Ogawa N, Asanuma M, Kondo Y, Hirata H, Nakayama N, Mori A
Department of Neuroscience, Okayama University Medical School, Japan.
Brain Res. 1994 Jan 7;633(1-2):167-70. doi: 10.1016/0006-8993(94)91536-9.
Thyrotropin-releasing hormone (TRH) injected intraperitoneally at doses of 10 mg/kg and 20 mg/kg induced marked hyperactivity in rats. Although regional levels of brain dopamine and its metabolites (DOPAC and HVA) in vagotomized rats did not differ from those in sham-operated controls, the (DOPAC + HVA)/dopamine ratio, an indicator of dopamine turnover, was significantly higher in the nucleus accumbens of TRH-treated sham-operated rats than that in untreated sham-operated controls. TRH injection induced hyperactivity only in sham-operated rats and not in subdiaphragmatic bilaterally vagotomized rats. Similarly, bilateral vagotomy completely abolished the TRH-induced increases in dopaminergic turnover in the nucleus accumbens. These results suggest that the dopaminergic system in the nucleus accumbens is involved in hyperactivity induced by TRH, and that TRH mainly affects peripheral receptors. The vagal nerve may be the major pathway from the visceral organs to the brain involved in the etiology of hyperactivity.
以10毫克/千克和20毫克/千克的剂量腹腔注射促甲状腺激素释放激素（TRH）可诱发大鼠明显的多动。虽然迷走神经切断大鼠脑内多巴胺及其代谢产物（3,4-二羟基苯乙酸和高香草酸）的区域水平与假手术对照组无异，但作为多巴胺周转指标的（3,4-二羟基苯乙酸+高香草酸）/多巴胺比值，在经TRH处理的假手术大鼠伏隔核中显著高于未处理的假手术对照组。TRH注射仅在假手术大鼠中诱发多动，而在双侧膈下迷走神经切断大鼠中未诱发。同样，双侧迷走神经切断完全消除了TRH诱导的伏隔核多巴胺能周转增加。这些结果表明，伏隔核中的多巴胺能系统参与了TRH诱导的多动，并且TRH主要影响外周受体。迷走神经可能是从内脏器官到大脑参与多动病因的主要通路。
