Sasaki K, Suda H, Watanabe H, Yagi H
Scientific Instrument Center, Toyama Medical and Pharmaceutical University, Japan.
Brain Res Bull. 1990 Jul;25(1):121-7. doi: 10.1016/0361-9230(90)90262-x.
The lateral habenula receives massive afferents from dopamine-rich forebrain areas through the stria medullaris and sends efferents to mesencephalic dopaminergic systems through the fasciculus retroflexus. In the present study, effects of electrolytic lesions of the habenula, transections of the stria medullaris, and kainic acid-induced lesions of the entopeduncular nucleus on methamphetamine-induced inhibition of substantia nigra dopamine neurons were investigated in rats. Following these lesions or transections the methamphetamine-induced inhibition on the dopamine neuronal activity was significantly attenuated compared to those in control animals with sham lesions or sham transections. Intravenous administration of methamphetamine at a dosage of 6.4 mg/kg produced only a 62.7 to 71.2% inhibition in lesioned or transected animals, whereas in control animals the activity of dopamine neurons was almost completely inhibited with this dose. The amounts of methamphetamine required to induce 50% inhibition of dopamine neurons in lesioned or transected animals was 3.3 to 4.7 times greater than those in control animals. There was no significant difference in cumulative dose-response curves between habenular-lesioned, stria medullaris-transected and entopeduncular-lesioned animals. These results, along with other findings, indicate possibly that the pathways running through the entopeduncular nucleus, the stria medullaris, the habenula, probably the lateral habenula, and the fasciculus retroflexus are involved in a feedback loop from the striatum to the substantia nigra and regulate the activity of dopamine neurons.
外侧缰核通过髓纹接受来自富含多巴胺的前脑区域的大量传入纤维，并通过后屈束向中脑多巴胺能系统发出传出纤维。在本研究中，研究了大鼠缰核电解损伤、髓纹横断以及内苍白球核 kainic 酸诱导损伤对甲基苯丙胺诱导的黑质多巴胺能神经元抑制的影响。与假损伤或假横断的对照动物相比，在这些损伤或横断后，甲基苯丙胺诱导的对多巴胺神经元活动的抑制明显减弱。以 6.4mg/kg 的剂量静脉注射甲基苯丙胺，在损伤或横断的动物中仅产生 62.7%至 71.2%的抑制，而在对照动物中，该剂量几乎完全抑制了多巴胺神经元的活动。在损伤或横断的动物中，诱导多巴胺神经元 50%抑制所需的甲基苯丙胺量比对照动物大 3.3 至 4.7 倍。缰核损伤、髓纹横断和内苍白球核损伤的动物之间累积剂量-反应曲线没有显著差异。这些结果以及其他发现可能表明，通过内苍白球核、髓纹、缰核（可能是外侧缰核）和后屈束的通路参与了从纹状体到黑质的反馈回路，并调节多巴胺神经元的活动。
