Abstract
During the first 2 days after operation resting plasma corticosterone levels were high, but thereafter returned to normal in both midbrain-transected and sham-operated animals. Ether anesthesia induced a significant rise in plasma corticosterone 48 hr after midbrain transection. Three days after operation dexamethasone suppressed plasma corticosterone levels to an equivalent level in both midbrain-transected and sham-operated rats. It is concluded that the hypothalamic-adenohypophysial complex is capable of regulating ACTH release in response to selected stimulatory and inhibitory influences in midbrain-transected rats. We found no evidence that the effect of a tonic inhibitory neural center on ACTH release is abolished by midbrain transection. (Endocrinology 77: 1091, 1965)
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