Search NEL Online

Journal Article 2001; 22(3): 169-174 PubMed PMID: 11449194 Citation  Keywords:  Animals, Humans, Hypothalamus:drug effects, In Vitro Techniques, Melatonin:pharmacology, Oxytocin:biosynthesis, Photoperiod, Pineal Gland:physiology, Pituitary Gland, Posterior:drug effects, Vasopressins:biosynthesis,.   

: The present paper reviews the findings accumulated on the role of pineal gland and its hormone - melatonin - in regulation of the hypothalamo-neurohypophysial system activity. Effects of modified photoperiod, pinealectomy or treatment with melatonin on the vasopressin and oxytocin biosynthesis and/or secretion have been described. Taken together, the in vivo and in vitro data suggest that the effect of melatonin on the vasopressin and oxytocin secretion depends on this pineal hormone concentration and experimental conditions....

Read abstract  Full text PDF

Journal Article 2001; 22(3): 199-207 PubMed PMID: 11449192 Citation  Keywords:  Animals, Apamin:pharmacology, Calcium:pharmacology, Cyclooxygenase Inhibitors:pharmacology, Dinoprost:pharmacology, Female, In Vitro Techniques, Indomethacin:pharmacology, Melatonin:pharmacology, Oxytocin:pharmacology, Potassium Channels:drug effects, Pot.   

OBJECTIVE: The aim of this study was to investigate the effects of melatonin on spontaneous and oxytocin-induced contractility of pregnant and non-pregnant rat myometrium in vitro.

DESIGN: Myometrial strips were removed from virgin or late pregnant (21 days gestation) Wistar rats following decapitation and placed in an organ bath containing Krebs' solution at 37 degrees C and pH 7.4, constantly bubbled with 95% oxygen-5% carbon dioxide and isometric contractions were recorded. Effects of cumulative concentrations of melatonin (0.1 to 10 microM) on spontaneous and oxytocin-induced contractions were studied. Possible involvement of Ca(2+)-activated K (+) channels in inhibitory actions of melatonin was investigated by using apamin (100 nM).

RESULTS: Melatonin inhibited spontaneous and oxytocin-induced contractions of myometrium from both virgin and late pregnant rats in a dose-dependent manner. After inhibition of oxytocin-induced contractions by melatonin, application of prostaglandin F (2alpha) (1 microM) but not high KCl (30 mM) containing solution initiated contractile activity. Inhibitory response induced by melatonin (13 microM) was not affected by apamin (100 nM).

CONCLUSIONS: Data from this study demonstrates that melatonin inhibits spontaneous and oxytocin-induced contractions of myometrium from pregnant and non-pregnant rats. Although the exact mechanism is not clear, melatonin-induced inhibition of myometrial contractions may results from its interactions with Ca(2+) channels....

Read abstract  Full text PDF

Journal Article 2001; 22(2): 101-108 PubMed PMID: 11335886 Citation  Keywords:  1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine:pharmacology, Animals, Apoptosis:drug effects, Brain:cytology, Cell Count, Corpus Striatum:cytology, DNA Fragmentation, Dopamine Agents:pharmacology, Male, Melatonin:pharmacology, Mesencephalon:cytology, Mice, .   

OBJECTIVES: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a neurotoxin that induces a Parkinsonian-type syndrome in animals which is similar to Parkinson's disease in humans. MPTP toxicity partially depends on the production of free radicals which in turn play a key role in the apoptotic death of neurons. In the present study melatonin, a potent free radical scavenger with antiapoptotic properties, was given to determine whether it would reduce oxidative stress in mice treated with MPTP.

MATERIALS AND METHODS: Male mice were given MPTP with or without melatonin and the brain was studied either 6h, 24h, 7 days or 15 days after the last MPTP injection.

RESULTS: The results show that melatonin counteracted in vivo MPTP-induced apoptosis in midbrain neurons at 6 and 24 h after MPTP treatment, and partially prevented apoptosis at 7 and 15 days after MPTP administration. MPTP treatment also produced time-dependent cell damage, whereas melatonin reduced the percentage of damaged cells at all time points, the effect being most evident at 15 days after treatment. Moreover, melatonin counteracted MPTP-dependent DNA fragmentation in the midbrain and striatum at 7 and 15 days after drug administration.

CONCLUSION: These results support a role for melatonin in protecting neurons against MPTP toxicity in vivo, and suggest that its antiapoptotic action is one of the mechanisms by which melatonin protects neuronal cells from neurotoxic insults....

Read abstract  Full text PDF