The acute administration of monosodium-l-glutamate (MSG, 8 mg/g) to neonatal hamsters (Mesocricetus auratus) destroys the neurons of the inner retina, although some ganglion cells survive. Despite the severe optic nerve degeneration, MSG-treated hamsters synchronize their circadian locomotor activity to light:dark signals. The central projections of the surviving ganglion cells in these animals were determined using anterograde tracing techniques. The retinohypothalamic pathway responsible for the photic synchronization of the locomotor activity was unaffected by the neurotoxin, although the remaining visual pathways were markedly reduced. The results indicate a differential sensitivity of retinal ganglion cells to MSG. The resistance of the retinal ganglion cells that innervate the suprachiasmatic nucleus of the hypothalamus to neonatal MSG treatment is discussed in relationship to other findings. The results from this study and other physiological and morphological findings suggest that the retino-hypothalamic system is an anatomically independent component of the optic system.
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