Chesire R M, Cheng J T, Teitelbaum P
Physiol Behav. 1983 May;30(5):809-18. doi: 10.1016/0031-9384(83)90182-8.
Electrolytic damage of the nucleus reticularis tegmenti pontis (NRTP) in rats produces a form of accelerating forward locomotion, indicating that this region is part of a system that inhibits locomotion and movement. In animals with such damage, 5 mg/kg haloperidol does not block forward locomotion although it produces complete akinesia in normal rats [2]. Our present results demonstrate that doses of morphine sulfate that render normal rats completely akinetic (40, 50, or 60 mg/kg) also fail to block forward locomotion. Furthermore, 200 micrograms gamma-aminobutyric acid applied intracranially in the region of the NRTP can reverse the akinesia produced by systemically administered haloperidol or morphine. We suggest that there are two types of akinesia--direct and indirect--and that morphine and haloperidol may produce akinesia indirectly via an inhibitory system which includes the NRTP.
大鼠脑桥被盖网状核（NRTP）的电解损伤会导致一种加速向前运动的形式，这表明该区域是抑制运动和活动的系统的一部分。在有此类损伤的动物中，5毫克/千克的氟哌啶醇虽然能使正常大鼠完全产生运动不能，但却不能阻止向前运动[2]。我们目前的结果表明，能使正常大鼠完全产生运动不能的硫酸吗啡剂量（40、50或60毫克/千克）也无法阻止向前运动。此外，在NRTP区域颅内注射200微克γ-氨基丁酸可以逆转全身注射氟哌啶醇或吗啡所产生的运动不能。我们认为存在两种类型的运动不能——直接型和间接型，并且吗啡和氟哌啶醇可能通过包括NRTP在内的抑制系统间接产生运动不能。
