We investigated the effects of daily melatonin (MEL) injection on phase angle of entrainment, duration of wheel-running activity (alpha), and frequency of suprachiasmatic nuclei (SCN) neuronal discharge in the photo-nonresponsive phenotype of the Djungarian hamster, Phodopus sungorus. Photo-nonresponsiveness is characterized by an absence of physiological adjustments to short days (SD). With respect to wheel-running activity, photo-nonresponsive hamsters have a large negative phase angle of entrainment and a compressed alpha under SD. These hamsters also have a delayed nocturnal MEL pulse. These circadian differences are correlated with the daily profile of SCN neuronal activity. In the present experiments, daily MEL injections to photo-nonresponsive hamsters resulted in molt, gonadal regression, and expansion in alpha until entrainment to lights off. Vehicle-injected controls did not exhibit any of these responses. SCN neuronal activity patterns recorded from MEL-injected photo-nonresponders, but not vehicle-injected controls, resembled electrical activity profiles of photoresponsive hamsters. These results demonstrate that MEL induces "photoresponsiveness" in previously photo-nonresponsive hamsters, that MEL modifies circadian behavior to resemble that of photoresponders, and that MEL injections affect the circadian rhythm of SCN neuronal firing.

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Aging increases mitochondrial dysfunction and susceptibility to hypoxia. Previous reports have indicated an association between post-hypoxic hyperoxidation of intra-mitochondrial enzymes and delayed neuronal injury. Therefore we investigated the relationship between NADH fluorescence and neuronal function during and after hypoxia across the lifespan. Hippocampal slices were prepared from adult (1 to >22 months) F344 rats. NADH fluorescence, extracellular voltage and tissue PO 2 were recorded from the CA1 region during hypoxia (95% N 2 ) of various lengths following onset of hypoxic spreading depression (hsd). Slices from younger rats recovered evoked neuronal responses to a greater degree and exhibited less hyperoxidation after a hypoxic episode, than slices from older rats. However, the use of Ca 2+ free-media in slices from >22 month old rats improved recovery and delayed NADH hyperoxidation (2.5 min hypoxia after hsd). Post-hypoxic decrease of NADH fluorescence (hyperoxidation) was age dependent and correlated with decreased neuronal recovery. Slices exposed to repeated hypoxic episodes yielded data suggesting depletion of the NAD + pool, which may have contributed to the deterioration of neuronal function.

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