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Objective:To investigate the relationship between lateral hypothalamus and melatonin-induced reduction of wakefulness in rats and the receptor mechanism.Methods:Forty clean-grade adult male Sprague-Dawley rats, weighing 250-300 g, were divided into 4 groups ( n=10 each) using a random number table method: control group (group C), melatonin group (group M), melatonin type-1/2 receptor (MT 1R) antagonist luzindole plus melatonin group (group L+ M), and melatonin type-2 receptor (MT 2R) antagonist 4P-PDOT plus melatonin group (P+ M group). In group C, 0.5 μl of 0.9% NaCl solution was microinjected into the lateral hypothalamus.In group M, 1 μmol/L melatonin 0.5 μl was microinjected into the lateral hypothalamus.In group L+ M, 1 μmol/L MT 1/2R and 1 μmol/L melatonin (0.5 μl in total) was microinjected into the lateral hypothalamus.The microinjection time was from 19: 30 to 20: 00.The changes in sleep-wake duration and the oscillating energy in different frequency bands of electroencephalogram were detected by using electroencephalogram and electromyogram recording technology. Results:Compared with group C, the percentage of wakefulness time was significantly decreased, the percentage of non-rapid eye movement sleep and rapid eye movement sleep time was increased, the energy for delta oscillation was increased, the energy for theta oscillation was decreased, and no significant change was found in the energy for alpha oscillation in M and P+ M groups ( P<0.01), and no significant change was found in the parameters mentioned above in group L+ M ( P>0.05). Compared with group M, the percentage of wakefulness time was significantly increased, the percentage of non-rapid eye movement sleep and rapid eye movement sleep time was decreased, the energy for delta oscillation was decreased, and the energy for theta oscillation was increased in group L+ M ( P<0.01), and no significant change was found in the parameters mentioned above in group P+ M ( P>0.05). Conclusion:The lateral hypothalamus may be involved in melatonin-induced reduction of wakefulness in rats, and the mechanism may be related to activating MT 1R in the lateral hypothalamus.
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AIM: To determine the effect of electrical stimulation of lateral hypothalamic area(LHA) on gastric ischemia-reperfusion injury(GI-RI) in rats and to analyse its possible neuroregulatory mechanisms. METHODS: The methods of electrical stimulation(ES), chemical stimulation, electrolytic lesion(EL) and denervation were used to investigate the effect of LHA ES on gastric mucosal injury in rats subjected to 30 min gastric ischemia followed by 60 min reperfusion and to analyse the role of dorsal vagal complex(DVC), vagus and sympathetic nerve in this effect. RESULTS: ①Electrical stimulation of LHA and microinjection of L-glutamic acid into LHA obviously aggravated GI-RI; ②Electrolytic lesion of the LHA attenuated the GI-RI;③DVC lesion eliminated the effect of electrical stimulation of LHA on GI-RI; ④Vagotomy or sympathectomy eliminated the effect of electrical stimulation of LHA on GI-RI too.CONCLUSION: These results indicate that the LHA is a specific area in the CNS for exerting aggravative effects on the GI-RI; the DVC, vagus and sympathetic nerve may be involved in regulatory effects of LHA on GI-RI.
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The pulmonary edema produced by electrolytic lesions of the lateral pre optic area (POA) of the hypotalamus can be reproduced by kainic acid (KA) microinfused in the POA of rats. KA group and electrolytic group showed similar patterns of lung pathology on gross and microscopic examination. The arterial blood pressdre and the frequency of discharge from the greater splanchnic nerve in KA group was increased more severely than in electrolytic group.The data indicate that there is a special and close ralation between lesion of POA and development of pulmonary edema. They also suggest that the changes in hemodynamics may not be a major factor in mechanisms of neurog enic pulmonary edema.