The Role of Extracellular Calcium in Generating and in Phase-Shifting the Bulla Ocular Circadian Rhythm

Khalsa, Sat Bir S.; Ralph, Martin R.; Block, Gene D.

doi:10.1177/074873049300800203

Cited by 22 publications

(4 citation statements)

References 38 publications

(48 reference statements)

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“…, 2007). Similarly, earlier work also indicates that a Ca 2+ influx is required for light regulation of the circadian oscillator found in the retinas of marine mollusks (McMahon & Block, 1987; Khalsa et al. , 1993; Colwell et al.…”

Section: Discussionmentioning

confidence: 60%

“…In addition, ryanodine receptors may mediate lightand glutamate-induced phase delays of the circadian system (Ding et al, 1997) as well as regulate the electrical activity of SCN neurons (Aguilar-Roblero et al, 2007). Similarly, earlier work also indicates that a Ca 2+ influx is required for light regulation of the circadian oscillator found in the retinas of marine mollusks (McMahon & Block, 1987;Khalsa et al, 1993;Colwell et al, 1994) and more recently in mammals (Lundkvist et al, 2005). Thus, the NMDA receptormediated Ca 2+ influx is likely to be a major transducer of light information to the circadian system.…”

Section: Discussionmentioning

confidence: 86%

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Role for the NR2B subunit of the N‐methyl‐d‐aspartate receptor in mediating light input to the circadian system

Wang

Schroeder

Loh

et al. 2008

Eur J of Neuroscience

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Light information reaches the suprachiasmatic nucleus (SCN) through a subpopulation of retinal ganglion cells that utilize glutamate as a neurotransmitter. A variety of evidence suggests that the release of glutamate then activates N-methyl-D-aspartate (NMDA) receptors within the SCN and triggers a signaling cascade that ultimately leads to phase shifts in the circadian system. In this study, we first sought to explore the role of the NR2B subunit in mediating the effects of light on the circadian system of hamsters and mice. We found that localized microinjection of the NR2B subunit antagonist ifenprodil into the SCN region reduces the magnitude of light-induced phase shifts of the circadian rhythm in wheel-running activity. Next, we found that the NR2B message and levels of phospho-NR2B vary with time of day in SCN tissue using semiquantitative real-time polymerase chain reaction and western blot analysis, respectively. Functionally, we found that blocking the NR2B subunit with ifenprodil significantly reduced the magnitude of NMDA currents recorded in SCN neurons. Ifenprodil also significantly reduced the magnitude of NMDA-induced Ca2+ changes in SCN cells. Together, these results demonstrate that the NR2B subunit is an important component of NMDA receptor-mediated responses within SCN neurons and that this subunit contributes to light-induced phase shifts of the mammalian circadian system.

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Section: Discussionmentioning

confidence: 60%

Section: Discussionmentioning

confidence: 86%

Role for the NR2B subunit of the N‐methyl‐d‐aspartate receptor in mediating light input to the circadian system

Wang

Schroeder

Loh

et al. 2008

Eur J of Neuroscience

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“…In addition, there is recent evidence that ryanodine receptors mediate light-and glutamate-induced phase delays of the circadian system (Ding et al, 1998). Similarly, earlier work also indicates that a Ca 2+ influx is required for light regulation of the circadian oscillator found in the retinas of marine mollusks (e.g., McMahon and Block, 1987;Khalsa et al, 1993;Colwell et al, 1994). Finally, other likely components of this light-induced signal transduction cascade in the SCN include the release of nitric oxide (NO), activation of the Ras/MAP kinase cascade, and, ultimately, changes in gene expression (Ding et al, 1994;Obrietan et al, 1998;Reppert, 1998).…”

Section: Discussionmentioning

confidence: 92%

Serotonin Modulation of Calcium Transients in Cells in the Suprachiasmatic Nucleus

Flett¹,

Colwell

1999

J Biol Rhythms

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Information about environmental lighting conditions is conveyed to the suprachiasmatic nucleus (SCN), at least in part, via a glutamatergic fiber pathway originating in the retina, known as the retinohypothalamic tract (RHT). Previous work indicates that serotonin (5HT) can inhibit this pathway, although the underlying mechanisms are unknown. The authors became interested in the possibility that 5HT can inhibit the glutamatergic regulation of Ca2+ in SCN neurons and, by this mechanism, modulate light-induced phase shifts of the circadian system. To start to examine this hypothesis, optical techniques were used to measure Ca2+ levels in SCN cells in a brain slice preparation. First, it was found that 5HT produced a reversible and significant inhibition of Ca2+ transients evoked by synaptic stimulation. Next, it was found that 5HT did not alter the magnitude or duration of Ca2+ transients evoked by the bath application of glutamate or N-methyl-D-aspartate acid (NMDA) in the presence of tetrodotoxin (TTX). The authors feel that the simplest explanation for these results is that 5HT can act presynaptically at the RHT/SCN synaptic connection to inhibit the release of glutamate. The demonstration that 5HT can have a dramatic modulatory action on synaptic-evoked Ca2+ transients measured in SCN neurons adds support to the notion that the serotonergic innervation of the SCN may function to regulate environmental input to the circadian system. In addition, it was found that the administration of higher concentrations of 5HT can increase Ca2+ in at least a subpopulation of SCN neurons. This effect of 5HT was concentration dependent and blocked by a broad-spectrum 5HT antagonist (metergoline). In addition, both TTX and the gamma-amino-N-butyric acid (GABA) receptor blocker bicuculline inhibited the 5HT-induced Ca2+ transients. Therefore, the interpretation of this data is that 5HT can act within the SCN to alter GABAergic activity and, by this mechanism, cause changes in intracellular Ca2+. It is also suggested that this 5HT-induced Ca2+ increase might play a role in 5HT-induced phase shifts of the SCN circadian oscillator.

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“…The steps which occur after membrane potential changes are unknown although ultimately changes in protein synthesis may be involved (Eskin et al 1984b;Yeung and Eskin 1987;Raju et al 1990; Koumenis and Eskin 1992). In the related mollusk Bulla gouldiana, evidence suggests that a transmembrane calcium flux is a part of the phase shifting mechanism which occurs after changes in membrane potential (McMahon and Block 1987;Block 1988, 1990;Khalsa et al 1993). The present study was designed to investigate the role of extracellular calcium in mediating both 5-HT and light-induced phase shifts of the circadian ocular rhythm of the marine mollusk Aplysia.…”

Section: Introductionmentioning

confidence: 97%

Calcium plays a central role in phase shifting the ocular circadian pacemaker of Aplysia

et al. 1994

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The eye of the marine mollusk Aplysia californica contains an oscillator that drives a circadian rhythm of spontaneous compound action potentials in the optic nerve. Both light and serotonin are known to influence the phase of this ocular rhythm. The aim of the present study was to evaluate the role of extracellular calcium in both light and serotonin-mediated phase shifts. Low calcium treatments were found to cause phase shifts which resembled those produced by the transmitter serotonin. However, unlike serotonin, low calcium neither increased ocular cAMP levels nor could these phase shifts be prevented by increasing extracellular potassium concentration. Low calcium-induced phase shifts were prevented by the simultaneous application of the translational inhibitor anisomycin and low calcium treatment resulted in changes in [35S]methionine incorporation into several proteins as measured by a two-dimensional electrophoresis gel analysis. Finally, light treatments failed to produce phase shifts in the presence of low calcium or the calcium channel antagonist nickel chloride. These results are consistent with a model in which serotonin phase shifts the ocular pacemaker by decreasing a transmembrane calcium flux through membrane hyperpolarization while light-induced phase shifts are mediated by an increase in calcium flux.

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The Role of Extracellular Calcium in Generating and in Phase-Shifting the Bulla Ocular Circadian Rhythm

Cited by 22 publications

References 38 publications

Role for the NR2B subunit of the N‐methyl‐d‐aspartate receptor in mediating light input to the circadian system

Role for the NR2B subunit of the N‐methyl‐d‐aspartate receptor in mediating light input to the circadian system

Serotonin Modulation of Calcium Transients in Cells in the Suprachiasmatic Nucleus

Calcium plays a central role in phase shifting the ocular circadian pacemaker of Aplysia

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