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Indirect evidence for an association of 5‐HT1B binding sites with retinal and geniculate axon terminals in the rat suprachiasmatic nucleus

The purpose of the present study was to investigate the possible cellular location of 5‐HT1B receptors on retinal and geniculate afferents in the rat suprachiasmatic nucleus (SCN). Biocular enucleation significantly decreased 5‐HT1B binding site labeling (35%), specifically in the ventral part of the SCN, while monocular enucleation produced a decrease of smaller magnitude (12%), limited to the ventral part of the contralateral SCN, these results being consistent with the known distribution of retinal afferents in the nucleus. By contrast, bilateral geniculate lesion did not induce any significant variation of 5‐HT1B binding site labeling in the SCN. Previously, we reported that serotonin (5‐HT) synthesis inhibition by parachlorophenylalanine increases 5‐HT1B binding site labeling in the SCN. Using saturation studies, we have now demonstrated that this upregulation reflected an increase in the total number of 5‐HT1B binding sites (+41% in the dorsal and +67% in the ventral part of the SCN). Furthermore, we evaluated the effects of bilateral geniculate lesion after 5‐HT stores depletion in order to overcome problems of technical resolution limits. The magnitude of upregulation was significantly decreased (27%) after bilateral geniculate lesion, suggesting that part of the 5‐HT1B receptor population was located on geniculate axon terminals within the SCN. The possible involvement of 5‐HT1B receptors, according to their cellular locations evidenced in the present study, in photic and nonphotic entrainment of the circadian clock is discussed. Synapse 33:314–323, 1999. © 1999 Wiley‐Liss, Inc.