Acute foot shock stress elicits a selective and time-dependent increas
e of neuroactive steroid (pregnenolone, progesterone, allotetrahydrode
oxycorticosterone) concentrations in rat brain cortex, accompanied by
a marked increase of plasma corticosterone. The brain cortical neuroac
tive steroid levels peaked between 10 and 30 min poststress and return
ed to control values by 2 h. Abecarnil (0.3 mg/kg, IP), a beta-carboli
ne derivative with anxiolytic properties, completely antagonized the e
ffect of foot shock on brain cortical neuroactive steroids. A single a
dministration of the anxiogenic beta-carboline FG 7142 (15 mg/kg, IP),
in contrast, mimicked the effect of foot shock. These data support th
e hypothesis for the existence of a functional relationship between br
ain neuroactive steroid concentrations and GABA(A) receptor function/e
motional state of the animal.