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Methamphetamine‐induced changes in the mice hippocampal neuropeptide Y system: implications for memory impairment
Author(s) -
Gonçalves Joana,
Baptista Sofia,
Olesen Mikkel V.,
FontesRibeiro Carlos,
Malva João O.,
Woldbye David P.,
Silva Ana P.
Publication year - 2012
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/jnc.12052
Subject(s) - meth , neuropeptide y receptor , methamphetamine , hippocampal formation , hippocampus , neuroscience , antagonist , receptor , endocrinology , medicine , receptor antagonist , central nervous system , neuropeptide , psychology , biology , chemistry , monomer , organic chemistry , acrylate , polymer
Abstract Methamphetamine (METH) is a psychostimulant drug that causes irreversible brain damage leading to several neurological and psychiatric abnormalities, including cognitive deficits. Neuropeptide Y (NPY) is abundant in the mammalian central nervous system (CNS) and has several important functions, being involved in learning and memory processing. It has been demonstrated that METH induces significant alteration in mice striatal NPY, Y 1 and Y 2 receptor mRNA levels. However, the impact of this drug on the hippocampal NPY system and its consequences remain unknown. Thus, in this study, we investigated the effect of METH intoxication on mouse hippocampal NPY levels, NPY receptors function, and memory performance. Results show that METH increased NPY, Y 2 and Y 5 receptor mRNA levels, as well as total NPY binding accounted by opposite up‐ and down‐regulation of Y 2 and Y 1 functional binding, respectively. Moreover, METH‐induced impairment in memory performance and AKT/mammalian target of rapamycin pathway were both prevented by the Y 2 receptor antagonist, BIIE0246. These findings demonstrate that METH interferes with the hippocampal NPY system, which seems to be associated with memory failure. Overall, we concluded that Y 2 receptors are involved in memory deficits induced by METH intoxication.