EFFECTS OF ACUTE AND CHRONIC MORPHINE ON DOPAC AND GLUTAMATE AT SUBCORTICAL DA TERMINALS IN AWAKE RATS

Citation
Nk. Huang et al., EFFECTS OF ACUTE AND CHRONIC MORPHINE ON DOPAC AND GLUTAMATE AT SUBCORTICAL DA TERMINALS IN AWAKE RATS, Pharmacology, biochemistry and behavior, 56(3), 1997, pp. 363-371
Citations number
43
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
00913057
Volume
56
Issue
3
Year of publication
1997
Pages
363 - 371
Database
ISI
SICI code
0091-3057(1997)56:3<363:EOAACM>2.0.ZU;2-8
Abstract
Effects of morphine and naloxone on the levels of 3,4-dihydroxy-phenyl acetic acid (DOPAC) and glutamate in the striatum and nucleus accumben s of awake rats were studied with in vivo microdialysis. Acute morphin e (50 mg/kg, IP) treatment increased the levels of DOPAC and glutamate in the striatum and nucleus accumbens: but both decreased from the el evated levels when naloxone (10 mg/kg, IP) was given 2 h later. Chroni c morphine treatment, twice daily for 5 days in incremental doses (5, 10, 20, 40 and 50 mg/kg, IP), increased the level of DOPAC but decreas ed that of glutamate in the striatum and nucleus accumbens. When nalox one was given 2 h later, the reverse of the above:phenomena are found. After given repeated morphine treatment and experiencing naloxone-pre cipitated withdrawal, the rats with an intact cortex and the rats with ibotenic acid (5 mu g/0.5 mu l/2.5 min) lesions on the medial prefron tal cortex and sulcal cortex have similar alternations in the levels o f DOPAC and glutamate in the striatum. However, in the nucleus accumbe ns, the level of DOPAC dropped more and the level of glutamate increas ed more in the intact rats than the lesioned rats during the withdrawa l stage. These data suggested that the intact cortex ordinarily exerte d an inhibitory role to influence the level of DOPAC in the striatum a nd nucleus accumbens during chronic morphine treatment. In conclusion, morphine seems to activate different pathways in dependent and non-de pendent rats. Copyright (C) 1997 Elsevier Science Inc.