Abstract
Effects of elec-trical stimulation of brainstem sites on ACTH release have been assessed in cats chronically implanted with electrodes and indwelling jugular venous catheters. Log-dose response for bioassay of ACTH in the 2-hr. hypophysectomized rat revealed a sensitivity to 0.05 mU/ml by measurement of adrenal venous effluent ascorbic acid, and to 0.075 mU/ml by effluent corticosteroid determinations. By these assays, control levels of ACTH in 1 ml plasma from unrestrained, unstimulated cats were undetectable. Measurable ACTH was released 1-2 min. after stimulation of sites in dorsal midbrain, or 4 of 8 sites in diencephalon; 30 min. later, levels were again below the minimum detectable. Inhibition of the pituitary-adrenal axis was demonstrated by paired stimulation of a potentially inhibitory site with a demonstrably facilitative one: diencephalically evoked release of ACTH was blocked by concurrent stimulation of sites in the ventral midbrain or the preoptic region. In spite of differences in preparation and prestimulation stress, results confirm those reported previously on effluent corticosteroid levels in encephale isole'' cats.