Linked Life Data

18079206

Source:http://linkedlifedata.com/resource/pubmed/id/18079206

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2008-2-22
pubmed:abstractText
CRH, the primary regulator of the neuroendocrine responses to stress, has been shown to modulate synaptic efficacy and the process of learning and memory in hippocampus. However, effects of CRH on N-methyl-d-aspartate (NMDA) receptor, the key receptor for synaptic plasticity, remain unclear. In primary cultured hippocampal neurons, using the technique of whole-cell patch-clamp recordings, we found that CRH (1 pmol/liter to 10 nmol/liter) inhibited NMDA-induced currents in a dose-dependent manner. This effect was reversed by the CRH receptor type 1 (CRHR1) antagonist antalarmin but not by the CRHR2 antagonist astressin-2B, suggesting that CRHR1 mediated the inhibitory effect of CRH. Investigations on the signaling pathways of CRH showed that CRH dose-dependently induced phosphorylated phospholipase C (PLC)-beta3 expression and increased intracellular cAMP content in these cells. Blocking PLC activity with U73122 prevented CRH-induced depression of NMDA current, whereas blocking protein kinase A (H89) and adenylate cyclase (SQ22536) failed to affect the CRH-induced depression of NMDA current. Application of inositol-1,4,5-triphosphate receptor (IP(3)R) antagonist, Ca(2+) chelators or protein kinase C (PKC) inhibitors also mainly blocked CRH-induced depression of NMDA currents, suggesting involvement of PLC/IP(3)R/Ca(2+)and PLC/PKC signaling pathways in CRH down-regulation of NMDA receptors. Our results suggest that CRH may exert neuromodulatory actions on hippocampus through regulating NMDA receptor function.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
149
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1389-98
pubmed:meshHeading
pubmed-meshheading:18079206-Action Potentials, pubmed-meshheading:18079206-Adenylate Cyclase, pubmed-meshheading:18079206-Animals, pubmed-meshheading:18079206-Cells, Cultured, pubmed-meshheading:18079206-Corticotropin-Releasing Hormone, pubmed-meshheading:18079206-Cyclic AMP, pubmed-meshheading:18079206-Cyclic AMP-Dependent Protein Kinases, pubmed-meshheading:18079206-Dose-Response Relationship, Drug, pubmed-meshheading:18079206-Hippocampus, pubmed-meshheading:18079206-Neurons, pubmed-meshheading:18079206-Patch-Clamp Techniques, pubmed-meshheading:18079206-Phospholipase C beta, pubmed-meshheading:18079206-Rats, pubmed-meshheading:18079206-Rats, Sprague-Dawley, pubmed-meshheading:18079206-Receptors, Corticotropin-Releasing Hormone, pubmed-meshheading:18079206-Receptors, N-Methyl-D-Aspartate, pubmed-meshheading:18079206-Signal Transduction
pubmed:year
2008
pubmed:articleTitle
Corticotropin-releasing hormone (CRH) depresses n-methyl-D-aspartate receptor-mediated current in cultured rat hippocampal neurons via CRH receptor type 1.
pubmed:affiliation
Department of Physiology, Ministry of Education, Second Military Medical University, 800 Xiangyin Road, Shanghai 200433, People's Republic of China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't