CHANGES IN THE EEC OF THE HYPOTHALAMUS AND LIMBIC SYSTEM AFTER ADMINISTRATION OF ACTH, SU-4885 AND ACH IN RABBITS WITH SPECIAL REFERENCE TO NEUROHUMORAL FEEDBACK REGULATION OF PITUITARY-ADRENAL SYSTEM
- 1 January 1966
- journal article
- research article
- Published by Physiological Society of Japan in The Japanese Journal of Physiology
- Vol. 16 (5) , 551-569
- https://doi.org/10.2170/jjphysiol.16.551
Abstract
EEG activity showed the following alterations: Injection of ACTH caused a decrease in 2-13 cps components in the dorsalhippocampus and median eminence-periventricular arcuate nucleus, and an increase in the amygdala, anterior hypo-thalamic area, mammillary body and midbrain reticular formation. Medial preoptic area revealed an increase and then a decrease in the slower components. Little change occurred in posterior hypothalamic area. SU-4885 [methopyrapone] caused an increase in the slower frequency components in the dorsal hippocampus, anterior hypothalamic area, median eminence-periventricular arcuate nucleus and posterior hypothalamic area. In the amygdala these components 1st decreased, but from 2-4 hr. after injection increased. In the midbrain reticular formation the slower components showed a decrease and then an increase. Hydrocortisone acetate caused an increase in the slower components of the dorsal hippocampus and the median eminence-periventricular arcuate nucleus, but these components markedly decreased in the amygdala, anterior hypothalamic area and the midbrain reticu- lar formation. After implantation of hydrocortisone acetate or localized electrolytic destruction in the median eminence-periventricular arcuate nucleus and the nucleus ventromedialis hypothalami, the stress response of the rabbit showed a depression. In cases of the septum pellucidum, posterior hypothalamic area, central grey and the midbrain reticular formation, no remarkable change in the stress response occurred. The basal hypothalamus might be a focus for the negative feedback control for the maintenance of homeostasis of ACTH and adrenocortical hormone, and the hippocampus and amygdala might participate in this mechanism by acting on the basal hypothalamus when their activities were influenced by ACTH or adrenocortical hormone level.This publication has 16 references indexed in Scilit:
- INVESTIGATION OF THE RELEASE OF ACTH1Endocrinology, 1959
- A COMPARISON OF THE INHIBITORY EFFECTS OF 2-METHYL-l,2-BIS(3-PYRIDYL)-l-PROPANONE AND AMPHENONE B ON ADRENAL CORTICAL SECRETION IN THE DOG1Endocrinology, 1959
- BLOOD ACTH: EFFECTS OF ETHER, PENTOBARBITAL, EPINEPHRINE AND PAIN1Endocrinology, 1958
- ALTERATIONS OF ADRENAL STEROID PATTERNS IN MAN RESULTING FROM TREATMENT WITH A CHEMICAL INHIBITOR OF 11 βHYDROXYLATIONJournal of Clinical Endocrinology & Metabolism, 1958
- Corticotropin Releasing Activity of a Pepsin Labile Factor in the Hypothalamus.Experimental Biology and Medicine, 1958
- RELATION BETWEEN THE ADRENAL CORTEX AND THE CENTRAL NERVOUS SYSTEM1958
- PLASMA 17-HYDROXYCORTICOSTEROID LEVELS AND CONDITIONED BEHAVIOR IN THE RHESUS MONKEYEndocrinology, 1957
- EVIDENCE OF SEPARATE HYPOTHALAMIC CENTERS CONTROLLING CORTICOTROPIN AND THYROTROPINSECRETION BY THE PITUITARY1Endocrinology, 1956
- Suppression of Adrenal Compensatory Hypertrophy by Hypothalamic Lesions.Experimental Biology and Medicine, 1955
- The rabbit diencephalon in stereotaxic coordinatesJournal of Comparative Neurology, 1954