HORMONAL BASIS FOR IMPAIRMENTS IN MILK SYNTHESIS AND MILK EJECTION FOLLOWING HYPOTHALAMIC LESIONS

1961 ◽  
Vol 23 (3) ◽  
pp. 303-316 ◽  
Author(s):  
C. C. GALE ◽  
S. TALEISNIK ◽  
H. M. FRIEDMAN ◽  
S. M. McCANN
Keyword(s):  
Median Eminence ◽  
Adrenal Glands ◽  
Regulatory Mechanisms ◽  
Adrenocorticotrophic Hormone ◽  
Milk Ejection ◽  
Hypothalamic Lesions ◽  
Severe Impairment ◽  
Electrolytic Lesions ◽  
Hypophysectomized Rats ◽  
Pituitary Secretion

SUMMARY The placing of electrolytic lesions in the median eminence of the hypothalamic tuber cinereum induces severe impairment of lactation in rats by causing deficiencies in pituitary secretion of adrenocorticotrophic hormone (ACTH; essential for milk synthesis) and of oxytocin (necessary for milk ejection). Thus, in rats with lesions given oxytocin × 2/day to permit milk ejection, it was observed that: (1) the severity of impairment in lactation correlated significantly with the degree of atrophy of the dams' adrenal glands; (2) administration of luteotrophin (LTH) failed to repair this defect in lactation; (3) when cortisol was administered milk production was markedly improved—to about 70–80% of normal for days 5–10—(a further slight increase in milk yield resulted when oxytocin injections were given every 4 hr. 'around the clock' to rats receiving cortisol therapy); and (4) administration of regimens consisting of either LTH and cortisol, or LTH, growth hormone (GH), and cortisol failed to improve lactation beyond levels attained with cortisol therapy alone. In hypophysectomized rats replacement with cortisol and LTH, plus oxytocin × 2/day, permitted substantial synthesis which was not significantly improved further when GH was added to the regimen, and which promptly declined when LTH therapy was withdrawn. Since no deficiency in secretion of LTH could be demonstrated in lactating rats with lesions given hormonal replacement, these data provide evidence that elimination of hypothalamic regulatory mechanisms by hypothalamic lesions is compatible with secretion of large amounts of LTH. This demonstration that lesions in the median eminence block release of ACTH while permitting continued secretion of LTH indicates that the hypothalamic mechanisms regulating their release are not identical.

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.

Production of diabetes insipidus in hypophysectomized rats by hypothalamic lesions

1961 ◽  
Vol 201 (5) ◽  
pp. 811-814 ◽  
Author(s):  
C. C. Gale ◽  
S. Taleisnik ◽  
S. M. McCann
Keyword(s):  
Diabetes Insipidus ◽  
Water Intake ◽  
Median Eminence ◽  
Urine Volume ◽  
Water Turnover ◽  
Hypothalamic Lesions ◽  
Significant Augmentation ◽  
Hypophysectomized Rats ◽  
Somatotrophic Hormone ◽  
Made In

Lesions in the median eminence produced permanent diabetes insipidus (DI) in chronically hypophysectomized rats. Water turnover in these animals, however, was only about half of that observed when lesions were made in rats with intact pituitaries and was further characterized by absence of the normal interphase. Conversely, when hypophysectomy was performed in rats with DI, an immediate and sustained 50% reduction in water intake occurred. Administration of adrenocorticotropin to hypophysectomized rats with lesions caused significant augmentation of DI, but not to levels found in rats with DI and intact pituitaries. Neither somatotrophic hormone (STH) nor triiodothyronine increased water turnover when given to hypophysectomized animals with DI. Lesions in the median eminence of hypophysectomized rats induced an immediate increase in urine volume in the absence of water intake, which indicates that primary polyuria was responsible at least in part for the development of DI in hypophysectomized rats with lesions.

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.

HYPOTHALAMIC CONTROL OF PITUITARY GONADOTROPHINS

1961 ◽  
Vol 22 (1) ◽  
pp. 107-117 ◽  
Author(s):  
C. C. GALE ◽  
S. M. McCANN
Keyword(s):  
Diabetes Insipidus ◽  
Median Eminence ◽  
Oestrogen Therapy ◽  
Milk Ejection ◽  
Pregnant Rats ◽  
Tuber Cinereum ◽  
Severe Diabetes ◽  
Hypothalamic Control ◽  
Electrolytic Lesions ◽  
Experienced Difficulty

SUMMARY Impairments in gestation, parturition, and milk ejection were produced when electrolytic lesions were placed in the median eminence of the tuber cinereum of pregnant rats at various stages of gestation. Thus, uterine implantation of ova was blocked in 65% of rats following placement of lesions on day 1 of gestation, and implantation of ova was induced in these animals by administration of oestrogen. When lesions localized to the caudal median eminence were placed on days 4–9, implantation was not blocked but abortion-resorption resulted in 90% of cases. Replacement studies during pregnancy in rats with lesions in the caudal median eminence suggest that (1) all aborting rats were deficient in gonadotrophins necessary for secretion of oestrogen, and (2) half of them were deficient in luteotrophin as well. (That is, luteotrophin had no replacement value, while oestrogen therapy permitted maintenance of gestation in 54% of cases, and oestrogen plus progesterone allowed 100% to remain pregnant.) In rats receiving lesions on days 7–9 and maintaining gestation to term, 32% of those with severe diabetes insipidus experienced difficulty during delivery. Placement of lesions after day 13 impaired neither gestation nor parturition. The observation that most rats with lesions were able to deliver their litters normally but were unable to eject milk following suckling stimuli suggests that oxytocin is not essential for parturition in this species. Most of the rats with lesions failed to resume oestrous cycles; of the few showing return of normal or irregular cycles, the majority failed to mate.

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 MAINTENANCE OF LACTATION IN THE RAT AFTER HYPOPHYSIAL ANTERIOR LOBECTOMY DURING PREGNANCY

1961 ◽  
Vol 22 (4) ◽  
pp. 403-408 ◽  
Author(s):  
A. T. COWIE ◽  
J. S. TINDAL
Keyword(s):  
Anterior Pituitary ◽  
Pituitary Hormones ◽  
Anterior Lobe ◽  
Milk Secretion ◽  
Adrenocorticotrophic Hormone ◽  
Milk Ejection ◽  
Growth Indices ◽  
Partial Restoration ◽  
Hypophysectomized Rats ◽  
Milk Ejection Reflex

SUMMARY Experiments to determine the pituitary hormones necessary for the maintenance of lactation in the rat in the absence of either the anterior lobe of the pituitary or the entire pituitary are described. The anterior pituitary or the whole of the pituitary was removed on the 12th day of pregnancy and prolactin (25 i.u. twice daily) plus adrenocorticotrophic hormone (ACTH) (2 i.u./day) was given to the animals from parturition to the 10th day of lactation inclusive. The lactational performances of the two operated groups of rats, as judged by the litter-growth indices, were 53% (anterior lobectomy) and 43% (hypophysectomy) of normal. The milk-ejection reflex was completely restored in the anterior-lobectomized rats by the time of parturition, but the hypophysectomized rats required a further 2 days before milk ejection appeared to be normal. Our experiments confirm that prolactin and ACTH are two important factors in the maintenance of milk secretion in the rat. Since only partial restoration was achieved, however, it is clear that other factors, presumably of anterior-pituitary origin, are required for the full restoration of lactation.

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.

CONTRIBUTION TO THE EXISTENCE OF REGULATORY MECHANISMS AT THE ADRENAL LEVEL

1972 ◽  
Vol 70 (4) ◽  
pp. 741-757
Author(s):  
Otto Linèt
Keyword(s):  
Orotic Acid ◽  
Adrenal Glands ◽  
Actinomycin D ◽  
Delay Period ◽  
Regulatory Mechanisms ◽  
Leucine Incorporation ◽  
Total Period ◽  
Free Media

ABSTRACT Rat adrenal glands atrophied by the administration of cortisol acetate in vivo were used as a model for the study of early metabolic processes occurring in vitro. Atrophied adrenals incubated in the presence of 14C-leucine incorporated subnormal quantities of this amino acid per mg of protein for the first 120 min. When the incubation lasted for a total period of 180 or 240 min a supranormal rise in the 14C-leucine incorporation was observed. Similar changes occurred with some delay with regard to corticosterone production as expressed per 100 mg of tissue. No differences in 14C-leucine incorporation were observed between the control and atrophied adrenals in vivo. Homogenates from atrophied glands incorporated 14C-leucine to a greater extent than the control homogenates. The in vitro incorporation of 14C-orotic acid into the RNA was also higher in atrophied adrenals. The in vitro use of actinomycin D, cycloheximide and amphenone indicated that corticosterone production depended on the incorporation of 14C-leucine. The addition of cortisol to the incubation media markedly decreased the enhancement of 14C-lysine incorporation into the protein of atrophied adrenals. These, as well as additional results suggest rebound phenomena: once atrophic adrenals are transferred to cortisol-free media, reparative processes begin after a delay period. Such phenomena seem to be mediated by regulatory mechanisms at the adrenal level.

LONG-TERM EFFECTS OF INTRACEREBRAL CORTICOID IMPLANTS

1967 ◽  
Vol 55 (3) ◽  
pp. 440-450 ◽  
Author(s):  
Shaul Feldman ◽  
Nisim Conforti ◽  
Julian M. Davidson
Keyword(s):  
Ascorbic Acid ◽  
Median Eminence ◽  
Adrenal Glands ◽  
Long Term Effects ◽  
Unilateral Adrenalectomy ◽  
Post Operative Period ◽  
Steady Decrease ◽  
Medial Hypothalamus ◽  
Post Implantation

ABSTRACT Chronic implantation of cortisol acetate in the basal medial hypothalamus resulted in a steady decrease in weight of the adrenal glands which remained severely atrophic up to 70 days post-implantation. At this time, however, the adrenal ascorbic acid depletion response to unilateral adrenalectomy was normal. The compensatory adrenal hypertrophy (CAH) response, which was inhibited in the immediate post-operative period, reappeared later, and had returned to normal by 21 days postoperatively. Intramuscular administration of cortisol in unimplanted rats inhibited CAH at 14 or 21 days following onset of treatment, and prevented the recovery of CAH in animals implanted 21 days previously with cortisol in the median eminence. The possibility is discussed that the differential recovery of the responses to unilateral adrenalectomy in implanted animals with continuing atrophy of the adrenal cortex is due to some adaptation of central nervous mechanisms subserving the CAH response.

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