Premium
Alterations in brain‐derived neurotrophic factor following withdrawal from a chronic, escalating dose regimen of d‐amphetamine (1145.2)
Author(s) -
Fuller Jasmine,
Murray Ryan,
Horner Kristen
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1145.2
Subject(s) - nucleus accumbens , anhedonia , amphetamine , brain derived neurotrophic factor , neurotrophic factors , psychology , amygdala , medicine , hippocampus , dorsal raphe nucleus , endocrinology , drug withdrawal , prefrontal cortex , ventral tegmental area , neuroscience , psychiatry , dopamine , receptor , drug , dopaminergic , serotonin , serotonergic , cognition
Withdrawal from chronic, escalating doses of D‐amphetamine (AMPH) induces a syndrome with symptoms that are similar to those seen in major depressive disorder (MDD), such as dysphoria and anhedonia. These changes in affect may underlie relapse and the maintenance of addiction. Changes in brain‐derived neurotrophic factor (BDNF) may underlie the pathophysiology of MDD, but it is unclear whether alterations in BDNF occur following withdrawal from a chronic, escalating dose regimen of AMPH. The goal of this study was to examine changes in BDNF after exposure to chronic, escalating doses of D‐AMPH, followed by 24h or 4d of withdrawal. Animals were sacrificed, the tissue processed for immunohistochemistry and changes in BDNF examined in the nucleus accumbens, amygdala, hippocampus, dorsal raphe and prefrontal cortex, which are regions that mediate emotion and are impaired following psychostimulant withdrawal. Our data show that at 24h post‐AMPH BDNF protein levels are increased in the nucleus accumbens and decreased in the hippocampus. At 4d post‐AMPH, BDNF protein levels are significantly decreased in all areas examined. Our data suggest that while some of the initial dysphoric/anhedonic effects of AMPH withdrawal, mediated by increased BDNF in the nucleus accumbens, may abate as withdrawal progresses, other impairments, mediated by widespread decreases in BDNF may persist in longer‐term withdrawal from AMPH. Grant Funding Source : Mercer Univeristy Seed Grant