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Neuroendocrine correlates of antisocial personality disorder in abstinent heroin‐dependent subjects
Author(s) -
GERRA G,
ZAIMOVIC A,
MOI G,
BUSSANDRI M,
DELSIGNORE R,
CACCAVARI R,
BRAMBILLA F
Publication year - 2003
Publication title -
addiction biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.445
H-Index - 78
eISSN - 1369-1600
pISSN - 1355-6215
DOI - 10.1080/1355621031000069846
Subject(s) - antisocial personality disorder , medicine , psychology , dopaminergic , clonidine , endocrinology , serotonergic , fenfluramine , dopamine , stimulation , prolactin , serotonin , receptor , hormone , poison control , environmental health , injury prevention
The function of the central alpha‐adrenergic, serotoninergic and dopaminergic systems was investigated in 30 heroin‐dependent subjects, 6–8 weeks after detoxification and in 22 psychophysically healthy controls (group C). Twelve heroin‐dependent subjects with antisocial personality disorder (ASPD) (group A), 18 heroin‐dependent subjects without other Axis I and II pathologies (group B) were included among abstinent substance abusers. The norepinephrine (NE) function was evaluated by the GH responses to acute stimulation with clonidine (clon); the serotonin (5‐HT) function by the PRL and cortisol (CORT) responses to acute stimulation with d‐fenfluramine (d‐fen) and the dopamine (DA) function was investigated by growth hormone (GH) and prolactin (PRL) responses to acute administration of bromocriptine (brom). Alpha‐adrenergic sensitivity, as measured by the GH‐clon test, was found significantly reduced in A subjects (ASPD), in comparison with B subjects and controls. PRL and CORT responses to d‐fen were significantly blunted both in A and B subjects, in comparison with control subjects. DA receptors sensitivity seems to be reduced significantly in ASPD (A subjects); in contrast, heroin addicts without open psychiatric co‐morbidity showed unimpaired responses to brom challenge; a significantly lower GH response to brom and a lack of PRL suppression in ASPD subjects could express D2 postsynaptic receptor hyposensitivity possibly related to DA gene variants associated to co‐morbid disorder. In sum, the study of central monoamine function revealed an alteration of the 5‐HT system in all detoxified heroin‐dependent subjects. A significant reduction of alpha‐adrenergic receptors sensitivity and the hyposensitivity of postsynaptic DA receptors in ASPD subjects suggest once again that specific biological correlates of psychiatric co‐morbidity may characterize substance abusers subtypes.