Melatonin has been reported to reduce infarct volumes induced by transient middle cerebral artery (MCA) occlusion. We examined whether melatonin could improve electrophysiological and neurobehavioral recoveries in rats after 72 hr of reperfusion following 1.5 hr of MCA occlusion. Melatonin (5 mg/kg) or vehicle was given intravenously at the commencement of reperfusion. Neurobehavioral outcome was serially examined, and somatosensory evoked potentials (SSEP) were recorded prior to ischemia and at 72 hr after the onset of reperfusion. Brain infarction was assessed upon killing. Before ischemia-reperfusion, stable SSEP waveforms were consistently recorded after individual fore- or hindpaw stimulation. The amplitude between the first positive (P1) and the first negative (N1) peaks and the P1 latency did not differ significantly between controls and melatonin-treated animals. At 72 hr of reperfusion, controls had severely depressant SSEPs recorded from ischemic fore- and hindpaw cortical fields, and the amplitudes decreased to 36 and 35% of baselines, respectively (P < 0.001). These animals also had transcallosal electrophysiological diaschisis in the SSEPs recorded at the contralateral hindpaw cortical field (P < 0.01). Relative to controls, melatonin-treated animals not only had significantly improved amplitudes of the SSEPs recorded from both ischemic fore- and hindpaw cortical fields, by 33 and 37% of baselines, respectively (P < 0.001), but also exhibited diminished transcallosal electrophysiological diaschisis following ischemia-reperfusion. In addition, melatonin improved sensory and motor neurobehavioral outcomes by 40 and 28%, respectively (P < 0.001), and reduced cortical and striatal infarct sizes by 32 and 40%, respectively (P < 0.05). Thus, delayed intravenous administration with melatonin both enhances electrophysiological and neurobehavioral recoveries and reduces cortical and striatal infarct sizes after cerebral ischemia and reperfusion injury.

中文翻译：

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褪黑素的延迟治疗可增强大鼠短暂性局灶性脑缺血后的电生理恢复。

据报道，褪黑激素可减少由短暂性大脑中动脉（MCA）阻塞引起的梗塞体积。我们检查了褪黑激素是否可以改善MCA闭塞1.5小时后再灌注72小时后大鼠的电生理和神经行为恢复。在再灌注开始时静脉内注射褪黑激素（5 mg / kg）或赋形剂。连续检查神经行为的预后，并在缺血前和再灌注后72小时记录体感诱发电位（SSEP）。杀死后评估脑梗塞。在缺血再灌注之前，单独的前爪或后爪刺激后，稳定地记录了稳定的SSEP波形。在对照组和褪黑激素治疗的动物之间，第一个阳性峰（P1）和第一个阴性峰（N1）之间的幅度和P1潜伏期没有显着差异。在再灌注72小时后，对照组从缺血前爪和后爪皮层记录到严重抑制性SSEP，振幅分别降至基线的36％和35％（P <0.001）。这些动物在对侧后爪皮层区域记录到的SSEP中也有经皮电生理异常（P <0.01）。相对于对照，褪黑素治疗的动物不仅从缺血性前爪和后爪皮层区域记录到的SSEP幅度均显着改善，分别达到基线的33％和37％（P <0.001），但在缺血再灌注后也表现出减少的经trans电生理障碍。此外，褪黑素分别将感觉和运动神经行为改善40％和28％（P <0.001），并将皮层和纹状体梗死面积分别减少32％和40％（P <0.05）。因此，褪黑激素的静脉内延迟给药既可以增强电生理和神经行为的恢复，又可以减少脑缺血和再灌注损伤后皮质和纹状体梗死的面积。