Increased expression of synapsin I mRNA in defined areas of the rat central nervous system following chronic morphine treatment

Chronic opiate administration leads to a selective regulation of several cellular proteins and mRNAs. This phenomenon has been viewed as a compensatory mechanism to the opiate signaling leading to the development of opiate addiction. In this study, in situ hybridization histochemistry experiments we...

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Published in:Brain research. Molecular brain research. 1995-12, Vol.34 (2), p.221-230
Main Authors: Matus-Leibovitch, Noa, Ezra-Macabee, Vittoria, Saya, Daniella, Attali, Bernard, Avidor-Reiss, Tomer, Barg, Jacob, Vogel, Zvi
Format: Article
Language:English
Subjects:
Amygdala
Analgesics
Animals
Biological and medical sciences
Blotting, Northern
Brain - metabolism
Brain Stem - metabolism
Cerebellum - metabolism
In situ hybridization
Locus coeruleus
Male
Medical sciences
Morphine
Morphine - pharmacology
Neuropharmacology
Opiate tolerance
Pharmacology. Drug treatments
Rats
Rats, Wistar
RNA, Messenger - biosynthesis
Spinal cord
Spinal Cord - metabolism
Synapsin I mRNA
Synapsins - genetics
Telencephalon - metabolism
Time Factors
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Summary:Chronic opiate administration leads to a selective regulation of several cellular proteins and mRNAs. This phenomenon has been viewed as a compensatory mechanism to the opiate signaling leading to the development of opiate addiction. In this study, in situ hybridization histochemistry experiments were employed to investigate the effect of chronic morphine treatment on synapsin I gene expression. We show here for the first time that prolonged morphine exposure causes a selective increase in the mRNA levels of synapsin I in several brain regions which are considered to be important for opiate action. Quantitative analysis of the signals, obtained by hybridization of digoxigenin-labeled antisense RNA probe, revealed a 5.8- and 7-fold increase of synapsin I mRNA levels in the locus coeruleus and the amygdala of morphine-treated rats, respectively, as compared with control untreated rats. Increased expression of synapsin I mRNA was also observed in the spinal cord of morphine-treated rats (by 3.8-fold). Since opiates were shown to attenuate neurotransmitter release and reduce synapsin I phosphorylation, it is suggested that the increase in synapsin I levels would lead to the requirement of higher amounts of opiate agonists to obtain the opiate physiological effects. These results suggest that the increases in mRNA levels of synapsin I in these specific areas can be part of the molecular mechanism(s) underlying opiate tolerance and withdrawal.
ISSN:0169-328X
1872-6941
DOI:10.1016/0169-328X(95)00166-P