John P. Allen

Role of the Amygdaloid Complexes in the Stress-Induced Release of ACTH in the Rat

The participation of the amygdaloid complexes in the stress-induced release of ACTH was studied in the adult male rat. Unilateral and/or bilateral radiofrequency lesions were placed in the amygdalae o

NYCTOHEMERAL VARIATION AND SUPPRESSIBILITY OF PLASMA ACTH IN VARIOUS STAGES OF CUSHING'S DISEASE

In order to define nyctohemeral plasma ACTH secretory patterns, frequent plasma ACTH samples were obtained in seven patients with untreated Cushings disease (i.e. pituitary‐dependent Cushings syndrome), five Cushings patients treated by bilateral adrenalectomy, four of whom had Nelsons syndrome, and one patient with 21‐hydroxylase deficiency (congenital adrenal hyperplasia). A nyctohemeral rhythm of plasma ACTH concentration was apparent in the one patient with the adrenogenital syndrome but not in those with Nelsons syndrome or Cushings disease.

Lack of Adaptation of Acth Secretion to Sequential Ether, Tourniquet, or Leg-Break Stress

Adaptation to a repeated stress in male rats was studied by measuring plasma ACTH by radioimmunoassay 2.5 min or plasma corticosterone by acid fluorescence 20 min alter initiation of the stress. No adaptation was seen in the secretion of ACTH in response to ether, tourniquet, or leg-break stresses repeated at 90 min intervals 1–3 times. A marked rise in plasma ACTH concentration was produced within 2.5 min after application of each stress. Plasma ACTH always returned to basal levels by 90 rain after application of stress. Ether stress repeated at 24-hr intervals for 3 days did not produce any decrease in either the plasna ACTH or corticosterone response by the third day. These data indicate that no adaptation in ACTH secretion in response to repeated stress occurs under the conditions of our experiments.

Anterolateral Hypothalamic Deafferentation Prevents Compensatory Hypersecretion of ACTH Following Adrenalectomy in the Rat

Summary Complete or anterolateral, but not anterior, basal hypothalamic deafferen-tation prevented the increased basal secretion of ACTH in chronically adrenalecto-mized rats. ACTH secretion in response to ether stress was at least as great in the de-afferented, adrenalectomized rats as in intact controls. The data suggest that extra-hypothalamic influences which enter the lateral basal hypothalamus are necessary to achieve a high basal ACTH secretion when plasma ghicocorticoids are depressed.

Spinal cord pathways involved in tourniquet stimulation of ACTH secretion.

The effect of complete transection or hemisection at various levels from the lumbar through the cervical spinal cord on a stress-induced change in plasma corticosterone concentration was studied in adult male pentobarbital-anesthetized rats. Stressors were a hind-leg tourniquet 1–5 days and a hind-leg break 5 or 10 days postoperatively. A rise in plasma corticosterone concentration 20 min after the onset of the stress was generally used as an index of ACTH secretion. Neither stressor stimulated ACTH secretion in rats with complete cord transection between L1 and T2. Hemisection between L1 and T10 did not consistently block ACTH secretion following ipsilateral or contralateral tourniquet or leg break, but hemisection above T10 blocked the effect of only the contralateral stressors. Complete cord transection above T2 was associated with elevated ‘basal’ plasma immunoreactive ACTH and corticosterone concentrations in unanesthetized rats. These elevations were partially suppressed by pre-treatment with dexamethasone 12 h prior to sacrifice. We conclude that both tourniquet and leg break stimulate ACTH secretion through pathways in the spinal cord. These pathways are not consistently lateralized between L1 and T10 but are contralateral to the stimulated extremity above T10.