Lesions in the anterior bed nucleus of the stria terminalis in Syrian hamsters block short-photoperiod-induced testicular regression.

To elucidate the neural circuitry involved in the photoperiodic control of seasonal reproduction, adult male Syrian hamsters, previously housed under long photoperiods (LD; 14 h of light per day), received sham or bilateral radiofrequency-current lesions directed towards one of three anterior-to-posterior levels of the bed nucleus of the stria terminalis (BNST; far anterior, anterior, posterior). They were then transferred to a short photoperiod (SD; 6 h of light per day) for 12 wk, and their testicular weights and plasma FSH, LH, and testosterone concentrations were determined. All of these parameters became markedly inhibited in the sham-lesioned SD controls and also in the far anterior and posterior BNST lesioned groups. In contrast, this inhibitory response to SD was completely abolished in 8 of 14 animals that had received anterior BNST lesions; only in these 8 animals did the lesion encompass the lateral aspect of the anterior BNST. In a second experiment, hamsters that had previously been exposed to SD for 12 wk in order to induce testicular regression were lesioned in the anterior BNST and for the next 4 weeks were either exposed to LD or further maintained in SD. However, in neither case did the anterior BNST lesions perturb the normal photoperiodic response. Paired testes weights and plasma FSH, LH, and testosterone concentrations at 4 wk did not differ significantly (p > 0.05) between the lesioned animals and their respective sham-lesioned LD and SD controls, which, respectively, showed recrudescence of the reproductive axis or remained in a regressed condition. Taken together, the results suggest that lateral aspects of the anterior BNST contain a cell group that is critical for perception of the SD neuro-inhibitory signal; obliteration of this cell group interrupts the transmission of the inhibitory signal to the reproductive axis but does not directly stimulate it.