The role of melatonin receptor and GABAA receptor in the sleeping time prolonged by melatonin in mice / 中国应用生理学杂志

<p><b>AIM</b>To observe the role of melatonin receptor and GABAA receptor in sleeping time prolonged by melatonin in mice.</p><p><b>METHODS</b>The absence of the righting reflex was considered as the sleep onset and the duration of the loss of the righting reflex was recorded as the sleeping time. The effects of receptor agonist and antagonist on hypnotic activity of melatonin were studied in the paper.</p><p><b>RESULTS</b>Prazosin hydrochloride, the blocker of melatonin 3 receptor, didn't affect the sleeping time prolonged by melatonin in mice. GABA, the endogenous agonist of GABA receptor, significantly potentiated the hypnotic activity of melatonin. When picrotoxin, the ligand of picrotoxin site on GABAA receptor, used together with melatonin, it significantly antagonized the sleeping time prolonged by melatonin, however, bicuculline, the specific antagonist of GABA binding site in GABAA receptor, didn't affect the hypnotic activity of melatonin in mice.</p><p><b>CONCLUSION</b>Melatonin does not exhibit its potentiation sleeping time in mice through melatonin 3 receptor. Hypnotic activity of melatonin may be mediated through picrotoxin site on GABAA receptor.</p>

Effect of atropine on the inhibition of melatonin to the unit discharges evoked in the posterior group of thalamic nuclei in cats / 药学学报

<p><b>AIM</b>To study the effect of atropine, muscarinic cholinergic antagonist, on the central analgesic action of melatonin (MT) and to explore the mechanism of MT analgesia.</p><p><b>METHODS</b>As an indicator of visceral pain, the unit discharges of the neurons in the posterior group of thalamic nuclei (PO) were caused by stimulating the great splanchnic nerve (GSN) of the cat. The cranial stereotaxic and extracellular glass microelectrode record technique were used. The drugs were given through the intra-cranial-ventricle (icv).</p><p><b>RESULTS</b>0.1% MT (10 micrograms.kg-1, icv) was shown to inhibit the unit discharge of the neurons in PO of the cat, whether the long latency or the short latency, which was evoked by stimulating GSN. The inhibition of 0.1% MT (10 micrograms.kg-1, icv) on the short latency discharge of neurons in PO was antagonized by 0.1% atropine (20 micrograms, icv). However, 0.1% atropine (20 micrograms, icv) did not show antagonistic effect on the inhibition of 0.1% morphine (5 micrograms, icv) at the same latency.</p><p><b>CONCLUSION</b>MT exhibited central analgesic action with mechanism different from morphine. It was suggested that the cholinergic system may be involved in analgesic process of MT.</p>