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Subjective Night (subjective + night)
Selected AbstractsRoles of light and serotonin in the regulation of gastrin-releasing peptide and arginine vasopressin output in the hamster SCN circadian clockEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 7 2010Jessica M. Francl Abstract Daily timing of the mammalian circadian clock of the suprachiasmatic nucleus (SCN) is regulated by photic input from the retina via the retinohypothalamic tract. This signaling is mediated by glutamate, which activates SCN retinorecipient units communicating to pacemaker cells in part through the release of gastrin-releasing peptide (GRP). Efferent signaling from the SCN involves another SCN-containing peptide, arginine vasopressin (AVP). Little is known regarding the mechanisms regulating these peptides, as literature on in vivo peptide release in the SCN is sparse. Here, microdialysis,radioimmunoassay procedures were used to characterize mechanisms controlling GRP and AVP release in the hamster SCN. In animals housed under a 14/10-h light,dark cycle both peptides exhibited daily fluctuations of release, with levels increasing during the morning to peak around midday. Under constant darkness, this pattern persisted for AVP, but rhythmicity was altered for GRP, characterized by a broad plateau throughout the subjective night and early subjective day. Neuronal release of the peptides was confirmed by their suppression with reverse-microdialysis perfusion of calcium blockers and stimulation with depolarizing agents. Reverse-microdialysis perfusion with the 5-HT1A,7 agonist 8-OH-DPAT ((±)-8-hydroxydipropylaminotetralin hydrobromide) during the day significantly suppressed GRP but had little effect on AVP. Also, perfusion with the glutamate agonist NMDA, or exposure to light at night, increased GRP but did not affect AVP. These analyses reveal distinct daily rhythms of SCN peptidergic activity, with GRP but not AVP release attenuated by serotonergic activation that inhibits photic phase-resetting, and activated by glutamatergic and photic stimulation that mediate this phase-resetting. [source] Nerve growth factor-induced circadian phase shifts and MAP kinase activation in the hamster suprachiasmatic nucleiEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2005Gastón A. Pizzio Abstract Circadian rhythms are entrained by light and by several neurochemical stimuli. In hamsters housed in constant darkness, i.c.v. administration of nerve growth factor (NGF) at various times in their circadian cycle produced phase shifts of locomotor activity rhythms that were similar in direction and circadian timing to those produced by brief pulses of light. Moreover, the effect of NGF and light were not additive, indicating signalling points in common. These points include the immediate-early gene c-fos and ERK1/2, a component of the mitogen-activated protein kinases (MAPK) family. NGF activates c-FOS and ERK1/2-MAPK in the suprachiasmatic nuclei, the site of a circadian clock in mammals, when administered during the subjective night but not during the day. The effect of NGF on ERK1/2 activation was not inhibited by the administration of MK-801, a glutamate/NMDA receptor antagonist. These results suggest that NGF, acting through MAPK activation, plays a role in photic entrainment of the mammalian circadian clock. [source] Blockade of the NPY Y5 receptor potentiates circadian responses to light: complementary in vivo and in vitro studiesEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 4 2004P. C. Yannielli Abstract Neuropeptide Y (NPY) is delivered to the suprachiasmatic nuclei (SCN) circadian pacemaker via an input from the thalamic intergeniculate leaflet. NPY can inhibit light-induced responses of the circadian system of Syrian hamsters. Here we studied whether an antagonist to NPY receptors can be used to potentiate photic phase shifts late in the subjective night. First we determined by in situ hybridization that both NPY Y1 and Y5 receptor mRNA are expressed in the SCN of Syrian hamsters. Second, similar to our previous findings at Zeitgeber time 14 (ZT 14, where ZT 12 was the time of lights off), we found that NPY applied at ZT 18.5 onto the SCN region of brain slices maintained in vitro could block NMDA-induced phase advances of the spontaneous firing rate rhythm, and this blocking effect was probably mediated by the Y5 receptor, since co-application of Y5 receptor antagonists completely reversed the effect of NPY, while application of a Y1 receptor antagonist had no effect under the same conditions. Third, we found that co-treatment with a Y5 receptor antagonist in vivo (s.c., 10 mg/kg) not only reversed the effect of NPY applied to the SCN in vivo through a cannula but also significantly potentiated the light-induced phase advance in the absence of NPY. This is the first report of a NPY receptor antagonist having such an effect, and indicates that NPY Y5 receptor antagonists could be clinically useful for potentiating circadian system responses to light. [source] Differential adrenergic regulation of the circadian expression of the clock genes Period1 and Period2 in the rat pineal glandEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2000Seiichi Takekida Abstract Precise temporal regulation of transcription is pivotal to the role of the mammalian pineal gland as a transducer of circadian and seasonal information. The circadian clock genes Per1 and Per2 encode factors implicated in temporally gated transcriptional programmes in brain and pituitary. Here we show that the nocturnal circadian expression of Per1 and Per2 in the rat pineal gland parallels that of serotonin N-acetyltransferase (NAT) mRNA, which encodes the rate-limiting enzyme of melatonin biosynthesis. This rhythm is dependent upon an intact sympathetic innervation. Increases in rPer1 (r indicates rat) and rPer2, as well as rNAT, expression during subjective night were blocked completely by superior cervical ganglionectomy (SCGX). In SCGX rats, the ,-adrenergic receptor agonist isoproterenol rapidly induced the rPer1 mRNA with dynamics very similar to its effect on rNAT mRNA. In contrast, isoproterenol was without effect on expression of rPer2 mRNA. These findings demonstrate that circadian pineal expression of both rPer1 and rPer2 is controlled by sympathetic afferent innervation, but whereas ,-adrenergic signalling regulates rPer1 and rNAT, an alternative route mediates sympathetic regulation over rPer2 expression. [source] Circadian rhythm of aromatic l -amino acid decarboxylase in the rat suprachiasmatic nucleus: gene expression and decarboxylating activity in clock oscillating cellsGENES TO CELLS, Issue 5 2002Yoshiki Ishida Background: Aromatic l -amino acid decarboxylase (AADC) is the enzyme responsible for the decarboxylation step in both the catecholamine and indoleamine synthetic pathways. In the brain, however, a group of AADC containing neurones is found outside the classical monoaminergic cell groups. Since such non-monoaminergic AADC is expressed abundantly in the suprachiasmatic nucleus (SCN), the mammalian circadian centre, we characterized the role of AADC in circadian oscillation. Results : AADC gene expression was observed in neurones of the dorsomedial subdivision of the SCN and its dorsal continuant in the anterior hypothalamic area. These AADC neurones could uptake exogenously applied L-DOPA and formed dopamine. AADC was co-expressed with vasopressin and the clock gene Per1 in the neurones of the SCN. Circadian gene expression of AADC was observed with a peak at subjective day and a trough at subjective night. The circadian rhythm of AADC enzyme activity in the SCN reflects the expression of the gene. Conclusions: Non-monoaminergic AADC in the SCN is expressed in clock oscillating cells, and the decarboxylating activity of master clock cells are under the control of the circadian rhythm. [source] Photic Regulation of mt1 Melatonin Receptors in the Siberian Hamster Pars Tuberalis and Suprachiasmatic Nuclei: Involvement of the Circadian Clock and Intergeniculate LeafletJOURNAL OF NEUROENDOCRINOLOGY, Issue 3 2000Schuster In the Siberian hamster suprachiasmatic nuclei and pars tuberalis of the pituitary, high affinity mt1 melatonin receptors are present. We have previously shown that night applied light pulse induced an increase in mt1 mRNA expression in the suprachiasmatic nuclei of this species, independently of the endogenous melatonin. Here, we report the photic regulation of melatonin receptor density and mRNA expression in the suprachiasmatic nuclei and pars tuberalis of pinealectomized Siberian hamsters and the implication in this control of either the circadian clock or the intergeniculate leaflet. The results show that: (1) A 1-h light pulse, delivered during the night, induces a transitory increase in mt1 mRNA expression in the suprachiasmatic nuclei and pars tuberalis. After 3 h this increase has totally disappeared (suprachiasmatic nuclei) or is greatly reduced (pars tuberalis). (2) The melatonin receptor density, in the suprachiasmatic nuclei, is not affected by 1 or 3 h of light, while it is strongly increased in the pars tuberalis. (3) In hamsters kept in constant darkness, the mt1 mRNA rise is gated to the subjective night in the suprachiasmatic nuclei and pars tuberalis. In contrast, the light-induced increase in melatonin binding is also observed in the subjective day in the pars tuberalis. (4) intergeniculate leaflet lesion totally inhibits the mt1 mRNA expression rise in the suprachiasmatic nuclei, while it has no effect on the light-induced increase in mt1 mRNA in the pars tuberalis. However, the light-induced increase in melatonin receptor density is totally prevented by the intergeniculate leaflet lesion in the pars tuberalis. These results show that: (1) the photic regulations of mt1 mRNA expression and receptor density are independent of each other in both the suprachiasmatic nuclei and pars tuberalis; and (2) the circadian clock and the intergeniculate leaflet are implicated in the photic regulation of melatonin receptors but their level of action differs totally between the suprachiasmatic nuclei and pars tuberalis. [source] Effect of stimulation of endogenous melatonin secretion during constant light exposure on 6-sulphatoxymelatonin rhythmicity in ratsJOURNAL OF PINEAL RESEARCH, Issue 1 2000D.J. Kennaway When light is presented unexpectedly at night to rats, melatonin production and secretion is acutely inhibited and the time of onset of production on the subsequent night is altered. In a series of experiments, we examined the effects of 6,12 hr light (200 lux) at night on melatonin metabolite excretion (6-sulphatoxymelatonin, aMT.6S). During the light exposure, we administered isoproterenol to stimulate endogenous production of melatonin by the pineal gland to determine if replacement of melatonin would block any phase shifting effects of the light. Exposure to 6 hr of light either during the first or second half of the night suppressed aMT.6S excretion during the light treatment and delayed the onset of melatonin secretion by 3.7±0.6 and 2.5±0.6 hr, respectively, compared to a change of 0.5±0.1 hr in animals maintained in darkness. Twelve hours light exposure (i.e. one night of continuous light) suppressed aMT.6S excretion completely and resulted in a delay in the onset the next night of 2.1±0.7 hr. When propranolol (10 mg/kg) was administered at 2-hr intervals during darkness, aMT.6S excretion was suppressed throughout the night, but on the subsequent release into constant darkness the onset of excretion was not delayed (0.6±0.1 hr delay). Administration of isoproterenol (10 mg/kg) to animals in constant light, at the time of expected lights off (CT12), and 5 hr later (CT17) resulted in an increase in melatonin production and aMT.6S excretion that was similar in duration and amount to the control night. The stimulation of endogenous melatonin production failed to block the phase shifting effects of the light exposure and, in fact, appeared to potentiate the delay at least on the first night (4.2±0.9 hr). The timing of the release into constant darkness following the light treatment had an unexpected effect on melatonin production on the cycle after treatment. Thus, animals exposed to 12 hr light and released into darkness at the normal time of lights off as above had a delay of about 2 hr and excreted 71±18% of the aMT.6S excreted on a control night. Animals released into darkness at the expected time of lights on failed to excrete more than 20 pmol/hr (i.e. no onset of excretion could be determined) at any time on the first subjective night after light treatment, which was no different from the excretion during the light treatment. On the next subjective night, the onset was delayed as expected and the amount of aMT.6S produced was restored. Treatment with isoproterenol at CT12 and CT17 failed to affect either the amount of aMT.6S excreted on the first subjective night after light treatment or the phase delay on the second night after treatment. The failure to produce melatonin on the first subjective night after 12 hr light exposure and release into darkness at CTO was not due to failure at the level of the pineal gland since injection of isoproterenol at CT12 and CT17 on the first subjective night after light restored the normal amount of melatonin production. These results suggest that the absence of melatonin during light stimulation at night is not responsible for the phase delay in melatonin production and excretion on subsequent nights. The basis of the failure of the rats to commence melatonin production following 12 hr extended light exposure followed immediately by continuous darkness is not known. [source] Circadian rhythms and the evolution of photoperiodic timing in insectsPHYSIOLOGICAL ENTOMOLOGY, Issue 4 2009DAVID S. SAUNDERS Abstract. This review discusses possible evolutionary trends in insect photoperiodism, mainly from a chronobiological perspective. A crucial step was the forging of a link between the hormones regulating diapause and the systems of biological rhythms, circadian or circannual, which have independently evolved in eukaryotes to synchronize physiology and behaviour to the daily cycles of light and darkness. In many of these responses a central feature is that the circadian system resets to a constant phase at the beginning of the subjective night, and then ,measures' the duration of the next scotophase. In ,external coincidence', one version of such a clock, light now has a dual role. First, it serves to entrain the circadian system to the stream of pulses making up the light/dark cycle and, second, it regulates the nondiapause/diapause switch in development by illuminating/not illuminating a specific light sensitive phase falling at the end of the critical night length. Important work by A. D. Lees on the aphid Megoura viciae using so-called ,night interruption experiments' demonstrates that pulses falling early in the night lead to long-day effects that are reversible by a subsequent dark period longer than the critical night length and also show maximal sensitivity in the blue,green range of the spectrum. Pulses falling in the latter half of the night, however, produce long-day effects that are irreversible by a subsequent long-night and show a spectral sensitivity extending into the red. With movement to higher latitudes, insects develop genetic clines in various parameters, including critical night length, the number of long-night cycles needed for diapause induction, the strength of the response, and the ,depth' or intensity of the diapause thus induced. Evidence for these and other types of photoperiodic response suggests that they provided strong selective advantages for insect survival. [source] | ||||||||||