GABAergic modulation of gap junction communication in slice cultures of the rat suprachiasmatic nucleus

Shinohara, Kazuyuki; Hiruma, Hiromi; Funabashi, Toshiya; Kimura, Fukuko

doi:10.1016/s0306-4522(99)00556-4

Cited by 56 publications

(38 citation statements)

References 39 publications

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“…1C). Gap junction inhibitors reduce the frequency of small APs and alter the normal firing rate of large APs, suggesting that gap junctions are involved in modulating membrane excitability of lLN v s. This is consistent with observations of cockroach lateral neurons (Schneider and Stengl, 2006), where gap junction blockers also influence spontaneous AP firing rate, and clock neurons in mammalian SCN (Colwell, 2000;Shinohara et al, 2000;Long et al, 2005;Rash et al, 2007). However, none of the three gap junction blockers had any effect on the amplitude of either large or small APs, thus making it highly unlikely that APs generated in coupled cells are propagating passively to the site of recording at the soma through gap junctions.…”

Section: Discussionsupporting

confidence: 78%

Circadian Control of Membrane Excitability in Drosophila melanogaster Lateral Ventral Clock Neurons

Cao¹,

Nitabach²

2008

Journal of Neuroscience

147

182

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Section: Discussionsupporting

confidence: 78%

Circadian Control of Membrane Excitability in Drosophila melanogaster Lateral Ventral Clock Neurons

Cao¹,

Nitabach²

2008

Journal of Neuroscience

147

182

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“…We report that GABA reduces the extent and strength of electrical coupling (see also Piccolino et al, 1982;Shinohara et al, 2000). Surprisingly, we found no effect of GABA on the input resistance Figure 7.…”

Section: Gabaergic Modulation Of Gap Junctional Couplingmentioning

confidence: 55%

Removal of GABA within Adult Modulatory Systems Alters Electrical Coupling and Allows Expression of an Embryonic-Like Network

Ducret¹,

Feuvre²,

Meyrand³

et al. 2007

J. Neurosci.

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The maturation and operation of neural networks are known to depend on modulatory neurons. However, whether similar mechanisms may control both adult and developmental plasticity remains poorly investigated. To examine this issue, we have used the lobster stomatogastric nervous system (STNS) to investigate the ontogeny and role of GABAergic modulatory neurons projecting to small pattern generating networks. Using immunocytochemistry, we found that modulatory input neurons to the stomatogastric ganglion (STG) express GABA only after metamorphosis, a time that coincides with the developmental switch from a single to multiple pattern generating networks within the STNS. We demonstrate that blocking GABA synthesis with 3-mercapto-propionic acid within the adult modulatory neurons results in the reconfiguration of the distinct STG networks into a single network that generates a unified embryoniclike motor pattern. Using dye-coupling experiments, we also found that gap-junctional coupling is greater in embryos and GABAdeprived adults exhibiting the unified motor pattern compared with control adults. Furthermore, GABA was found to diminish directly the extent and strength of electrical coupling within adult STG networks. Together, these observations suggest the acquisition of a GABAergic phenotype by modulatory neurons after metamorphosis may induce the reconfiguration of the single embryonic network into multiple adult networks by directly decreasing electrical coupling. The findings also suggest that adult neural networks retain the ability to express typical embryonic characteristics, indicating that network ontogeny can be reversed and that changes in electrical coupling during development may allow the segregation of multiple distinct functional networks from a single large embryonic network.

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“…Several studies have addressed the question of the physiological role of GABA in the SCN 45,46 . GABA may be a coupling agent between SCN cells 45 , as it is able to acutely inhibit SCN neuron firing rate (through GABA B receptors) and shift the phase of these neurons (through GABA A receptors).…”

Section: Discussionmentioning

confidence: 99%

Light induces chromatin modification in cells of the mammalian circadian clock

et al. 2000

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The central mammalian circadian clock is located in neurons of the hypothalamic suprachiasmatic nucleus [1][2][3] . The pacemaker activity of the SCN is autonomous, as it functions in constant darkness and in the absence of external light stimuli 1-3 ; however, it can be entrained by environmental light-dark cycles 4 . In rodents, at least three neural pathways link the retina to the SCN: first, the direct, monosynaptic retino-hypothalamic tract (RHT), whose main neurotransmitters seem to be excitatory amino acids such as glutamate 5,6 ; second, the indirect multisynaptic projection from the intergeniculate leaflet (IGL), which acts via the release of the protein neurotransmitter neuropeptide Y and the inhibitory neurotransmitter γ-aminobutyric acid (GABA) 7,8 ; third, an indirect pathway arising from the dorsal and median raphe nucleus, in which serotonin is the main neurotransmitter 9 . Although the RHT alone seems necessary and sufficient to mediate light entrainment 10 , interference with the IGL and/or dorsal raphe nucleus transmission 11 can modify the response of the SCN to light. In mammals kept in darkness, a light pulse during the subjective night (that is, the time of the day corresponding to the dark period in a normal light-dark cycle) causes phase-shifting of the SCN-controlled rhythms 4 . The phase-shift stimulated by light triggers gene expression within the SCN, including the rapid and transient activation of clock genes, such as Per1 and Per2 (refs. 12, 13) and of immediate early genes (IEGs), such as c-fos, fos -B, jun-B, nur77 and zif268 (refs. 14, 15). These changes in gene expression have been implicated in phase-shifting the pacemaker 16,17 . Although the photic regulation of c-fos expression in the SCN has been extensively studied, the pivotal events enabling dynamic regulation at the chromosomal level are not yet known.Light pulses induce activation of the mitogen activated protein kinase (MAPK) 18 , and thus possibly modulate the physiological function of substrates within the SCN. In particular, light pulses induce phosphorylation of transcription factor CREB (cAMP response-element binding protein) on serine 133 (ref. 19), the essential phospho-acceptor site that enables the recruiting of the co-activator CBP, a protein with histone acetyltransferase (HAT) activity 20 . Factors of the CREB family are involved in circadian rhythmicity both in Drosophila 21 and mammals 22 .Modifications occurring on histone tails are primary events that contribute to the dynamic process of chromatin remodeling, an essential step in transcriptional regulation 23 . Both chromatin remodeling factors and covalent histone modifications facilitate access of transcription factors to chromatin, and regulate expression of a wide range of genes 24 . A number of post-translational modifications occur on histone tails (for review, see ref. 23). Among these, inducible phosphorylation at serine 10 of the histone H3 N-terminal tail in response to a mitogenic stimulus represents the best characterized link between ac...

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GABAergic modulation of gap junction communication in slice cultures of the rat suprachiasmatic nucleus

Cited by 56 publications

References 39 publications

Circadian Control of Membrane Excitability in Drosophila melanogaster Lateral Ventral Clock Neurons

Circadian Control of Membrane Excitability in Drosophila melanogaster Lateral Ventral Clock Neurons

Removal of GABA within Adult Modulatory Systems Alters Electrical Coupling and Allows Expression of an Embryonic-Like Network

Light induces chromatin modification in cells of the mammalian circadian clock

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