Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1996-12-5
pubmed:abstractText
Previous work demonstrated that systemic administration of the benzodiazepine receptor (BZR) partial inverse agonist beta-carboline FG 7142 (FG) augments the cardiovascular response to non-signal stimuli, similar to the effects of an aversive context. Analysis of the parasympathetic and sympathetic contributions to the effects of FG prompted the hypothesis that increases in central cholinergic activity mediates the potentiation of the cardioacceleratory response by FG. Consistent with this hypothesis, the present experiments demonstrate: (a) intracerebroventricular (ICV) infusion of the cholinergic receptor agonist carbachol mimics the response-potentiating effects of FG; (b) this effect of carbachol was blocked by ICV co-administration of the muscarinic antagonist atropine; (c) ICV infusions of atropine blocked the potentiation of the cardioacceleratory response by systemically administered FG, but did not alter the basal response to the stimulus; and (d) 192 IgG-saporin-induced lesions of basal forebrain cholinergic neurons prevented the FG-induced potentiation of the cardioacceleratory response, again without altering the basal cardiac response. These data strongly support the hypothesis that the effects of FG on cardiac reactivity are mediated via an activation of central muscarinic cholinergic mechanisms.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/192 IgG-saporin, http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal, http://linkedlifedata.com/resource/pubmed/chemical/Appetite Depressants, http://linkedlifedata.com/resource/pubmed/chemical/Atropine, http://linkedlifedata.com/resource/pubmed/chemical/Carbachol, http://linkedlifedata.com/resource/pubmed/chemical/Carbolines, http://linkedlifedata.com/resource/pubmed/chemical/Cholinergic Agents, http://linkedlifedata.com/resource/pubmed/chemical/FG 7142, http://linkedlifedata.com/resource/pubmed/chemical/GABA-A Receptor Agonists, http://linkedlifedata.com/resource/pubmed/chemical/Immunotoxins, http://linkedlifedata.com/resource/pubmed/chemical/Muscarinic Antagonists, http://linkedlifedata.com/resource/pubmed/chemical/N-Glycosyl Hydrolases, http://linkedlifedata.com/resource/pubmed/chemical/Parasympathomimetics, http://linkedlifedata.com/resource/pubmed/chemical/Ribosome Inactivating Proteins...
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0166-4328
pubmed:author
pubmed:issnType
Print
pubmed:volume
74
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
91-103
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:8851918-Animals, pubmed-meshheading:8851918-Antibodies, Monoclonal, pubmed-meshheading:8851918-Appetite Depressants, pubmed-meshheading:8851918-Atropine, pubmed-meshheading:8851918-Blood Pressure, pubmed-meshheading:8851918-Carbachol, pubmed-meshheading:8851918-Carbolines, pubmed-meshheading:8851918-Cholinergic Agents, pubmed-meshheading:8851918-GABA-A Receptor Agonists, pubmed-meshheading:8851918-Hemodynamics, pubmed-meshheading:8851918-Humans, pubmed-meshheading:8851918-Immunotoxins, pubmed-meshheading:8851918-Injections, Intraventricular, pubmed-meshheading:8851918-Muscarinic Antagonists, pubmed-meshheading:8851918-N-Glycosyl Hydrolases, pubmed-meshheading:8851918-Parasympathetic Nervous System, pubmed-meshheading:8851918-Parasympathomimetics, pubmed-meshheading:8851918-Prosencephalon, pubmed-meshheading:8851918-Rats, pubmed-meshheading:8851918-Rats, Sprague-Dawley, pubmed-meshheading:8851918-Ribosome Inactivating Proteins, Type 1
pubmed:year
1996
pubmed:articleTitle
A central cholinergic link in the cardiovascular effects of the benzodiazepine receptor partial inverse agonist FG 7142.
pubmed:affiliation
Department of Psychology and Neuroscience Program, Ohio State University, Columbus 43210, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't