Persson S A
Psychopharmacology (Berl). 1978 Oct 31;59(2):113-6. doi: 10.1007/BF00427743.
In the rat, lysergic acid diethylamide (LSD) 0.5 mg/kg and 2-bromo lysergic acid diethylamide (BOL) 0.5 mg/kg increased the rate of the striatal in vivo tyrosine hydroxylation as measured by the DOPA accumulation after decarboxylase inhibition. Neither LSD nor BOL significantly changed the DOPA accumulation in the olfactory tubercle, a dopamine-rich part of the limbic system. LSD but not BOL increased the DOPA accumulation in the cerebral cortex and in the brain stem. LSD and BOL appeared not to alter the rate of alpha-MT-induced disappearance of DA or of NA in the whole brain, nor did they change the rate of the alpha-MT-induced disappearance of DA in the striatum. It is suggested that in the striatum LSD and BOL block autoreceptorss (presynaptic receptors) regulating the tyrosine hydroxylation. These receptors may be DA receptor, but may also be 5-HT- or LSD-sensitive receptors. The regional differences observed between LSD and BOL suggest that LSD in the cerebral cortex and in the brain stem increases the DOPA accumulation by mechanism other than that functioning in the striatum. One possible explanation is that LSD and BOL may differ in their effects on 5-hydroxytryptaminergic systems in the cerebral cortex and in the brain stem.
在大鼠中,通过抑制脱羧酶后测定多巴积累量发现,0.5毫克/千克的麦角酸二乙酰胺(LSD)和0.5毫克/千克的2-溴麦角酸二乙酰胺(BOL)可提高纹状体中体内酪氨酸羟化的速率。LSD和BOL均未显著改变边缘系统中富含多巴胺的嗅结节中的多巴积累量。LSD可增加大脑皮层和脑干中的多巴积累量,而BOL则无此作用。LSD和BOL似乎并未改变α-甲基酪氨酸(alpha-MT)诱导的全脑中多巴胺(DA)或去甲肾上腺素(NA)消失的速率,也未改变α-甲基酪氨酸诱导的纹状体中多巴胺消失的速率。提示在纹状体中,LSD和BOL阻断调节酪氨酸羟化的自身受体(突触前受体)。这些受体可能是多巴胺受体,但也可能是5-羟色胺或对LSD敏感的受体。LSD和BOL之间观察到的区域差异表明,大脑皮层和脑干中的LSD通过与纹状体中起作用的机制不同的其他机制增加多巴积累量。一种可能的解释是,LSD和BOL对大脑皮层和脑干中5-羟色胺能系统的作用可能不同。