Chesire R M, Cheng J T, Teitelbaum P
Behav Neurosci. 1984 Aug;98(4):739-42. doi: 10.1037//0735-7044.98.4.739.
Focal application of 5 micrograms of morphine sulfate to the nucleus reticularis tegmenti pontis (NRTP) in rats reversed the akinesia induced by 5 mg/kg systemic haloperidol or 40 mg/kg systemic morphine and released festinating forward locomotion. gamma-Aminobutyric acid (200 micrograms) applied to this nucleus also reversed such akinesia. Intraventricular naloxone (10 micrograms) or picrotoxin (0.1 microgram), respectively, blocked the effects of such focally applied drugs. Thus, morphine and gamma-aminobutyric acid appear to act physiologically on the cells of the NRTP. The results suggest that systemic morphine, in addition to producing immobility, simultaneously facilitates a readiness for locomotion by inactivating a final common inhibitory system in the region of the NRTP.
向大鼠脑桥被盖网状核（NRTP）局部应用5微克硫酸吗啡，可逆转5毫克/千克全身注射氟哌啶醇或40毫克/千克全身注射吗啡所诱导的运动不能，并引发急促的向前运动。向该核团应用γ-氨基丁酸（200微克）也可逆转此类运动不能。脑室内分别注射纳洛酮（10微克）或印防己毒素（0.1微克）可阻断此类局部应用药物的作用。因此，吗啡和γ-氨基丁酸似乎在生理上作用于NRTP的细胞。结果表明，全身注射吗啡除了会导致不动外，还会通过使NRTP区域的最终共同抑制系统失活，同时促进运动准备状态。
