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NMDA‐mediated modulation of dopamine release is modified in rat prefrontal cortex and nucleus accumbens after chronic nicotine treatment
Author(s) -
Grilli Massimo,
Pittaluga Anna,
MerloPich Emilio,
Marchi Mario
Publication year - 2009
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2008.05792.x
Subject(s) - nucleus accumbens , nmda receptor , nicotine , dopamine , prefrontal cortex , chemistry , endocrinology , medicine , pharmacology , anesthesia , neuroscience , receptor , psychology , cognition
In this study, we investigate the effects of chronic administration of (−)nicotine on the function of the NMDA‐mediated modulation of [ 3 H]dopamine (DA) release in rat prefrontal cortex (PFC) and nucleus accumbens (NAc). In the PFC synaptosomes NMDA in a concentration‐dependent manner evoked [ 3 H]DA release in rats chronically treated with vehicle (14 days) with an EC 50 of 13.1 ± 2.0 μM. The NMDA‐evoked overflow of the [ 3 H]DA in PFC nerve endings of rats treated with (−)nicotine was significantly lower (−43%) than in vehicle treated rats. The EC 50 was 9.0 ± 1.4 μM. Exposure of NAc synaptosomes of rats treated with vehicle to NMDA produced an increase in [ 3 H]DA overflow with an EC 50 of 14.5 ± 5.5 μM. This effect was significantly enhanced in chronically treated animals. The EC 50 was 10.5 ± 0.5 μM. The K + ‐evoked release of [ 3 H]DA was not modified by the (−)nicotine administration. Both the changes of the NMDA‐evoked [ 3 H]DA overflow in the NAc and PFC disappeared after 14 days withdrawal. The results show that chronic (−)nicotine differentially affects the NMDA‐mediated [ 3 H]DA release in the PFC and NAc of the rat.