Catherine F. 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

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.

Brain-Dependent ACTH Secretion from Multiple Heterotopic Pituitaries.

Summary Hypophysectomized rats with multiple heterotopic pituitaries have nearly normal adrenal weight and significant, though subnormal, corticosterone secretion. Removal of the entire forebrain, but not decortication, in these animals reduced corticosterone secretion nearly to values found in hypophysectomized control animals. These results indicate that heterotopic pituitary ACTH secretion is dependent on some subcortical portion of the forebrain.

The effect of pentobarbital on basal and ether-stimulated ACTH secretion in intact and adrenalectomized rats.

Pentobarbital in a dose of 3.5 mg/100 g b.w. did not suppress the high basal a.m. levels of plasma ACTH in adrenalectomized male rats. In both intact and adrenalectomized rats prior administration of the drug slightly depressed the rise in plasma ACTH induced by 2.5 min of ether inhalation, but this depression is of questionable statistical significance.

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.

Relationship of nycthemeral cycles of running activity and plasma corticosterone concentration following basal hypothalamic isolation

Abstract Rats with established normal nycthemeral rhythms of plasma corticosterone and spontaneous running activity were subjected to complete basal hypothalamic deafferentation. Immediately postoperatively, there was an abolition of both the adrenal and spontaneous activity rhythms. Postoperative AM and PM plasma corticosterone concentrations were not significantly different from each other; both were between the preoperative AM nadir and PM zenith. Postoperative running activity was nearly abolished in both the hours of light and darkness; the values for both were less than the low level of activity seen in the preoperative daylight hours.

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.