Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1999-3-18
pubmed:abstractText
Previous studies have indicated that intracerebroventricular (i.c.v.) infusions of corticotropin-releasing factor (CRF) activate locus coeruleus (LC) noradrenergic neurons and increase the metabolism and extracellular concentrations of norepinephrine (NE) in several brain regions, suggesting increased release. To examine the temporal aspects and mechanism of the presumed release of NE, CRF was infused i.c.v. and the oxidation current was recorded using carbon fiber voltammetric electrodes placed in rat hippocampus or cortex. The CRF (1 microg, i.c.v.) caused a significant increase of oxidation current with a delay of approximately 5 min, and a peak at approximately 35 min. Similar responses were observed in the medial prefrontal cortex. The hippocampal response was markedly attenuated when CRF was infused into rats pretreated with DSP-4 to deplete NE, suggesting that the observed changes in current resulted from oxidation of NE. The increase of NE-like current did not occur when 25 microg alpha-helical CRF9-41 (ahCRF) was injected immediately before 1 microg CRF, suggesting that the response was mediated by cerebral CRF-receptors. Subcutaneous pretreatment with the ganglionic blocker, chlorisondamine, at a dose of 3 mg/kg had no effect on the voltammetric response to CRF, but a 6 mg/kg dose completely prevented the response. The beta-adrenoceptor antagonists, S-propranolol (5 mg/kg), nadolol (5 and 10 mg/kg), and timolol (5 mg/kg) attenuated the NE response to i.c.v. CRF to varying degrees. When chlorisondamine (3 microg) or nadolol (5 microg) were given i.c.v. before the CRF, the hippocampal responses were not blocked. These results suggest peripheral actions of ganglionic and beta-adrenergic blockers. We conclude that peripheral autonomic mechanisms, and probably both central and peripheral beta-adrenoceptors, contribute to the increased secretion of hippocampal NE in response to i.c.v. CRF.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0361-9230
pubmed:author
pubmed:issnType
Print
pubmed:volume
47
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
277-84
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:9865861-Adrenergic beta-Antagonists, pubmed-meshheading:9865861-Animals, pubmed-meshheading:9865861-Benzylamines, pubmed-meshheading:9865861-Chlorisondamine, pubmed-meshheading:9865861-Corticotropin-Releasing Hormone, pubmed-meshheading:9865861-Electric Conductivity, pubmed-meshheading:9865861-Electrochemistry, pubmed-meshheading:9865861-Extracellular Space, pubmed-meshheading:9865861-Ganglionic Blockers, pubmed-meshheading:9865861-Hippocampus, pubmed-meshheading:9865861-Injections, Intraventricular, pubmed-meshheading:9865861-Male, pubmed-meshheading:9865861-Neurotransmitter Uptake Inhibitors, pubmed-meshheading:9865861-Norepinephrine, pubmed-meshheading:9865861-Osmolar Concentration, pubmed-meshheading:9865861-Oxidation-Reduction, pubmed-meshheading:9865861-Prefrontal Cortex, pubmed-meshheading:9865861-Rats, pubmed-meshheading:9865861-Rats, Sprague-Dawley
pubmed:year
1998
pubmed:articleTitle
Intracerebroventricular infusion of CRF increases extracellular concentrations of norepinephrine in the hippocampus and cortex as determined by in vivo voltammetry.
pubmed:affiliation
Department of Pharmacology and Therapeutics, Louisiana State University Medical Center, Shreveport 71130-3932, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.