| The striatonigral dynorphin pathway of the rat studied with in vivo microdialysis--I. Effects of K(+)-depolarization, lesions and peptidase inhibition. | |
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MedLine Citation:
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PMID: 7891855 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Extracellular levels of dynorphin B were analysed with in vivo microdialysis in the neostriatum and substantia nigra of halothane-anaesthetized rats. Dopamine and its metabolites, 3,4-dihydroxyphenyl-acetic acid and homovanillic acid, as well as GABA were simultaneously monitored. Chromatographic analysis revealed that the dynorphin B-like immunoreactivity measured in perfusates collected under basal and K(+)-depolarizing conditions co-eluted with synthetic dynorphin B. Dynorphin B, GABA and dopamine levels were Ca(2+)-dependently increased by K(+)-depolarization, while 3,4-dihydroxyphenylacetic acid and homovanillic acid levels were decreased. Dopamine and its metabolites, but not dynorphin B or GABA levels, were significantly decreased after a unilateral 6-hydroxydopamine injection into the left medial forebrain bundle. In contrast, following a unilateral injection of ibotenic acid into the striatum, dynorphin B and GABA levels were decreased by > 50% in striatum and substantia nigra on the lesioned side, whereas no significant changes were observed in basal dopamine levels. The inclusion of the peptidase inhibitor captopril (50-500 microM) into the nigral perfusion medium produced a concentration-dependent increase in nigral extracellular levels of dynorphin B. In the striatum, a delayed increase in dynorphin B and GABA levels could be observed following the nigral captopril administration, but this effect was not concentration-dependent. Thus, we demonstrate that extracellular levels of dynorphin B, dopamine and GABA can simultaneously be monitored with in vivo microdialysis. Extracellular dynorphin B appears to originate from neurons, since the levels were (i) increased in a Ca(2+)-dependent manner by K(+)-depolarization, and (ii) decreased by a selective lesion of the striatum, known to contain cell bodies of dynorphin neurons in the striatonigral pathway. Furthermore, (iii) the increase in nigral dynorphin B levels by peptidase inhibition suggests the presence of clearance mechanisms for the released dynorphin peptides. |
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Authors:
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Z B You; I Nylander; M Herrera-Marschitz; W T O'Connor; M Goiny; L Terenius |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Neuroscience Volume: 63 ISSN: 0306-4522 ISO Abbreviation: Neuroscience Publication Date: 1994 Nov |
Date Detail:
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Created Date: 1995-04-18 Completed Date: 1995-04-18 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 7605074 Medline TA: Neuroscience Country: ENGLAND |
Other Details:
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Languages: eng Pagination: 415-25 Citation Subset: IM |
Affiliation:
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Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Captopril / pharmacology Chromatography Corpus Striatum / physiology* Dopamine / metabolism Dynorphins / chemistry, metabolism, physiology* Electrophysiology Endorphins / chemistry, metabolism Extracellular Space / metabolism Male Microdialysis Neural Pathways / physiology Potassium / pharmacology* Rats Rats, Sprague-Dawley Substantia Nigra / physiology* gamma-Aminobutyric Acid / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Endorphins; 56-12-2/gamma-Aminobutyric Acid; 62571-86-2/Captopril; 7440-09-7/Potassium; 74913-18-1/Dynorphins; 83335-41-5/rimorphin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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