The intergeniculate leaflet does not mediate the disruptive effects of constant light on circadian rhythms in the rat

Prolonged constant light exposure causes disruptions in circadian rhythms, resulting in splitting of circadian activity rhythms in hamsters and arrhythmicity in rats. Hamsters with lesions of the thalamic intergeniculate leaflet do not exhibit constant light-induced disruptions in rhythmicity. We have shown that circadian rhythms of rats with monosodium glutamate-induced neurotoxic damage to visual pathways persist under constant light, and hypothesized that monosodium glutamate damaged the retinogeniculate pathway, thus preventing constant light-induced arrhythmicity. The present study demonstrates, however, that the intergeniculate leaflet does not mediate these effects in rats. Rats with bilateral electrolytic intergeniculate leaflet lesions showed the same rate of disruption of circadian temperature rhythms as did sham-operated animals, housed under constant light. We also show that, unlike intergeniculate leaflet-lesioned rats, rats treated neonatally with monosodium glutamate exhibit neuropeptide Y fiber staining in the suprachiasmatic nucleus, indicating that the geniculohypothalamic tract is functionally intact following monosodium glutamate treatment. Taken together, these data demonstrate that the disruption of circadian rhythms during constant light exposure is not mediated directly via the geniculohypothalamic tract in rats. Whether this disruption in rhythmicity results from effects of constant light exposure on the circadian pacemaker, or is a direct effect of light on body temperature, is unknown. Retinal or collicular damage in monosodium glutamate-treated rats may render these animals insensitive to the disruptive effects of constant light.