The purpose of this study was to identify sites of action of melatonin in the human fetal brain by in vitro autoradiography and in situ hybridization. Specific, guanosine triphosphate (GTP) sensitive, binding of 2-[(125)I]iodomelatonin was localized to the leptomeninges, cerebellum, thalamus, hypothalamus, and brainstem. In the hypothalalmus, specific binding was present in the suprachiasmatic nuclei (SCN) as well as the arcuate, ventromedial and mammillary nuclei. In the brainstem specific binding was present in the cranial nerve nuclei including the oculomotor nuclei, the trochlear nuclei, the motor and sensory trigeminal nuclei, the facial nuclei, and the cochlear nuclei. The localization of MT1 receptor subtype gene expression as determined by in situ hybridization matched the localization of 2-[(125)I]iodomelatonin binding. No MT2 receptor subtype gene expression was detected using this technique. Thus, melatonin may act on the human fetus via the MT1 receptor subtype at a number of discrete brain sites. A major site of action of melatonin in both fetal and adult mammals is the pars tuberalis of the pituitary gland. However, no 2-[(125)I]iodomelatonin binding or melatonin receptor gene expression was detected in the pituitary gland in the present study, indicating that the pituitary, particularly the pars tuberalis, is not a site of action of melatonin in the human fetus.
The midline thalamus (e.g., the paraventricular thalamic nuclei and the reuniens nucleus) of Siberian hamsters and other mammals has been reported to contain specific binding sites for melatonin, a hormone that is essential for photoperiodically induced winter adaptations such as reproductive quiescence, loss of body weight, daily torpor, and the winter molt. The first experiment investigated whether the midline thalamus is necessary for these winter adaptations. Adult Siberian hamsters received discrete neurotoxic lesions of the paraventricular thalamic nuclei or the reuniens nucleus while under pentobarbital sodium-induced anesthesia. After recovery, the hamsters were monitored for winter adaptations while they were exposed to short photoperiods (10 h light/day) for 12 wk at 22 degrees C then for 60 days at 7 degrees C. Lesions of the reuniens nucleus, but not of the paraventricular thalamic nuclei, significantly inhibited short photoperiod-induced loss of body weight and tended to increase food consumption and decrease daily torpor. The second experiment showed that lesions of the reuniens nucleus increased body weight gain compared with that in controls during exposure to long photoperiods at 22 degrees C for 16 wk. In summary, these findings show that the reuniens nucleus is an important site for regulation of body weight and suggest that lesions of the reuniens nucleus may attenuate winter metabolic adaptations by causing an increase in body weight.
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