Svensson T H, Engberg G
Adv Exp Med Biol. 1980;126:535-50. doi: 10.1007/978-1-4684-3632-7_40.
The effect of ethanol (2 g/kg) on brain catecholamine neurons in the rat as well as its interaction with catecholamine receptor agonists was studied utilizing single unit recording techniques. Identified dopamine (DA) neurons of the zona compacta, substantia nigra as well as noradrenaline (NA) neurons of the locus coeruleus showed no alterations in firing rate at ethanol administration. Also the function of their presynaptic DA and NA receptors, respectively, appeared normal judging from the unaltered inhibitory response to systemically or microiontophoretically applied receptor agonists, apomorphine and clonidine, respectively, when applied in small doses. In contrast, the catecholamine releasing agent amphetamine caused inhibition of firing of the central catecholamine neurons in the same anesthetized preparation. The rate of tryosine hydroxylation in vivo in central DA and NA neurons measured as the amount of Dopa accumulated in various brain regions following inhibition of aromatic l-amino acid decarboxylase by NSD 1015, 150 md/kg i.p., was significantly increased by ethanol in anesthetized rats. Consequently, the present data do not support the hypothesis derived largely from behavioural evidence that ethanol causes inactivation of central DA and NA neurons. The antagonism by catecholamine receptor agonists, apomorphine and clonidine of ethanol's behaviourally stimulant action may thus be of unspecific character. The results indicate that alterations in tyrosine hydroxylase activity, when measured as Dopa formation after decarboxylase inhibition, can occur without concomitantly altered impulse activity in central DA or NA neurons. At present the action of ethanol on brain DA and NA neurons remains unclear and necessitates further studies.
利用单单位记录技术研究了乙醇（2克/千克）对大鼠脑内儿茶酚胺神经元的影响及其与儿茶酚胺受体激动剂的相互作用。已鉴定的黑质致密部多巴胺（DA）神经元以及蓝斑去甲肾上腺素（NA）神经元在给予乙醇后放电率未发生改变。从分别对全身或微量离子导入应用的受体激动剂阿扑吗啡和可乐定（小剂量应用时）的抑制反应未改变来看，它们各自的突触前DA和NA受体功能似乎正常。相比之下，儿茶酚胺释放剂苯丙胺在相同的麻醉制剂中导致中枢儿茶酚胺神经元放电受到抑制。在麻醉大鼠中，通过NSD 1015（150毫克/千克腹腔注射）抑制芳香族L-氨基酸脱羧酶后，以各脑区积累的多巴量来衡量的中枢DA和NA神经元体内酪氨酸羟化速率被乙醇显著提高。因此，目前的数据不支持主要基于行为学证据得出的乙醇导致中枢DA和NA神经元失活的假说。儿茶酚胺受体激动剂阿扑吗啡和可乐定对乙醇行为兴奋作用的拮抗作用可能因此具有非特异性。结果表明，当以脱羧酶抑制后多巴形成来衡量时，酪氨酸羟化酶活性的改变可以在中枢DA或NA神经元冲动活动未同时改变的情况下发生。目前，乙醇对脑内DA和NA神经元的作用仍不清楚，需要进一步研究。
