Activity-Induced Expression of Common Reference Genes in Individual CNS Neurons

Chen, Jian; Сочивко, Д. Г.; Beck, Hanno; Maréchal, Daniel; Wiestler, Otmar D.; Becker, Albert

doi:10.1038/labinvest.3780300

Cited by 72 publications

(45 citation statements)

References 6 publications

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“…The signal threshold was set within the exponential phase of the reaction for determination of the threshold cycle (C t ). Synaptophysin was used as an endogenous, neuron-specific reference gene, because it does not show expression changes at early (1-3 d, 5 d, and 10 d; data not shown; n ϭ 5 each) or late (Chen et al, 2001) stages after pilocarpine-induced SE. Relative quantification started from 5.0 -10.0 ng of mRNA.…”

Section: Methodsmentioning

confidence: 99%

Transcriptional Upregulation of Ca_v3.2 Mediates Epileptogenesis in the Pilocarpine Model of Epilepsy

Becker¹,

Pitsch²,

et al. 2008

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In both humans and animals, an insult to the brain can lead, after a variable latent period, to the appearance of spontaneous epileptic seizures that persist for life. The underlying processes, collectively referred to as epileptogenesis, include multiple structural and functional neuronal alterations. We have identified the T-type Ca 2ϩ channel Ca v 3.2 as a central player in epileptogenesis. We show that a transient and selective upregulation of Ca v 3.2 subunits on the mRNA and protein levels after status epilepticus causes an increase in cellular T-type Ca 2ϩ currents and a transitional increase in intrinsic burst firing. These functional changes are absent in mice lacking Ca v 3.2 subunits. Intriguingly, the development of neuropathological hallmarks of chronic epilepsy, such as subfield-specific neuron loss in the hippocampal formation and mossy fiber sprouting, was virtually completely absent in Ca v 3.2 Ϫ/Ϫ mice. In addition, the appearance of spontaneous seizures was dramatically reduced in these mice. Together, these data establish transcriptional induction of Ca v 3.2 as a critical step in epileptogenesis and neuronal vulnerability.

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Section: Methodsmentioning

confidence: 99%

Transcriptional Upregulation of Ca_v3.2 Mediates Epileptogenesis in the Pilocarpine Model of Epilepsy

Becker¹,

Pitsch²,

et al. 2008

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“…mRNA was isolated (RNAqueous; Ambion, Austin, TX) and reverse-transcribed (Superscript III; Invitrogen). Sequence-specific primer/probe sets (Invitrogen) for the mouse receptor (NM_011013) and the control gene, synaptophysin (NM_009305) (Chen et al, 2001), were used to determine the relative transcript level, quantified by the cycle number or count threshold (CT) at which the gene-specific fluorescence reached mid-linear levels, using the Taqman 7700 (Applied Biosystems, Union City, CA). The data are presented as the mean Ϯ S.E.M.…”

Section: Methodsmentioning

confidence: 99%

δ Receptors Are Required for Full Inhibitory Coupling of μ Receptors to Voltage-Dependent Ca²⁺ Channels in Dorsal Root Ganglion Neurons

Walwyn

John²,

Maga³

et al. 2009

Mol Pharmacol

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Recombinant and ␦ opioid receptors expressed in cell lines can form heterodimers with distinctive properties and trafficking. However, a role for opioid receptor heterodimerization in neurons has yet to be identified. The inhibitory coupling of opioid receptors to voltage-dependent Ca 2ϩ channels (VDCCs) is a relatively inefficient process and therefore provides a sensitive assay of altered opioid receptor function and expression. There was no change in -receptor mRNA levels. D-Phe-Cys-Tyr-D-Trp-Arg-Thr-PenThr-NH 2 -sensitive -receptor-coupling efficacy was fully restored to ␦(ϩ/ϩ) levels in ␦(Ϫ/Ϫ) neurons by expression of recombinant ␦ receptors. However, the dimerization-deficient ␦-15 construct expressed in ␦(Ϫ/Ϫ) neurons failed to fully restore the inhibitory coupling of receptors compared with that seen in ␦(ϩ/ϩ) neurons, suggesting that, although not essential for -receptor function, -␦ receptor dimerization contributes to full -agonist efficacy. Because DAMGO exhibited a similar potency in ␦(ϩ/ϩ) and ␦(Ϫ/Ϫ) neurons and caused similar levels of internalization, the role for heterodimerization is probably at the level of receptor biosynthesis.

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“…1 B). Finally, we measured levels of histone acetylation in the hippocampus at the promoters of the ␤-tubulin and synaptophysin genes, which are expressed in adult hippocampus but with expression levels that are reportedly unchanged in this region after ECS (Chen et al, 2001;Newton et al, 2003). Indeed, levels of histone modifications at these loci did not differ between control and ECS-treated animals (Figs.…”

Section: Quantification Of Histone Modifications By Chromatin Immunopmentioning

confidence: 99%

“…Several molecules, however, have been implicated to play a role in chronic ECS action, including BDNF and the transcription factor CREB (cAMPresponse element binding protein). Levels of BDNF and CREB are upregulated in the hippocampus by chronic ECS (Nibuya et al, 1995(Nibuya et al, , 1996, effects directly linked to antidepressant activity in animal models (Chen et al, 2001;Shirayama et al, 2002). Furthermore, chronic ECS causes a long-term downregulation of c-fos mRNA levels (Winston et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

Histone Modifications at Gene Promoter Regions in Rat Hippocampus after Acute and Chronic Electroconvulsive Seizures

Tsankova¹,

Kumar²,

Nestler³

2004

J. Neurosci.

395

296

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The mechanism of action of electroconvulsive seizures (ECS), one of the most effective treatments of major depression, may involve the regulation of gene expression. Chromatin remodeling at gene promoter regions is increasingly recognized as a key control point of gene expression and may, therefore, partly mediate acute and chronic effects of ECS on gene activity. Here, we assayed how posttranslational modifications of histones, a major form of chromatin remodeling, are altered at several gene promoters in rat hippocampus at 30 min, 2 hr, and 24 hr after acute or repeated ECS. We performed chromatin immunoprecipitation assays to measure levels of histone H3 and H4 acetylation and phosphoacetylation at the promoters of the c-fos, BDNF, and CREB (cAMP response element-binding protein) genes, the expression of which is altered by ECS. We found that, with few exceptions, levels of H4 acetylation correlated with mRNA levels for c-fos, BDNF, and CREB throughout the acute and chronic time course study, whereas acetylation and phosphoacetylation of H3 were detected more selectively. Our findings suggest that the chronic downregulation of c-fos transcription, observed in this study, may be achieved at the level of H4 acetylation, whereas chronic upregulation of BDNF transcription may be sustained via control of H3 acetylation, selectively at the BDNF P3 and P4 promoters. These data provide the first in vivo demonstration of the involvement of chromatin remodeling in ECS-induced regulation of gene expression in the brain and will help in understanding the mechanisms underlying the efficacy of ECS in the treatment of depression.

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Activity-Induced Expression of Common Reference Genes in Individual CNS Neurons

Cited by 72 publications

References 6 publications

Transcriptional Upregulation of Ca_v3.2 Mediates Epileptogenesis in the Pilocarpine Model of Epilepsy

Transcriptional Upregulation of Ca_v3.2 Mediates Epileptogenesis in the Pilocarpine Model of Epilepsy

δ Receptors Are Required for Full Inhibitory Coupling of μ Receptors to Voltage-Dependent Ca²⁺ Channels in Dorsal Root Ganglion Neurons

Histone Modifications at Gene Promoter Regions in Rat Hippocampus after Acute and Chronic Electroconvulsive Seizures

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Activity-Induced Expression of Common Reference Genes in Individual CNS Neurons

Cited by 72 publications

References 6 publications

Transcriptional Upregulation of Cav3.2 Mediates Epileptogenesis in the Pilocarpine Model of Epilepsy

Transcriptional Upregulation of Cav3.2 Mediates Epileptogenesis in the Pilocarpine Model of Epilepsy

δ Receptors Are Required for Full Inhibitory Coupling of μ Receptors to Voltage-Dependent Ca2+ Channels in Dorsal Root Ganglion Neurons

Histone Modifications at Gene Promoter Regions in Rat Hippocampus after Acute and Chronic Electroconvulsive Seizures

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Transcriptional Upregulation of Ca_v3.2 Mediates Epileptogenesis in the Pilocarpine Model of Epilepsy

Transcriptional Upregulation of Ca_v3.2 Mediates Epileptogenesis in the Pilocarpine Model of Epilepsy

δ Receptors Are Required for Full Inhibitory Coupling of μ Receptors to Voltage-Dependent Ca²⁺ Channels in Dorsal Root Ganglion Neurons