𝔖 Bobbio Scriptorium
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Interrupted expression of NAC-1 augments the behavioral responses to cocaine

✍ Scribed by Peter W. Kalivas; Patricia Duffy; Scott A. Mackler


Publisher
John Wiley and Sons
Year
1999
Tongue
English
Weight
147 KB
Volume
33
Category
Article
ISSN
0887-4476

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✦ Synopsis


NAC-1 is an mRNA that is increased selectively in the nucleus accumbens after acute and repeated cocaine administration. Antisense or control oligonucleotides were microinjected into the nucleus accumbens of rats to define the role of NAC-1 in the behavioral responses to acute systemic cocaine. Antisense oligonucleotides decreased NAC-1 mRNA levels by 26% and markedly enhanced the motor stimulant response to an acute cocaine injection compared to sense oligonucleotide microinjections. The augmentation in cocaine motor behavior produced by NAC-1 antisense pretreatment in the nucleus accumbens was not associated with increased dopamine release as estimated by microdialysis. In contrast, the behavioral response to dopamine microinjection into the nucleus accumbens was increased after antisense oligonucleotide treatment, while the motor response to Β΅-opioid receptor stimulation was unaltered. These data suggest that the induction of NAC-1 by cocaine may be a compensatory mechanism that minimizes the behavioral impact of cocaine administration by regulating postsynaptic dopamine transmission within the nucleus accumbens.


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