The dorsomedial nucleus (DMN) of the hypothalamus, the only site within the mediobasal hypothalamus of Syrian hamsters that both binds melatonin and has abundant concentrations of androgen receptors, has been proposed as a target tissue for induction of seasonal changes in brain sensitivity to steroid negative feedback. We tested whether DMN ablation, which does not interfere with pineal gland secretion of melatonin in short day lengths, prevents testicular regression by altering sensitivity to steroid negative feedback. Hamsters with DMN lesions, unlike control hamsters, failed to undergo testicular regression after transfer from a long (14 h light/day) to a short day length (8 h light/day); however, increased negative-feedback inhibition of follicle-stimulating hormone by testosterone was not compromised by ablation of the DMN, indicating that this tissue is not an essential mediator of seasonal changes in feedback sensitivity. We propose a redundant neural network comprised of multiple structures, each of which contributes to neuroendocrine mechanisms, that determines the effect of short days on gonadal function.

Long days (LDs) stimulate and short days (SDs) inhibit reproduction in photoperiodic rodents by modifying nocturnal pineal melatonin secretion. In LD Turkish hamsters, unlike other rodents, pinealectomy induces reproductive quiescence comparable to that produced by SDs. We assessed whether SDs and pinealectomy induce similar or different patterns of kisspeptin and gonadotropin-inhibitory hormone (also known as RFamide-related peptide-3 [RFRP-3] in mammals) expression, important mediators of seasonal reproductive changes in other species. Brains were harvested from sham-operated female Turkish hamsters maintained in LDs and SDs and LD-pinealectomized (pinx) females, all housed in their respective photoperiods for 12 weeks. Uterine weights were substantially higher in LD-sham than in LD-pinx and SD-sham females. RFRP-3-immunoreactive(-ir) cells in the dorsomedial hypothalamic nucleus were greater in number and size in the reproductively competent LD-sham hamsters than in both reproductively suppressed SD-sham and LD-pinx hamsters. LD-sham hamsters had more kisspeptin-ir cells in the anteroventral periventricular nucleus than did LD-pinx hamsters. Reproductive quiescence, whether induced by short-day lengths or pinealectomy, was generally accompanied by comparable changes in RFRP-3 and kisspeptin, suggesting that long-duration melatonin signaling and withdrawal of melatonin by pinealectomy may act through the same neural substrates to induce gonadal quiescence.

The dorsomedial nucleus (DMN) of the hypothalamus has been implicated in seasonal control of reproduction. Syrian hamsters with DMN lesions, unlike control hamsters, do not undergo testicular regression after transfer from a long day length (14 h of light per day; LD) to a short day length (8 h of light per day; SD). SDs also markedly reduce hamster locomotor activity (LMA). To assess whether the DMN is a component of the neural circuitry that mediates seasonal variation in LMA, neurologically intact males (controls) and hamsters that had sustained lesions of the DMN (DMNx) were housed in an LD or SD photoperiod for 26 weeks. DMNx that prevented testicular regression counteracted decreases in LMA during 8 to10 weeks of SD treatment; steroid-independent effects of SDs did not override high levels of LMA in DMNx males. As in previous studies, testosterone (T) restoration increased LMA in LD but not SD castrated control males. In the present study, T also failed to increase LMA in SD-DMNx hamsters. The DMN is not necessary to maintain decreased responsiveness of locomotor activity systems to T in SDs, which presumably is mediated by other central nervous system androgen target tissues. Finally, DMNx did not interfere with the spontaneous increase in LMA exhibited by photorefractory hamsters after 26 weeks of SD treatment. We propose that DMN is an essential part of the substrate that mediates seasonal decreases in LMA as day length decreases but is not required to sustain decreased SD responsiveness to T or for development of refractoriness to SDs.