SOUND STRESS ACTIVATION OF TRYPTOPHAN-HYDROXYLASE BLOCKED BY HYPOPHYSECTOMY AND INTRACRANIAL RU-38486

The rapidly reversible increase in cortical or midbrain tryptophan hyd roxylase activity observed ex vivo after exposure of rats to 1-h sound stress was blocked by hypophysectomy, but not sham hypophysectomy, an d restored by dexamethasone administration to the hypophysectomized an imals (500 mu g/day i.p. for 3 days). The response to sound stress was also lost with deafferentation of the hypothalamus. These results ind icate that hypothalamic control of adrenal glucocorticoids is required for the serotonergic response to sound stress. The glucocorticoid ant agonist, RU 38486, given intracerebroventricularly (200 mu g/day for 4 -5 days) or bilaterally, into the region of the central nucleus of the amygdala (100 mu g 15 min before stress), blocked the sound stress-in duced increase in tryptophan hydroxylase activity. In contrast, the an timineralocorticoid, RU 26752, was without effect. The block obtained with RU 38486 suggests that glucocorticoid is required by the neurons that relay the effects of sound stress to the rostrally projecting ser otonergic neurons.