(1-3 days) constant light exposure (brief LL) potentiates nonphotic phase shifting induced by sleep deprivation and serotonin (5-HT) agonist stimulation. The present assessments reveal that exposure to brief LL markedly alters the magnitude and shape of the 5-HT 1A,7 receptor agonist, 8-(ϩ)2-dipropyl-amino-8-hydroxyl-1,2,3,4-tetrahyronapthalene (8-OH-DPAT) phase-response curve, facilitating (ϳ12 h) phase-advance shifts during the early morning when serotonergics have no phase-shifting effect. Brief LL also reduces the threshold for 8-OH-DPAT shifting at midday, evidenced by 5-to 6-h phase-advance shifts elicited by dosages that have no effect without the LL treatment. The brief LL-potentiated phase advances to intraperitoneal 8-OH-DPAT at zeitgeber time 0 (ZT 0) were blocked by the 5-HT 1A antagonists, pindolol and WAY 100635, indicating that this shifting is mediated by 5-HT 1A receptors. Antagonists with action at 5-HT7 receptors, including ritanserin and metergoline, were without effect. Although autoradiographic analyses of [ 3 H]8-OH-DPAT binding indicate that brief LL does not upregulate suprachiasmatic nucleus (SCN) 5-HT 1A receptor binding, intra-SCN microinjection of 8-OH-DPAT at ZT 0 in brief LL-exposed hamsters induced shifts similar to those produced by intraperitoneal injection, suggesting that SCN 5-HT 1A receptors mediate potentiated 8-OH-DPAT-induced shifts during the early morning. Lack of shifting by intra-SCN 8-OH-DPAT at ZT 6 or 18 (when intraperitoneal 8-OH-DPAT induces large shifts), further indicates that brief LL-potentiated shifts at these time points are mediated by 5-HT target(s) outside the SCN. Significantly, sleep deprivation-induced phase-advance shifts potentiated by brief LL (ϳ9 h) at ZT 0 were blocked by pindolol, suggesting that these behavioral shifts could be mediated by the same SCN 5-HT 1A receptor phase-resetting pathway as that activated by 8-OH-DPAT treatment. suprachiasmatic nucleus; sleep deprivation; 8-OH-DPAT THE SUPRACHIASMATIC NUCLEUS (SCN) of the anterior hypothalamus is the site of the master circadian clock in mammals (21,23,40,47). The SCN clock is entrained by photic input received principally from the retina via the retinohypothalamic tract and nonphotic signaling received from the intergeniculate leaflet via the geniculohypothalamic tract, and possibly from the midbrain raphe nuclei (28). Inputs from these nonphotic sources to the SCN are mediated by neuropeptide Y and serotonin (5-HT), respectively (34, 41).In Syrian hamsters, nonphotic stimuli, in the form of behavioral manipulations (e.g., social interaction, cage changing, novel wheel exposure, or sleep deprivation) or pharmacological intervention (e.g., 5-HT agonists or benzodiazepines) can induce phase shifts similar in magnitude to photic shifts (ϳ1-2 h) (15,31,36). Recently, we demonstrated that nonphotic shifting responses of hamsters receiving sleep deprivation treatment or systemic application of the 5-HT 1A,7 receptor agonist 8-OH-DPAT are greatly potentiated (ϳ10 -12 h) by prior treatment with s...