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Neural Correlates of Inflexible Behavior in the Orbitofrontal–Amygdalar Circuit after Cocaine Exposure
Author(s) -
STALNAKER THOMAS A.,
ROESCH MATTHEW R.,
CALU DONNA J.,
BURKE KATHRYN A.,
SINGH TEGHPAL,
SCHOENBAUM GEOFFREY
Publication year - 2007
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1401.014
Subject(s) - orbitofrontal cortex , basolateral amygdala , amygdala , neuroscience , context (archaeology) , addiction , psychology , flexibility (engineering) , prefrontal cortex , biology , cognition , paleontology , statistics , mathematics
: Addiction is characterized by compulsive or inflexible behavior, observed both in the context of drug‐seeking and in contexts unrelated to drugs. One possible contributor to these inflexible behaviors may be drug‐induced dysfunction within circuits that support behavioral flexibility, including the basolateral amygdala (ABL) and the orbitofrontal cortex (OFC). Here we describe data demonstrating that chronic cocaine exposure causes long‐lasting changes in encoding properties in the ABL and the OFC during learning and reversal in an odor‐guided task. In particular, these data suggest that inflexible encoding in ABL neurons may be the proximal cause of cocaine‐induced behavioral inflexibility, and that a loss of outcome‐expectant encoding in OFC neurons could be a more distal contributor to this impairment. A similar mechanism of drug‐induced orbitofrontal–amygdalar dysfunction may cause inflexible behavior when animals and addicts are exposed to drug‐associated cues and contexts.