽管也必定涉及其他作用位点。上行去甲肾上腺素能系统似乎不影响氟哌啶醇诱导的僵住症。