Bhargava V, Salamy A, Shah S
Pharmacol Biochem Behav. 1981 Oct;15(4):587-9. doi: 10.1016/0091-3057(81)90214-8.
We have examined the role of serotonergic and/or dopaminergic mechanism in the mediation of the nicotine-induced depression of brainstem auditory evoked responses (BAER) to auditory stimuli. Nicotine produced dose- and time-dependent decreases in BAER amplitude. Administration of serotonin-depleting drugs (reserpine or p-chlorophenylalanine (PCPA), prevented this decrease. Administration of catecholamine-depleting drugs (alpha-methyl-p-tyrosine, disulfiram or Dopa), on the other hand, had no effect. These data thus suggest a role for serotonergic mechanisms in the mediation of nicotine-induced depression of the brainstem auditory pathway.
我们研究了血清素能和/或多巴胺能机制在介导尼古丁引起的脑干听觉诱发电位（BAER）对听觉刺激的抑制作用中的作用。尼古丁使BAER波幅呈剂量和时间依赖性降低。给予血清素耗竭药物（利血平或对氯苯丙氨酸（PCPA））可阻止这种降低。另一方面，给予儿茶酚胺耗竭药物（α-甲基对酪氨酸、双硫仑或多巴）则没有效果。因此，这些数据表明血清素能机制在介导尼古丁引起的脑干听觉通路抑制中发挥作用。
