期刊
NEUROREPORT
卷 20, 期 6, 页码 617-621出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/WNR.0b013e32832a2393
关键词
anabolic androgenic steroids; contextual fear conditioning; gamma-aminobutyric acid A receptors; neurosteroids; selective brain steroidogenic stimulants
资金
- CRB Award [2-611185]
Corticolimbic neurons express neurosteroid biosynthesis, which is altered during anabolic androgenic steroid (AAS) treatment. The brain circuits and neurons that underlie the behavioral deficits found after AAS treatment remain undefined. We studied the effects of testosterone propionate (testosterone) on fear conditioning responses and in primary output corticolimbic neurons on 5 alpha-reductase-type-I and 3 alpha-hydroxysteroid-dehydrogenase expression. Testosterone fails to change cued fear responses although it induces excessive contextual fear associated with corticolimbic 5 alpha-reductase-type-I mRNA expression downregulation in the prefrontal cortex, hippocampus, and basolateral amygdala glutamatergic neurons. Increased fear responses are abolished by normalizing corticolimbic allopregnanolone levels with allopregnanolone treatment (8 mu mol/kg) or selective brain steroidogenic stimulants, including S-norfluoxetine (1.8 mu mol/kg). Agents that increase corticolimbic allopregnanolone levels may be beneficial in treating AAS users. NeuroReport 20:617-621 (C) 2009 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
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