HYPOTHALAMIC LESIONS AND ADRENAL FUNCTION IN THE CAT

1961 ◽  
Vol 38 (1) ◽  
pp. 88-98 ◽  
Author(s):  
Dorothy T. Krieger ◽  
Irving H. Wagman
Keyword(s):  
Median Eminence ◽  
Adrenal Function ◽  
Cortical Function ◽  
Hypothalamic Lesions ◽  
Electrolytic Lesions ◽  
Response To Stress ◽  
Adrenal Response ◽  
Adrenal Cortical Function

ABSTRACT Bilateral electrolytic lesions limited to the median eminence were produced stereotaxically in four cats which had previously shown positive responses (as measured by blood corticoid elevations) to exogenous corticotrophin (ACTH) and insulin hypoglycaemia. Following operation these animals exhibited low basal corticoid levels and an inability to respond to ACTH and an impaired response to stress. At autopsy they showed an increase in adrenal size and stainable cortical lipid. Operated controls had normal responses to both exogenous ACTH and insulin hypoglycaemia and had normal adrenal histology. Thus a lesion of the median eminence depresses adrenal cortical function by interference with release of steroid from the adrenal and not by inducing adrenal atrophy. This may be explained in part by the observation that median eminence lesions interfere with the adrenal response to exogenous ACTH.

Adrenal cortical function following stepwise removal of the brain in the dog

1959 ◽  
Vol 196 (3) ◽  
pp. 583-588 ◽  
Author(s):  
J. L. Story ◽  
J. C. Melby ◽  
R. H. Egdahl ◽  
L. A. French
Keyword(s):  
Pituitary Gland ◽  
Venous Blood ◽  
Cortical Response ◽  
Cortical Function ◽  
Operative Trauma ◽  
Hypothalamic Lesions ◽  
Response To Stress ◽  
The Brain ◽  
Adrenal Cortical Function

Previous studies indicate that hypothalamic lesions will prevent adrenal cortical response to stress. The present study was undertaken to determine if higher centers of the brain are necessary for adrenal cortical hypersecretion of 17-hydroxycorticosteroids due to operative trauma. Intermittent samples of adrenal venous blood were obtained from dogs by means of adrenal cannulas and 17-hydroxycorticosteroid output was determined. Stepwise removal of the brain was performed, with collections of adrenal venous blood at various levels of anatomic integrity. Removal of the brain down to the hypothalamus resulted in no diminution in the maximal adrenal cortical response following operative trauma as measured by 17-OH-corticosteroid output. After removal of the hypothalamus there is a persistence of adrenal corticoid secretion up to 6 hours after removal of this structure leaving the pituitary gland intact. It is concluded that a) the CNS above the hypothalamus is not essential for adrenal 17-OH-corticosteroid production in response to operative trauma; and b) adrenal cortical secretion persists in response to stress up to 6 hours after removal of the hypothalamus.

THE EFFECT OF HYPOTHALAMIC LESIONS ON REPRODUCTIVE ACTIVITY IN SHEEP

1967 ◽  
Vol 39 (3) ◽  
pp. 415-NP ◽  
Author(s):  
H. M. RADFORD
Keyword(s):  
Median Eminence ◽  
Reproductive Activity ◽  
Mammillary Body ◽  
Optic Chiasma ◽  
Hypothalamic Lesions ◽  
Apparent Change ◽  
Electrolytic Lesions ◽  
Releasing Factors ◽  
Bilateral Lesions ◽  
Made In

SUMMARY Electrolytic lesions were made in the hypothalamus of 41 Merino ewes which were subsequently observed for 2–16 months. Ovarian inactivity resulted from bilateral medial and ventral lesions placed immediately posterior to the optic chiasma (four ewes) or immediately anterior to the mammillary body (five ewes). Failure to show oestrus while apparently still ovulating regularly was a feature in another four ewes in which bilateral medial and ventral lesions were placed between the sites already described. Small bilateral lesions in these ventral regions led initially to ovarian inactivity, but final re-establishment of apparently normal reproductive activity in three ewes. Bilateral lesions in regions other than those described above resulted in no apparent change in reproductive activity (eight ewes). Similarly, unilateral or asymmetrical lesions in the remaining 17 ewes failed to affect their reproductive activity. The results are consistent with the hypothesis that in sheep a region of the median eminence responsible for the production of gonadotrophin-releasing factors requires neural inputs traversing both anterior and posterior hypothalamic areas.

LOCALIZATION OF HYPOTHALAMIC LESIONS INHIBITING ADRENAL WEIGHT MAINTENANCE IN THE RAT

1960 ◽  
Vol XXXIV (I) ◽  
pp. 19-26 ◽  
Author(s):  
Johannes Moll
Keyword(s):  
Median Eminence ◽  
Weight Maintenance ◽  
Brain Lesions ◽  
Pituitary Stalk ◽  
Adrenal Weight ◽  
Hypothalamic Lesions ◽  
Electrolytic Lesions ◽  
The Right

ABSTRACT Electrolytic lesions, approximately 1 mm in diameter, were placed at 20 regularly distributed points in the midline of the hypothalamus of rats. Eighteen days later the left adrenals were removed and weighed. Six days after this operation the animals were sacrificed and the right adrenals weighed. Animals without brain lesions but otherwise similarly treated, served as controls. The brains of all lesioned animals were studied histologically. Following lesions in the antero-basal and mid-basal hypothalamus the weights of both adrenals were subnormal. Compensatory adrenal hypertrophy was only slightly inhibited by the lesions. Lesions destroying the pituitary stalk and lesions in the median eminence, had no effect on adrenal weight.

EFFECT OF HYPOTHALAMIC LESIONS ON PITUITARY MELANOCYTE-STIMULATING HORMONE

1967 ◽  
Vol 39 (4) ◽  
pp. 485-NP ◽  
Author(s):  
S. TALEISNIK ◽  
J. DE OLMOS ◽  
R. ORÍAS ◽  
MARÍA E. TOMATIS
Keyword(s):  
Median Eminence ◽  
Male Rats ◽  
Posterior Lobe ◽  
Melanocyte Stimulating Hormone ◽  
Mammillary Bodies ◽  
Hypothalamic Lesions ◽  
Paraventricular Nuclei ◽  
Inhibiting Factor ◽  
Electrolytic Lesions ◽  
Stimulating Hormone

SUMMARY The effect on the content of melanocyte-stimulating hormone (MSH) activity in the pituitary of electrolytic lesions placed in different regions of the hypothalamus was studied in male rats. Lesions in the paraventricular nuclei resulted, after 15 days, in a decrease of pituitary MSH activity to 20·4 ± 4·5%/mg. gland as compared with the controls, without changes in the weight of the hypophyses. In a group of animals in which the lesions failed to destroy the paraventricular nuclei completely the MSH activity in the pituitary was 66·4 ± 7·5% of that of controls and the weight of the gland was significantly higher. Hypothalamic lesions in the median eminence of the tuber cinereum produced 24 hr. later a decrease of pituitary MSH activity to 6·6 ± 0·8%, but 15 days later the values/mg. gland were almost normal. Lesions placed in the mammillary bodies or in the nucleus caudatus did not affect pituitary MSH content. Extracts of stalk-median eminence or posterior lobe from animals with lesions in the paraventricular nuclei, failed to show MSH-releasing factor as it is found in intact animals, nor did they contain MSH-release-inhibiting factor. The results support the concept that the paraventricular nuclei are involved in the control of pituitary MSH secretion and suggest that the MSH content of the disconnected hypophysis is to some degree regulated autonomously.

THE ASSESSMENT OF ADRENAL-CORTICAL FUNCTION IN PATIENTS RECEIVING CORTICOTROPHIN THERAPY

1970 ◽  
Vol 64 (2) ◽  
pp. 287-294
Author(s):  
M. J. Levell ◽  
S. R. Stitch ◽  
M. Noronha ◽  
C. Vas
Keyword(s):  
Plasma Cortisol ◽  
Therapeutic Trial ◽  
Urinary Cortisol ◽  
Cortical Function ◽  
Low Concentrations ◽  
Urine Concentrations ◽  
Adrenal Response ◽  
Urinary Steroid ◽  
Secretion Rates ◽  
Adrenal Cortical Function

ABSTRACT Plasma cortisol and urinary 17-hydroxycorticosteroids and cortisol secretion rates have been measured on patients with multiple sclerosis taking part in a therapeutic trial of corticotrophin. Patients who had not received corticotrophin showed no evidence of abnormal adrenal function, although the combination of normal levels of plasma cortisol with somewhat low concentrations of urinary cortisol metabolites suggested an abnormal steroid metabolism. Patients who had been treated continuously with corticotrophin (for at least 1 year) showed elevated plasma cortisol concentrations and an even greater disparity between plasma and urine concentrations than the untreated controls. Thus, the urinary steroid measurements did not give a useful measure of the degree of adrenal response and should not be used to monitor prolonged corticotrophin therapy.

EFFECTS OF IMPLANTATION OF CORTISOL INTO THE BRAIN STEM OR PITUITARY GLAND ON THE ADRENAL RESPONSE TO STRESS IN THE RABBIT

1962 ◽  
Vol 41 (4) ◽  
pp. 561-570 ◽  
Author(s):  
Peter G. Smelik ◽  
Charles H. Sawyer
Keyword(s):  
Pituitary Gland ◽  
Brain Stem ◽  
Median Eminence ◽  
Immobilization Stress ◽  
Observable Effect ◽  
Anterior Portion ◽  
Paraventricular Nuclei ◽  
Response To Stress ◽  
Adrenal Response ◽  
The Brain

ABSTRACT Small amounts of crystalline cortisol were implanted into the brain stem or the pituitary gland of rabbits; subsequently the adrenal response to immobilization stress was measured (as indicated by the rise in plasma corticoids) at weekly intervals for several weeks after implantation. The stress-induced adrenal activation was inhibited by implants into the anterior portion of the median eminence, the post-optic region and, to a lesser extent, the antero-medial part of the hypothalamus, between the supra-optic and paraventricular nuclei and the median eminence. No observable effect was induced by similar implants into the posterior hypothalamus, mesencephalon and adenohypophysis. Little correlation could be noted between inhibition of adrenal function and decline of adrenal weight.

Effects of chronic hypothalamic lesions on diurnal and stress corticosteroid levels

1964 ◽  
Vol 206 (5) ◽  
pp. 1161-1164 ◽  
Author(s):  
Margaret A. Slusher
Keyword(s):  
Acute Stress ◽  
Indwelling Catheter ◽  
Blood Samples ◽  
Tuber Cinereum ◽  
Hypothalamic Lesions ◽  
Acute Response ◽  
Response To Stress ◽  
Adrenal Response ◽  
Arcuate Nuclei ◽  
Stimulation Of

The effect of chronic lesions on plasma corticosteroid levels has been assessed in an attempt to differentiate neuronal areas affecting diurnal corticosteroid rise from those involved in acute response to stress. In unanesthetized, unrestrained rats blood samples were collected through a chronic indwelling catheter on each of four experimental days at 9 and 10 am and 5 pm with or without addition of a stress applied at 9:45 am. Anterior hypothalamic lesions bilaterally destroying the periventricular zone and arcuate nuclei were associated with inhibition of the normal 5 pm rise but with normal rise in plasma corticosteroid levels in response to sound or to a 1-min electrical stimulation of the posterior diencephalon. Posterior tuber cinereum lesions were associated with normal 5 pm rise but with inhibition of response to sound. Response to ether stress was unaffected by any lesion. Thus the integrity of anterior hypothalamic areas appears essential for normal diurnal rise in plasma corticosteroid levels while more posterior areas are involved in mediation of pituitary-adrenal response to acute stress of sound.

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