Excitatory Mechanisms in the Suprachiasmatic Nucleus: The Role of AMPA/KA Glutamate Receptors

Michel, Stephan; Itri, Jason N.; Colwell, Christopher S.

doi:10.1152/jn.2002.88.2.817

Cited by 66 publications

(63 citation statements)

References 74 publications

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“…Subsequently, GABAmediated IPSCs appear as inward currents because the reversal potential for chloride was more positive than the holding potential. Synaptic events were excluded if the decay time was Ͻ4.6 ms to eliminate AMPAmediated events (Michel et al, 2002).…”

Section: Whole-cell Patch-clamp Recordingmentioning

confidence: 99%

Evidence for Neuronal Desynchrony in the Aged Suprachiasmatic Nucleus Clock

Farajnia¹,

Michel²,

Deboer³

et al. 2012

J. Neurosci.

198

212

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Aging is associated with a deterioration of daily (circadian) rhythms in physiology and behavior. Deficits in the function of the central circadian pacemaker in the suprachiasmatic nucleus (SCN) have been implicated, but the responsible mechanisms have not been clearly delineated. In this report, we characterize the progression of rhythm deterioration in mice to 900 d of age. Longitudinal behavioral and sleep-wake recordings in up to 30-month-old mice showed strong fragmentation of rhythms, starting at the age of 700 d. Patch-clamp recordings in this age group revealed deficits in membrane properties and GABAergic postsynaptic current amplitude. A selective loss of circadian modulation of fast delayed-rectifier and A-type K ϩ currents was observed. At the tissue level, phase synchrony of SCN neurons was grossly disturbed, with some subpopulations peaking in anti-phase and a reduction in amplitude of the overall multiunit activity rhythm. We propose that aberrant SCN rhythmicity in old animals-with electrophysiological arrhythmia at the single-cell level and phase desynchronization at the network level-can account for defective circadian function with aging.

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Section: Whole-cell Patch-clamp Recordingmentioning

confidence: 99%

Evidence for Neuronal Desynchrony in the Aged Suprachiasmatic Nucleus Clock

Farajnia¹,

Michel²,

Deboer³

et al. 2012

J. Neurosci.

198

212

View full text Add to dashboard Cite

show abstract

“…Methods were similar to those described previously (Colwell, 2000;Michel et al, 2002;Paz Soldan et al, 2003). Briefly, a cooled CCD camera (Microview model; 1317 ϫ 1035 pixel format; Princeton Instruments, Monmouth Junction, NJ) was added to the Olympus (Melville, NY) fixed-stage microscope to measure fluorescence.…”

Section: Analysis Of the Golli Ko Transgenic Micementioning

confidence: 99%

Region-Specific Myelin Pathology in Mice Lacking the Golli Products of the Myelin Basic Protein Gene

Jacobs

Pribýl²,

Feng³

et al. 2005

J. Neurosci.

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The myelin basic protein (MBP) gene encodes two families of proteins, the classic MBP constituents of myelin and the golli-MBPs, the function of which is less well understood. In this study, targeted ablation of the golli-MBPs, but not the classic MBPs, resulted in a distinct phenotype unlike that of knock-outs (KOs) of the classic MBPs or other myelin proteins. Although the golli KO animals did not display an overt dysmyelinating phenotype, they did exhibit delayed and/or hypomyelination in selected areas of the brain, such as the visual cortex and the optic nerve, as determined by Northern and Western blots and immunohistochemical analysis with myelin protein markers. Hypomyelination in some areas, such as the visual cortex, persisted into adulthood. Ultrastructural analysis of the KOs confirmed both the delay and hypomyelination and revealed abnormalities in myelin structure and in some oligodendrocytes. Abnormal visual-evoked potentials indicated that the hypomyelination in the visual cortex had functional consequences in the golli KO brain. Evidence that the abnormal myelination in these animals was a consequence of intrinsic problems with the oligodendrocyte was indicated by an impaired ability of oligodendrocytes to form myelin sheets in culture and by the presence of abnormal Ca 2ϩ transients in purified cortical oligodendrocytes studied in vitro. The Ca 2ϩ results reported in this study complement previous results implicating golli proteins in modulating intracellular signaling in T-cells. Together, all these findings suggest a role for golli proteins in oligodendrocyte differentiation, migration, and/or myelin elaboration in the brain.

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“…Methods are similar to those described previously (Colwell 2001;Michel et al 2002). Slices were placed in a chamber (PH-1, Warner Instruments) attached to the stage of a fixed-stage upright microscope.…”

Section: Whole Cell Patch-clamp Electrophysiologymentioning

confidence: 99%

“…Once the whole cell configuration was established, whole cell capacitance was calculated from voltage transients produced by a 20-mV voltage step lasting 40 ms according to standard methods (Colwell 2001;Michel et al 2002). Whole cell capacitance and electrode resistance were neutralized.…”

Section: Whole Cell Patch-clamp Electrophysiologymentioning

confidence: 99%

Regulation of Inhibitory Synaptic Transmission by Vasoactive Intestinal Peptide (VIP) in the Mouse Suprachiasmatic Nucleus

Itri

Colwell

2003

Journal of Neurophysiology

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Itri, Jason and Christopher S. Colwell. Regulation of inhibitory synaptic transmission by vasoactive intestinal peptide (VIP) in the mouse suprachiasmatic nucleus. J Neurophysiol 90: 1589 -1597, 2003;; 10.1152/jn.00332.2003. Circadian rhythmicity in mammals is generated by a pair of nuclei in the anterior hypothalamus known as the suprachiasmatic nuclei (SCN), whose neurons express a variety of neuropeptides that are thought to play an important role in the circadian timing system. To evaluate the influence of VIP on inhibitory synaptic transmission between SCN neurons, we used whole cell patch-clamp recording in an acute brain slice preparation of mouse SCN. Baseline spontaneous GABAergic inhibitory postsynaptic currents (IPSCs) varied significantly between regions and across phases, with a greater frequency of IPSCs observed in the dorsomedial region during the early night. Bath-applied VIP caused a significant increase in the frequency of spontaneous inhibitory postsynaptic currents (sIPSC) in a reversible and dose-dependent manner with no effect on the mean amplitude or kinetic parameters. The effect of VIP was widespread throughout the SCN and observed in both ventrolateral (VL) and dorsomedial (DM) regions. In the presence of tetrodotoxin, VIP increased the frequency of miniature IPSCs without affecting the mean magnitude or kinetic parameters. The magnitude of the enhancement by VIP was significantly larger during the day than during the night. Pretreatment with the VIP-PACAP receptor antagonist [AcTyr 1 , D-Phe 2 ]-GHRF 1-29 or the selective VPAC 2 receptor antagonist PG 99-465 completely blocked the VIP-induced enhancement. The effect of VIP appears to be mediated by a cAMP/PKA-dependent mechanism as forskolin mimics, while the PKA antagonist H-89 blocks the observed enhancement of GABA currents. Our data suggest that VIP activates presynaptic VPAC 2 receptors to regulate inhibitory synaptic transmission within the SCN and that this effect varies from day to night.

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Excitatory Mechanisms in the Suprachiasmatic Nucleus: The Role of AMPA/KA Glutamate Receptors

Cited by 66 publications

References 74 publications

Evidence for Neuronal Desynchrony in the Aged Suprachiasmatic Nucleus Clock

Evidence for Neuronal Desynchrony in the Aged Suprachiasmatic Nucleus Clock

Region-Specific Myelin Pathology in Mice Lacking the Golli Products of the Myelin Basic Protein Gene

Regulation of Inhibitory Synaptic Transmission by Vasoactive Intestinal Peptide (VIP) in the Mouse Suprachiasmatic Nucleus

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