Open AccessCocaine-induced reduction of brain neuropeptide Y synthesis dependent on medial prefrontal cortex.
Author(s) -
Claes Wahlestedt,
Farouk Karoum,
George E. Jaskiw,
Richard Jed Wyatt,
Dan Larhammar,
Rolf Ekman,
Donald J. Reis
Publication year - 1991
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.88.6.2078
Subject(s) - neuropeptide y receptor , nucleus accumbens , dopamine , prefrontal cortex , lesion , neuroscience , neuropeptide , endocrinology , medicine , psychology , receptor , psychiatry , cognition
Repeated administration of cocaine elicits substantial, long-lasting, but reversible reductions in neuropeptide Y (NPY) and NPY mRNA in the rat cerebral cortex and nucleus accumbens. The NPY reduction appears to be mediated through a decrease in NPY biosynthesis, occurring transneuronally, perhaps in response to changes in synaptic dopamine associated with mesolimbic and mesocortical dopamine neurons. The medial prefrontal cortex appears necessary for maintenance of cocaine's action on this neuronal network since excitotoxic lesions of this area prevented (lesion before cocaine) and reversed (lesion after cocaine) the reductions in NPY elicited by the cocaine. NPY may be a sensitive marker for chronic cocaine use. Its decrease may relate to the anxiety and depression associated with cocaine withdrawal in humans.