Document Detail


Expression of fos protein in rat brain following administration of a nicotinic acetylcholine receptor agonist epibatidine.
MedLine Citation:
PMID:  9630573     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Epibatidine (exo-2-(6-chloro-3-pyridyl)-7-azabicyclo-[2.2.1]heptane), an extract of frog skin, is a novel and highly potent agonist for the nicotinic acetylcholine (ACh) receptor. The present study was undertaken to examine the expression of Fos protein in several rat brain regions following an acute administration of epibatidine. Furthermore, we also studied the role of the dopamine D1 and D2 receptors and the N-methyl-d-aspartate (NMDA) receptor, and nicotinic ACh receptor in the expression of Fos protein by epibatidine. A single administration of epibatidine (5, 10, 50 microgram/kg) caused a marked induction of Fos-immunoreactivity in the prefrontal cortex, medial striatum, nucleus accumbens, amygdala and superior colliculus of rat brain. In these regions, pretreatment with SCH 23390 (1.0 mg/kg), a dopamine D1 receptor antagonist, MK-801 (1.0 mg/kg), a NMDA receptor antagonist, and mecamylamine (5. 0 mg/kg), a nicotinic Ach receptor antagonist, inhibited the induction of Fos protein by epibatidine (10 microgram/kg). Pretreatment with sulpiride, a dopamine D2 receptor antagonist, blocked the induction of Fos protein in the prefrontal cortex and the core region of accumbens nucleus, but not in the medial striatum and the shell division of nucleus accumbens of rat brain. These results suggest that epibatidine induced the expression of Fos protein in several regions of rat brain, and that dopamine D1 receptor, NMDA receptor, and nicotinic ACh receptor may play a role in the expression of Fos protein by epibatidine in rat brain. Furthermore, dopamine D2 receptor may, in part, play a role in epibatidine induced expression of Fos protein in the prefrontal cortex and the core region of nucleus accumbens, but not in the medial striatum and the shell division of nucleus accumbens of rat brain.
Authors:
K Watanabe; K Hashimoto; T Nishimura; K Tsunashima; Y Minabe
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Brain research     Volume:  797     ISSN:  0006-8993     ISO Abbreviation:  Brain Res.     Publication Date:  1998 Jun 
Date Detail:
Created Date:  1998-08-06     Completed Date:  1998-08-06     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0045503     Medline TA:  Brain Res     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  135-42     Citation Subset:  IM    
Copyright Information:
Copyright 1998 Elsevier Science B.V. All rights reserved.
Affiliation:
Division of Cortical Function Disorder, National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4-1-1 Ogawahigashi, Kodaira, Tokyo, 187-8502, Japan. watanabe@ncnaxp.ncnp. go.jp
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MeSH Terms
Descriptor/Qualifier:
Animals
Benzazepines / pharmacology
Bicyclo Compounds, Heterocyclic / pharmacology*
Brain Chemistry / drug effects*
Dizocilpine Maleate / pharmacology
Dopamine Antagonists / pharmacology
Excitatory Amino Acid Antagonists / pharmacology
Male
Mecamylamine / pharmacology
Nicotinic Agonists / pharmacology*
Nicotinic Antagonists / pharmacology
Proto-Oncogene Proteins c-fos / analysis,  biosynthesis*
Pyridines / pharmacology*
Rats
Rats, Sprague-Dawley
Receptors, Dopamine D1 / physiology
Receptors, Dopamine D2 / physiology
Receptors, N-Methyl-D-Aspartate / physiology
Receptors, Nicotinic / physiology
Sulpiride / pharmacology
Chemical
Reg. No./Substance:
0/Benzazepines; 0/Bicyclo Compounds, Heterocyclic; 0/Dopamine Antagonists; 0/Excitatory Amino Acid Antagonists; 0/Nicotinic Agonists; 0/Nicotinic Antagonists; 0/Proto-Oncogene Proteins c-fos; 0/Pyridines; 0/Receptors, Dopamine D1; 0/Receptors, Dopamine D2; 0/Receptors, N-Methyl-D-Aspartate; 0/Receptors, Nicotinic; 140111-52-0/epibatidine; 15676-16-1/Sulpiride; 60-40-2/Mecamylamine; 77086-22-7/Dizocilpine Maleate

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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