Document Detail


Effects of morphine treatment and withdrawal on striatal and limbic monoaminergic activity and ascorbic acid oxidation in the rat.
MedLine Citation:
PMID:  8813393     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Since ascorbic acid (AA) reportedly suppresses tolerance to and dependence on morphine in humans and rodents, levels of dopamine (DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 3-methoxytyramine (3-MT), 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), AA, dehydroascorbic acid (DHAA), uric acid, xanthine, hypoxanthine, glutamate and gamma-aminobutyric acid (GABA) were determined by high-pressure liquid chromatography (HPLC) in the striatum and in the limbic forebrain of the rat following morphine treatment (single or repeated) and withdrawal. Single morphine administration (20 mg/kg s.c.) increased DOPAC + HVA/DA, 5-HIAA/5-HT and DHAA/AA ratios, uric acid levels, and decreased xanthine, hypoxanthine, glutamate and GABA levels in both regions. 3-MT levels were decreased in the striatum and increased in the limbic forebrain. After 7 days of morphine treatment, striatal DOPAC + HVA/DA and DHAA/AA ratios and uric acid levels were still higher and striatal and limbic xanthine levels still lower than in controls, while all other parameters were in the range of control values in both regions. Morphine treatment also increased the glutamate/GABA ratio in the striatum. In all morphine-treated rats, individual striatal DOPAC + HVA/DA and DHAA/AA ratio values were directly correlated. After a 48 h withdrawal period, both striatal AA oxidation and glutamate/GABA ratio further increased; limbic 3-MT levels further decreased, while all other parameters did not differ from control values. We conclude that: (i) tolerance to morphine-induced increase in hypoxanthine, xanthine and AA oxidation develops in the limbic forebrain faster than in the striatum; (ii) the morphine-induced increase in striatal and limbic AA oxidation may be considered a consequence of increased formation of reactive oxygen species due to increased DA, hypoxanthine and xanthine oxidative metabolism; (iii) a striatal excitotoxic imbalance characterizes the withdrawal state and may be taken into account to explain the further increase in striatal AA oxidation.
Authors:
M S Desole; G Esposito; L Fresu; R Migheli; P Enrico; M A Mura; G De Natale; E Miele; M Miele
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Brain research     Volume:  723     ISSN:  0006-8993     ISO Abbreviation:  Brain Res.     Publication Date:  1996 Jun 
Date Detail:
Created Date:  1996-12-03     Completed Date:  1996-12-03     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0045503     Medline TA:  Brain Res     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  154-61     Citation Subset:  IM    
Affiliation:
Institute of Pharmacology, University of Sassari, Italy.
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MeSH Terms
Descriptor/Qualifier:
3,4-Dihydroxyphenylacetic Acid / metabolism
Amines / metabolism*
Animals
Ascorbic Acid / metabolism*
Corpus Striatum / drug effects*
Dopamine / metabolism
Male
Morphine / pharmacology*
Prosencephalon / drug effects*
Rats
Rats, Wistar
Substance Withdrawal Syndrome
gamma-Aminobutyric Acid / metabolism
Chemical
Reg. No./Substance:
0/Amines; 102-32-9/3,4-Dihydroxyphenylacetic Acid; 50-81-7/Ascorbic Acid; 56-12-2/gamma-Aminobutyric Acid; 57-27-2/Morphine

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


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