Photoperiodic responsiveness of hamsters with lesions of the lateral geniculate nucleus is related to hippocampal damage.

We tested the hypothesis that the geniculohypothalamic tract is important for hamster photoperiodism. Adult male hamsters, maintained in a long photoperiod (LD 14:10), received either large bilateral neurotoxic lesions of the lateral geniculate nucleus (LGN) or sham lesions. One week later, half of the animals from each group were transferred to a short photoperiod (LD 8:16) where they were maintained for 15 weeks. Most lesions effectively destroyed the intergeniculate leaflet (IGL) and much of the lateral geniculate complex. They also caused substantial damage to the overlying hippocampus. The lesions had no effect on long-day animals, but significantly reduced the extent of testicular regression during short photoperiod exposure. This effect, however, appeared to be the result of hippocampal, rather than geniculate, damage. Four individuals with complete IGL lesions, but minimal hippocampal damage, underwent a pattern of regression that was indistinguishable from controls. Body weight was increased by lesions in short-day, but not long-day, animals. This effect was not related to the extent of hippocampal damage. We conclude that geniculate input to the suprachiasmatic nuclei is not essential for hamster photoperiodism and that hippocampal damage may modify the effect of short daylengths on testes size.