Linked Life Data

21781114

Source:http://linkedlifedata.com/resource/pubmed/id/21781114

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2011-9-2
pubmed:abstractText
The present study investigated regulation of histone acetylation by L-type voltage-dependent calcium channels (VDCCs), one of the machineries to provide Ca(2+) signals. Acetylation of histone through the phosphorylation of protein kinase C? (PKC?) in the development of methamphetamine (METH)-induced place preference was demonstrated in the limbic forebrain predominantly but also in the nucleus accumbens of ?1C subunit knockout mice. Chronic administration of METH produced a significant place preference in mice, which was dose-dependently inhibited by both chelerythrine (a PKC inhibitor) and nifedipine (an L-type VDCC blocker). Protein levels of acetylated histone H3 and p-PKC? significantly increased in the limbic forebrain of mice showing METH-induced place preference, and it was also significantly attenuated by pre-treatment with chelerythrine or nifedipine. METH-induced place preference was also significantly attenuated by deletion of half the ?1C gene, which is one of the subunits forming Ca(2+) channels. Furthermore, increased acetylation of histone H3 was found in specific gene-promoter regions related to synaptic plasticity, such as Nrxn, Syp, Dlg4, Gria1, Grin2a, Grin2b, Camk2a, Creb, and cyclin-dependent kinase 5, in wild-type mice showing METH-induced place preference, while such enhancement of multiple synaptic plasticity genes was significantly attenuated by a deletion of half the ?1C gene. These findings suggest that L-type VDCCs play an important role in the development of METH-induced place preference by facilitating acetylation of histone H3 in association with enhanced expression of synaptic plasticity genes via PKC? phosphorylation following an increase in the intracellular Ca(2+) concentration.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1471-4159
pubmed:author
pubmed:copyrightInfo
© 2011 The Authors. Journal of Neurochemistry © 2011 International Society for Neurochemistry.
pubmed:issnType
Electronic
pubmed:volume
118
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1056-66
pubmed:meshHeading
pubmed-meshheading:21781114-Acetylation, pubmed-meshheading:21781114-Animals, pubmed-meshheading:21781114-Blotting, Western, pubmed-meshheading:21781114-Calcium Channels, L-Type, pubmed-meshheading:21781114-Central Nervous System Stimulants, pubmed-meshheading:21781114-Chromatin, pubmed-meshheading:21781114-Conditioning, Operant, pubmed-meshheading:21781114-Histones, pubmed-meshheading:21781114-Immunoprecipitation, pubmed-meshheading:21781114-Injections, Intraventricular, pubmed-meshheading:21781114-Methamphetamine, pubmed-meshheading:21781114-Mice, pubmed-meshheading:21781114-Mice, Inbred C57BL, pubmed-meshheading:21781114-Mice, Knockout, pubmed-meshheading:21781114-Nucleus Accumbens, pubmed-meshheading:21781114-Phosphorylation, pubmed-meshheading:21781114-Prosencephalon, pubmed-meshheading:21781114-Protein Kinase C, pubmed-meshheading:21781114-Reinforcement (Psychology), pubmed-meshheading:21781114-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:21781114-Subcellular Fractions
pubmed:year
2011
pubmed:articleTitle
L-type voltage-dependent calcium channels facilitate acetylation of histone H3 through PKC? phosphorylation in mice with methamphetamine-induced place preference.
pubmed:affiliation
Department of Pharmacology, Kawa saki Medical School, Matsushima, Kurashiki, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't