Lesions in the bed nucleus of the stria terminalis, but not in the lateral septum, inhibit short-photoperiod-induced testicular regression in Syrian hamsters.

The transfer of adult male hamsters from long days (LD) to short days (SD) (i.e. < 12 h of light per day) typically results in marked testicular regression and a decline in plasma testosterone concentrations. To help disclose key brain regions responsible for mediating this photoperiodic response male hamsters received either chemical (i.e. N-methyl-D-aspartate; NMDA) or radiofrequency current lesions in the bed nucleus of the stria terminalis (BNST), and were then exposed to SD for 15 or 12 weeks, respectively. Although body weights were similar between sham-lesioned controls and the NMDA-lesioned hamsters, the latter showed a significant attenuation of testicular regression; additionally, their plasma testosterone concentrations remained at typical LD levels. When radiofrequency current-lesioned hamsters were transferred from LD to SD they also failed to show significant signs of testicular regression, nor a decline in plasma testosterone concentrations, nor a complete arrest of spermatogenesis. In contrast, sham-lesioned controls or hamsters that were lesioned dorsally to the BNST at a site primarily involving the lateral septum all showed the expected degree of testicular regression, a decline in plasma testosterone concentrations, and complete arrest of spermatogenesis; body weights were similar in all of the experimental group. Taken together, these findings suggest that the BNST, a brain area traditionally not associated with reproductive function, may play an important role in mediating photoperiodic information to the neural circuits that control the reproductive axis.