Sorensen S M, Johnson S W, Freedman R
Brain Res. 1982 Sep 16;247(2):365-71. doi: 10.1016/0006-8993(82)91262-8.
The spontaneous discharge of cerebellar Purkinje neurons was studied in rats after withdrawal from chronic treatment with amphetamine (2 mg/kg per day x 21 days). Discharge rates in withdrawn animals remained significantly lower than those of controls for up to 50 days. Disruption of the adrenergic input to these neurons from the locus coeruleus by treatment with propranolol, clonidine or reserpine, partially restored these discharge rates. Acute administration of amphetamine in amphetamine-withdrawn rats did not further depress Purkinje neurons discharge rate, whereas in a previous study in this lab, Purkinje neurons from naive animals were markedly slowed. Moreover, Purkinje neurons from amphetamine-withdrawn rats were also significantly less sensitive than controls to locally applied norepinephrine. These results demonstrate that chronic amphetamine can lead to very long-term changes in neuronal activity, and suggest that these changes may be mediated, in part, by the noradrenergic transmitter systems.
研究了大鼠在撤掉慢性苯丙胺治疗（2毫克/千克/天，共21天）后小脑浦肯野神经元的自发放电情况。撤药后的动物在长达50天的时间里，其放电率仍显著低于对照组。用普萘洛尔、可乐定或利血平处理破坏蓝斑向这些神经元的肾上腺素能输入，可部分恢复这些放电率。对撤掉苯丙胺的大鼠急性给予苯丙胺，并未进一步降低浦肯野神经元的放电率，而在本实验室之前的一项研究中，来自未接触过药物的动物的浦肯野神经元放电明显减慢。此外，撤掉苯丙胺的大鼠的浦肯野神经元对局部应用去甲肾上腺素的敏感性也明显低于对照组。这些结果表明，慢性苯丙胺可导致神经元活动发生非常长期的变化，并提示这些变化可能部分由去甲肾上腺素能递质系统介导。
