LESIONS OF THE IODOMELATONIN-BINDING SITES OF THE MEDIOBASAL HYPOTHALAMUS SPARE THE LACTOTROPIC, BUT BLOCK THE GONADOTROPIC RESPONSE OF MALE SYRIAN-HAMSTERS TO SHORT PHOTOPERIOD AND TO MELATONIN

The aim of this study was to determine whether the iodomelatonin-binding sites identified within the preoptic area (POA) or mediobasal hypothalamus (MBH) are essential for the photoperiodic control of seasonal reproduction in male Syrian hamsters. Animals received sham or bilateral electrolytic lesions directed toward either the POA (POA-X; n = 11) or MBH (MBH-X; n = 12) and were then maintained on long days (16 h of light and 8 h of darkness) for at least 4 weeks before transfer to a short photoperiod (SD; 8 h of light and 16 h of darkness). The transscrotal width of the left testis and serum testosterone (Exp 1), PRL, and LH (Exp 2) levels were recorded every 4 weeks in lesioned and intact hamsters to monitor their reproductive state. Lesions of the MBH, but not the POA, abolished the SD-induced gonadal responses (transscrotal width of the left testis after 12 weeks of SD: MBH-X, 10.0 +/- 0.2 mm; sham, 4.6 +/- 0.1 mm; POA-X, 4.0 +/- 0.1 mm; sham, 4.1 +/- 0.1 mm). Similarly, the decrease in serum LH concentrations was prevented by lesions of the MBH (serum LH after 12 weeks SD: MBH-X, 0.74 +/- 0.2 ng/ml; sham, 0.25 +/- 0.1 ng/ml). However, neither lesion prevented the SD-induced decline in serum PRL (serum PRL after 12 weeks SD: MBH-X, 4.7 +/- 1.0 ng/ml; sham, 3.1 +/- 0.1 ng/ml; POA-X, 2.0 +/- 0.1 ng/ml; sham, 2.0 +/- 0.1 ng/ml). To exclude the possibility that the lesion to the MBH prevented gonadal regression through disruption of nocturnal melatonin production, MBH-X animals were switched to a long day photoperiod, pinealectomized, and fitted with a sc cannula for the infusion of either melatonin (500 ng/10 h) or saline (50 mu l/h) once daily for 6 weeks. A group of neurally intact, pinealectomized control animals that received the same infusions showed the expected gonadal regression with melatonin treatment, whereas those receiving saline vehicle had large testes (melatonin, 0.5 +/- 0.1 g; saline, 3.3 +/- 0.3 g). Furthermore, after 6 weeks of infusions, serum LH and PRL concentrations in intact melatonin-infused hamsters were significantly reduced (LH: melatonin, 0.2 +/- 0.04 ng/ml; saline, 1.3 +/- 0.1 ng/ml; PRL: melatonin, 2.2 +/- 0.2 ng/ml; saline, 16.9 +/- 3.1 ng/ml). In contrast to the intact controls, none of the MBH-X animals infused with melatonin exhibited gonadal regression (MBH-X: melatonin, 2.8 +/- 0.5 g; saline, 2.9 +/- 0.5 g). In addition, serum LH concentrations were not significantly different between MBH-X animals infused with either melatonin or saline (melatonin, 0.78 +/- 0.2 ng/ml; saline, 0.70 +/- 0.1 ng/ml), whereas infusions of melatonin did have a significant effect on serum concentrations of PRL in MBH-X animals (melatonin, 2.4 +/- 0.3 ng/ml; saline, 8.0 +/- 1.0 ng/ml). These results show that an intact MBH, but not POA, is essential for the photoperiodic control of gonadotropic activity in the Syrian hamster. Neither site is essential for photoperiodic control of the lactotropic axis. The data are consistent with the hypothesis that melatonin acts via the melatonin-binding sites of the MBH to control photoperiodic rhythms of reproduction.