These results indicate that transcriptional activation of bspA is complex. The Ca 2+ ionophore, ionomycin, also induced GUS activity in excised shoots. Inhibition by EGTA was partially relieved by the addition of Ca 2+. Glutamine plus sucrose induction of GUS activity was inhibited by EGTA, okadaic acid, or K-252A. ![]() The addition of sucrose with either glutamine or NH 4NO 3 resulted in synergistic induction of GUS, whereas sucrose alone had no effect. Treatment with either glutamine or NH 4NO 3 resulted in increased stem GUS activity. Because changes in photoperiod and growth also alter carbon and nitrogen partitioning, the role of carbon and nitrogen metabolites in modulating the activity of the bspA promoter were investigated by treating excised stems with amino acids or NH 4NO 3 with or without sucrose. Stimulating shoot growth in plants treated with SD inhibited SD-induced increases in bark GUS activity. When growth was inhibited under growth permissive photoperiods ( SD with night break) levels of bark β-glucuronidase (GUS) activity increased. ![]() High levels of bspA expression usually occur in the bark of plants during SD but not long day or SD with a night break. Activity of the bspA promoter was also influenced by shoot growth. Photoperiodic activation of the bspA promoter was shown to involve perception by phytochrome and likely involves both a low fluence response and a parallel very low fluence response pathway. In this study, poplars transformed with a chimeric gene consisting of the bspA promoter fused to β-glucuronidase ( uidA) were used to investigate the transcriptional regulation of the bspA promoter. These findings suggest that buspirone affected the circadian system in a manner similar to the 5-HT 1A/7 agonist (±)-8-Hydroxy-2-dipropylaminotetralin hydrobromide, primarily through the 5-HT 1A receptor, and suggest that therapeutic use of buspirone to manage anxiety may impact circadian function.In poplars ( Populus), bspA encodes a 32-kD bark storage protein that accumulates in the inner bark of plants exposed to either short-day ( SD) photoperiods or elevated levels of nitrogen. Buspirone administration at midday produced non-photic phase advances in wildtype but not 5-HT 1A receptor knockout mice. Chronic buspirone treatment decreased the amplitude of wheel-running rhythms, lengthened the duration of the active phase and advanced the phase angle of entrainment. ![]() Attenuated photic phase shifts in buspirone-treated hamsters were accompanied by decreased phosphorylation of ERK and CREB. In wildtype mice, the attenuated phase shifts were accompanied by increased cFos expression in the suprachiasmatic nucleus, whereas potentiated phase shifts in knockouts were accompanied by increased phosphorylation of extracellular signal-regulated kinase (ERK) and cyclic AMP response element-binding protein (CREB), and decreased cFos expression. ![]() 5-HT 1A receptor knockout mice exhibited potentiated photic phase shifts when pretreated with buspirone. Phase advances to late subjective night light pulses in hamsters and wildtype mice were significantly attenuated by buspirone. Here we examined behavioral and molecular responses to phase-shifting light in mice and hamsters treated with buspirone. Given that buspirone is used therapeutically to manage generalised anxiety disorder, it would be useful to understand if and how this drug may modify circadian responses to light, not only to help manage side effects, but also to examine its potential use as a chronobiotic. The anxiolytic buspirone is a 5-HT 1A receptor partial agonist. Serotonergic drugs modify circadian responses to light, with agonists attenuating and some partial agonists or antagonists potentiating photic phase shifts.
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