Hypothalamic Islands Research Articles

Paradoxical Sleep — A Study of its Nature and Mechanisms

This chapter discusses the results of a study that analyzes the nature and mechanisms of paradoxical sleep (P.S.), or rhombencephalic phase of sleep. In this study, both tonic and phasic electroencephalogram (EEG)or peripheral index of P.S. are very different from EEG and behavioral slow sleep. The pontine origin of rapid eye movements and of the phasic ponto-geniculo-occipital activity occurring during P.S. is emphasized. Phylogenetic study shows that slow sleep may be observed in reptiles, birds, and mammals. In contrast, P.S. is not found at all in the tortoise, and is of very short duration in birds (its ratio to the total sleep being only 0.2%). In mammals, this ratio is about 6–30%. Ontogenetic studies in the kitten show that P.S. may appear immediately after wakefulness and constitutes 90% of total sleep during the first days. In chronic pontile animals, with hypothalamic islands, the rhombencephalic phase of sleep, showing all the pontine electrical and behavioral criteria of P.S. in the intact animal, can be completely identified with the latter. Its mean duration (6 min) is analogous to that of the intact animal. No behavioral or EEG index of slow sleep was observed in pontile animals.

STUDIES OF THE LOCATION OF THE RECEPTOR SITE FOR NEGATIVE FEEDBACK CONTROL OF ACTH RELEASE.

Dexamethasone-21-phosphate was administered to rats 20 hr after graded amounts of forebrain had been removed. Four hr later, its ability to suppress ACTH release was estimated by measuring corticosterone in a 3-min collection of left adrenal effluent, obtained immediately after laparotomy under ether anesthesia. Corticosterone secretion was suppressed in dexamethasone-treated hypothalamic island and median eminence island animals as well as in dexamethasone-treated intact controls. Untreated animals of all groups had relatively high corticosterone secretion rates. Untreated animals with pituitary islands usually had pituitary infarcts and low corticosterone secretion rates, even without dexamethasone suppression. While the dexamethasone-treated pituitary island animals tended to have lower secretion rates than untreated pituitary island animals, it was not possible to assess with certainty the effect of dexamethasone on ACTH release in these animals. Since dexamethasone unequivocally suppressed ACTH secre...

NEURAL CONTROL OF THYROTROPIN SECRETION: EFFECT OF FOREBRAIN REMOVAL ON THYROID FUNCTION.

The entire brain rostral to the superior colliculus was removed, leaving either a “hypothalamic island” or a “median eminence island” attached to the pituitary. Operated and control animals were force-fed for 10 days postoperatively; approximately half of each group additionally received 30 mg propylthiouracil (PTU) daily. Thyroid weights and radioiodine uptake were compared in various experimental and control groups. Thyrotropin secretion appeared approximately equal in similarly treated intact and hypothalamic island groups. No thyroid hypertrophy developed in the PTU-treated median eminence island rats, but only 3 of these survived the full 10 days. No pituitary infarction was found in any operated animal. It thus appears that the forebrain outside the limits of the hypothalamus is not essential for normal functioning of the servomechanism which results in increased TSH release in response to thyroxine deficiency.

Further Studies on Adrenal Cortical Function in Dogs with Isolated Pituitaries

Adrenal venous blood was analyzed for corticosteroid content in various dog preparations. Dogs with brain removal down to the pons and isolated pituitaries exhibited a period of depressed adrenal cortical function, followed by persistent elevated “resting” secretion. Removal of the entire brain and spinal cord in addition did not alter this response, nor did removal of the posterior pituitary or abdominal evisceration. Similar patterns of adrenal cortical function were present in dogs with hypothalamic islands.

Osmotic activation of neurohypophysial hormone release in rabbits with hypothalamic islands

Electroencephalographic (EEG) changes in response to elevations in the osmolarity of blood have been correlated in earlier studies with the release of both antidiuretic hormone and oxytocin from the neurohypophysis. To determine whether these phenomena are causally related, studies have been made of the effects of forebrain ablations on the osmotically-induced release of oxytocin. In acute rabbit preparations the injection of 10 per cent NaCl into the carotid artery provided an osmotic stimulus. The milk-ejection technique was used to assess neurohypophysial activation. The hypertonic stimulus induced both a synchronous EEG firing of elements in the olfactory bulb and release of neurohypophysial hormone. However, after removal of the olfactory bulbs by blunt dissection and suction, the neurohypophysis could still be activated by the osmotic stimulus. In fact, only an hypothalamic island containing the supraoptic but not the paraventricular nuclei was necessary. The osmotic stimulus was no longer effective (with one questionable exception) after removal of the island, though the neurohypophysis still responded to direct electrical stimulation. Electrolytic lesions of the infundibular stalk blocked the reflex release of hormone. It was concluded that the osmotically-induced EEG response in the olfactory bulb is not essential for activation of the neurohypophysis and that osmoreceptors responsible for hormone release are located in the anterobasal part of the hypothalamus.