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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7-8
pubmed:dateCreated
2010-10-25
pubmed:abstractText
Prokineticin 2 (PK2) is a newly identified regulatory protein, which is involved in a wide range of physiological processes including pain perception in mammals. However, the precise role of PK2 in nociception is yet not fully understood. Here, we investigate the effects of PK2 on GABA(A) receptor function in rat trigeminal ganglion neurons using whole-cell patch clamp technique. PK2 reversibly depressed inward currents produced by GABA(A) receptor activation (I(GABA)) with an IC?? of 0.26 ± 0.02 nM. PK2 appeared to decrease the efficacy of GABA to GABA(A) receptor but not the affinity. The maximum response of the GABA dose-response curve decreased to 71.2 ± 7.0% of control after pretreatment with PK2, while the threshold value and EC?? of curve did not alter significantly. The effects of PK2 on I(GABA) were voltage independent. The PK2-induced inhibition of I(GABA) was removed by intracellular dialysis of either GDP-?-S (a non-hydrolyzable GDP analog), EGTA (a Ca²+ chelator) or GF109203X (a selective protein kinase C inhibitor), but not by H89 (a protein kinase A inhibitor). These results suggest that PK2 down-regulates the function of the GABA(A) receptor via G-protein and protein kinase C dependent signal pathways in primary sensory neurons and this depression might underlie the hyperalgesia induced by PK2.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1873-7064
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Elsevier Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
59
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
589-94
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Prokineticin 2 suppresses GABA-activated current in rat primary sensory neurons.
pubmed:affiliation
Department of Pharmacology, Xianning College, 88 Xianning Road, Xianning 437100, Hubei, PR China.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't