Intrinsic Neuronal Rhythms in the Suprachiasmatic Nuclei and their Adjustment

Gillette, Martha U.; Medanic, M.; McArthur, Angela J.; Liu, C.; Ding, Jian; Faiman, Lia E.; Weber, E. Todd; Tcheng, Thomas K.; Gallman, Eve A.

doi:10.1002/9780470514597.ch8

Cited by 31 publications

(10 citation statements)

References 43 publications

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“…The SCN generates a circadian rhythm of spontaneous action potentials (12). For up to 3 days in vitro, we recorded this rhythm from SCN neurons within the murine brain slice using single-unit extracellular electrodes.…”

Section: Resultsmentioning

confidence: 99%

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HIV protein, transactivator of transcription, alters circadian rhythms through the light entrainment pathway

Clark¹,

Sampair²,

Kofuji³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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Patients infected with the human immunodeficiency virus (HIV), and other mammals infected with related lentiviruses, exhibit fatigue, altered sleep patterns, and abnormal circadian rhythms. A circadian clock in the hypothalamic suprachiasmatic nucleus (SCN) temporally regulates these functions in mammals. We found that a secretary HIV transcription factor, transactivator of transcription (Tat), resets the murine circadian clock, in vitro and in vivo, at clinically relevant concentrations (EC(50) = 0.31 nM). This effect of Tat occurs only during the subjective night, when N-methyl-D-aspartate (NMDA) receptor [D-2-amino-5-phosphonovaleric acid (0.1 mM)] and nitric oxide synthase (N(G)-nitro-L-arginine methyl ester, 0.1 mM) inhibitors block Tat-induced phase shifts. Whole cell recordings of SCN neurons within the brain slice revealed that Tat did not activate NMDA receptors directly but potentiated NMDA receptor currents through the enhancement of glutamate release. Consistent with this presynaptic mechanism, inhibitors of neurotransmission block Tat-induced phase shifts, such as tetrodotoxin (1 microM), tetanus toxin (1 microM), P/Q/N type-calcium channel blockers (1 microM omega-agatoxin IVA and 1 microM omega-conotoxin GIVA) and bafilomycin A(1) (1 microM). Thus the effect of Tat on the SCN may underlie lentiviral circadian rhythm dysfunction by operating as a disease-dependent modulator of light entrainment through the enhancement of excitatory neurotransmission.

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Section: Resultsmentioning

confidence: 99%

“…Action potentials generated from individual neurons were isolated on an oscilloscope with a window discriminator in real time on the basis of amplitude, waveform, polarity and cadence and counted by a customized program (Labview, National Instruments, Austin, TX). Running means were calculated to determine the time of peak activity (12).…”

Section: Methodsmentioning

confidence: 99%

HIV protein, transactivator of transcription, alters circadian rhythms through the light entrainment pathway

Clark¹,

Sampair²,

Kofuji³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Extracellular recording of spontaneous SUA of SCN neurons has been described previously [26]. Briefly, the firing rate of an individual neuron is recorded and its mean SUA determined over 4 min; the electrode is repositioned and the process repeated.…”

Section: Methodsmentioning

confidence: 99%

Circadian Integration of Glutamatergic Signals by Little SAAS in Novel Suprachiasmatic Circuits

et al. 2010

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BackgroundNeuropeptides are critical integrative elements within the central circadian clock in the suprachiasmatic nucleus (SCN), where they mediate both cell-to-cell synchronization and phase adjustments that cause light entrainment. Forward peptidomics identified little SAAS, derived from the proSAAS prohormone, among novel SCN peptides, but its role in the SCN is poorly understood.Methodology/Principal FindingsLittle SAAS localization and co-expression with established SCN neuropeptides were evaluated by immunohistochemistry using highly specific antisera and stereological analysis. Functional context was assessed relative to c-FOS induction in light-stimulated animals and on neuronal circadian rhythms in glutamate-stimulated brain slices. We found that little SAAS-expressing neurons comprise the third most abundant neuropeptidergic class (16.4%) with unusual functional circuit contexts. Little SAAS is localized within the densely retinorecipient central SCN of both rat and mouse, but not the retinohypothalamic tract (RHT). Some little SAAS colocalizes with vasoactive intestinal polypeptide (VIP) or gastrin-releasing peptide (GRP), known mediators of light signals, but not arginine vasopressin (AVP). Nearly 50% of little SAAS neurons express c-FOS in response to light exposure in early night. Blockade of signals that relay light information, via NMDA receptors or VIP- and GRP-cognate receptors, has no effect on phase delays of circadian rhythms induced by little SAAS.Conclusions/SignificanceLittle SAAS relays signals downstream of light/glutamatergic signaling from eye to SCN, and independent of VIP and GRP action. These findings suggest that little SAAS forms a third SCN neuropeptidergic system, processing light information and activating phase-shifts within novel circuits of the central circadian clock.

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“…Thus, evidence supports the involvement of glutamate, GABA, and serotonin signaling in the development of acute tolerance. Interestingly, these three neurotransmitter systems play critical roles in regulating the phase of the mammalian circadian clock (Gillette et al, 1995;Hastings et al, 1998). Furthermore, we and others have shown that ethanol profoundly disrupts phase regulation of mammalian circadian rhythms.…”

Section: Introductionmentioning

confidence: 99%

The Mammalian Circadian Clock Exhibits Acute Tolerance to Ethanol

Prosser

Glass²

2009

Alcoholism Clin & Exp Res

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Background-Tolerance to ethanol is observed over a variety of time courses, from minutes to days. Acute tolerance, which develops over 5-60 minutes, has been observed for both behavioral and neurophysiological variables, and may involve changes in signaling through NMDA, GABA, or other receptors. Previous work has shown that both acute and chronic ethanol treatments modulate photic and non-photic phase resetting of the mammalian circadian clock located in the suprachiasmatic nucleus (SCN). Although not specifically tested, the data thus far do not point to the development of chronic tolerance to the modulatory effects of ethanol. Here we investigated whether acute tolerance the ethanol occurs with respect to in vitro phase modulation of the SCN clock.

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Intrinsic Neuronal Rhythms in the Suprachiasmatic Nuclei and their Adjustment

Cited by 31 publications

References 43 publications

HIV protein, transactivator of transcription, alters circadian rhythms through the light entrainment pathway

HIV protein, transactivator of transcription, alters circadian rhythms through the light entrainment pathway

Circadian Integration of Glutamatergic Signals by Little SAAS in Novel Suprachiasmatic Circuits

The Mammalian Circadian Clock Exhibits Acute Tolerance to Ethanol

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