Showing papers on "Hypothalamus published in 1972"

A retinohypothalamic projection in the rat

Abstract: A direct projection from the retina to the hypothalamus was demonstrated in the rat. Following injection of tritiated leucine or proline into the posterior chamber of the eye, labelled protein was shown autoradiographically in the suprachiasmatic nuclei of the medial hypothalamus, both ipsilateral and contralateral to the injected eye. The labelling of the nucleus was heaviest in its ventral portion but extended throughout the nucleus. No evidence for a projection to the supraoptic nucleus or any other hypothalamic nucleus was observed. All of the known terminal nuclei of the primary and accessory optic tracts were heavily labelled. The projection to the suprachiasmatic nucleus could not be clearly confirmed in material prepared using the Fink-Heimer method for the demonstration of degenerating axon terminals. Electron microscopic study of the suprachiasmatic nucleus following orbital enucleation showed degenerating endings making synaptic contacts with small dendrites of the suprachiasmatic nucleus cells. These first appeared at three days after operation and were nearly gone by seven days. Thus, the retinohypothalamic tract in the rat appears to arise from the ganglion cells of the retina and to terminate on the smaller dendritic branches of the neurons of the suprachiasmatic nucleus.

An autoradiographic and electron microscopic study of retino-hypothalamic connections.

Abstract: Retino-hypothalamic connections have been studied autoradiographically in the rat, guinea pig, rabbit, cat and monkey following the intravitreal injection of 3H-leucine or 3H-proline, and electron microscopically following unilateral eye removal in the guinea pig and monkey. In each of the species examined evidence has been found for a direct projection from the retina to the suprachiasmatic nucleus, but to no other region of the hypothalamus. The projection to the suprachiasmatic nucleus is always bilateral (even in the albino guinea pig, in which all other components of the retinal projection are crossed) but from grain counts in our autoradiographs it appears that the input to the contralateral nucleus is about twice as heavy as that on the ipsilateral side. Most of the retinal fibers appear to terminate within the ventral part of the nucleus where they form asymmetric synapses either upon small dendritic branches or dendritic spines. The possible role of this retinal projection to the suprachiasmatic nucleus in mediating a variety of light-induced neuroendocrine responses is discussed.

Aromatization of Androstenedione by the Anterior Hypothalamus of Adult Male and Female Rats

Abstract: Homogenates of fresh tissue from adult male and female rats were incubated with appropriate co-factors and androstenedione-3H for one hour at 37° C. Extraction and identification of reaction products demonstrated the aromatization of androstenedione to estrone by anterior hypothalamus but not by posterior hypothalamus, anterior pituitary gland or frontal cortex. This finding confirms and expands the previous preliminary report of aromatization by human fetal hypothalamus to include adults of both sexes in a second species, the rat. Further localization of this reaction is consistent with concepts derived from experimental evidence which indicate central aromatization of androgens to be involved in sexual differentiation of the brain, initiation and maintenance of sexual behavior, control of gonadotropin secretion and “peripheral conversion” of circulating androgens to estrogens. (Endocrinology 90: 295, 1972)

Sexual differences in the hypothalamic regulation of prolactin secretion.

Abstract: Estrogen treatment of female rats ovariectomized when adult or of adult neonatally castrated males resulted, on the afternoon and evening of the 3rd day after initiation of treatment, in surges of prolactin secretion which reached 100 ng/ml. Males castrated when adult or androgen sterilized females ovariectomized when adult did not produce surges in response to estrogen treatment, prolactin levels remaining in the range of 10–20 ng/ml. In contrast to these sexual differences, baseline prolactin levels in untreated gonadectomized males or androgen sterilized females were significantly higher than in untreated gonadectomized females or neonatally castrated males. The surge of prolactin secretion in estrogen-treated female rats ovariectomized when adult was inhibited by a retrochiasmatic cut separating the anterior from the medial part of the hypothalamus. These results demonstrate fundamental sexual differences in the regulation of prolactin secretion. These differences may result from androgens inhibiting,...

The Ontogenesis of Human Fetal Hormones: I. GROWTH HORMONE AND INSULIN

Abstract: The content and concentration of immunoreactive growth hormone (GH) were measured in 117 human fetal pituitary glands from 68 days of gestation to term and in the pituitary glands of 20 children 1 month to 9 yr of age. Physicochemical and immunochemical properties of GH of fetal pituitary glands and GH from adult pituitary glands were indistinguishable by disc gel electrophoresis, immunoelectrophoresis, starch gel electrophoresis, and radioimmunoassay techniques. In the fetal pituitary gland, the GH content rose from mean levels of 0.44+/-0.2 mug at 10-14 wk of gestation, to 9.21+/-2.31 mug at 15-19 wk, to 59.38+/-11.08 mug at 20-24 wk, to 225.93+/-40.49 mug at 25-29 wk, to 577.67+/-90 mug at 30-34 wk, and to 675.17+/-112.33 mug at 35-40 wk. There was a significant positive correlation between growth hormone content of the pituitary and gestational age, crown-rump length, and the weight of the pituitary gland. The content and concentration (micrograms/milligram) of human growth hormone (HGH) in the fetal pituitary showed significant increments (P < 0.001) for each 4 wk period of gestation until 35 wk. Further increases in the HGH content were noted in pituitaries of children aged 1-9 yr (range of 832 to 11.211 mug). Immunoreactive GH was detected in fetal serum at a concentration of 14.5 ng/ml as early as 70 days gestation, the youngest fetus assayed. At 10-14 wk, the mean concentration of serum growth hormone was 65.2+/-7.6 ng/ml; at 15-19 wk 114.9+/-12.5 ng/ml; at 20-24 wk 119.3+/-19.8 ng/ml; at 25-29 wk 72.0+/-11.5 ng/ml; and 33.5+/-4.2 ng/ml at term. A significant negative correlation of serum growth hormone with advancing gestational age after 20-24 wk was observed (P < 0.001). In 17 fetuses paired serum and pituitary samples were assayed; no significant correlation between the concentration of serum GH and the pituitary content or concentration of GH was demonstrable. The serum concentration of chorionic somatomammotropin (HCS) in the fetus was unrelated to gestational age. Insulin (1-30 muU/ml) was detected in 42 of 46 fetal sera assayed. These data suggest that the appearance and development of the secretory capacity for GH by the human fetal pituitary gland coincides with developmental changes in the portal system and hypothalamus. Maturation of inhibitory central nervous system control mechanisms for secretion of GH may not occur until infancy.

Hypothalamic control of prolactin secretion.

Abstract: Publisher Summary This chapter emphasizes the current concepts and observations hypothalamic control of prolactin secretion. The regulation of prolactin secretion is exerted by the hypothalamus, and involves the action of a prolactin-inhibiting factor (PIF), a possible prolactin-releasing factor (PRF), catecholamines, serotonin, and other biogenic amines—all produced in the hypothalamus. Some other agents that stimulate or inhibit prolactin secretion including estrogen, the suckling stimulus, stresses, several drugs, and prolactin, act through hypothalamic mechanism. However, there are some hormones and drugs that can directly influence the anterior pituitary to increase or decrease prolactin secretion, although several of these also can act through the hypothalamus. The interference with hypothalamic pathways to the anterior pituitary by appropriate hypothalamic lesions, stalk section, pituitary transplantation or by administration of certain drugs, results in augmented prolactin release. PIF release from the median eminence is at least partially under the regulation of biogenic amines. The physiological importance of circulating prolactin in controlling secretion of pituitary prolactin remains to be elucidated. The ability of many drugs to either increase or depress prolactin release suggests a useful approach for controlling the secretion and functions of prolactin in the organism.

Nerve Growth Factor: Stimulation of Regenerative Growth of Central Noradrenergic Neurons

Abstract: The growth of new axonal sprouts was studied from transected, ascending noradrenergic axons into transplants of iris tissue in the caudal hypothalamus of the rat. A single intraventricular injection of nerve growth factor, given at the time of axonal damage, resulted in an increased formation and growth of new noradrenaline sprouts 7 days later. The effect seemed to be proportional to the administered dose of nerve growth factor.

Relation of Prolactin and Estrogen to Mammary Tumorigenesis in the Rat

Abstract: In rats estrogen and prolactin are the 2 most important hormones involved in development and growth of mammary tumors. Both are controlled by the pituitary gland and hypothalamous. Ovariectomy or hypophysectomy can inhibit development of mammary tumors or can cause regression. Growth of established mammary tumors can be increased by doses of estrogen estrogen with progesterone or prolactin. Estrogen increases prolactin and growth hormone secretion by the pituitary but has no effect on tumorigenesis in the absence of the pituitary. However prolactin or prolactin with growth hormone together may promote mammary tumor development in the absence of ovaries. In an experiment to study the effects of different doses of estrogen on mammary cancer de velopment and growth in ovariectomized rats tumors were induced with 5 mg of 712-dimethylbenz (a) anthracene (DMBA) at 52 days of age. Test animals received estradiol benzoate (EB) every other day for 150 days by sc injection; controls were given only the corn oil solvent. Mammary cancers developed in all 18 controls with an average latency period of 59 days. No cancers developed in ovariectomized rats who did not receive DMBA. Greatest tumor incidence (17 of 19) occurred in rats given 2 mcg EB. Average latency was 73 days. Regression occurred in 8% of mammary tumors in intact controls but in 20% of ovariectomized rats given .2 and 2.0 mcg EB. Regression rate was 39% in ovariectomized rats given 20 mcg EB. At 150 days ovariectomized rats not treated with EB showed reduced prolactin levels; those with .2 mcg EB showed a small inc rease; the highest doses (up to 2 mcg) produced increases ranging from 11.5 to 12-fold. In rats given 2 mcg EB fewer cancers followed and the latency period was longer than in intact controls. In another experiment a large dose of estrogen given 3 months after DMBA prevented tumor growth while prolactin alone increased mammary tumor growth about 190%. EB alone completely suppressed growth of tumors whereas EB with prolactin restored growth to that of controls. Large doses of estrogen may block binding of prolactin to receptor sites or otherwise prevent prolactin from acting on tumor cells. Changes in hypothalamic function may give rise to spontaneous mammary tumors by increasing prolactin secretion especially in old female rats. Whether this applies to humans is undetermined.

Dependence of hypothalamic obesity on insulin, the pituitary and the adrenal gland.

Abstract: . The obesity which follows destruction of the ventromedial nucleus (VMN) of the hypothalamus of rats is accompanied by hyperphagia and hypersecretion of insulin. The effects of weight gain after ventromedial lesions were examined after hypophysectomy, after adrenalectomy and in rats in which the secretory function of the (3-cells had been destroyed with streptozotocin. Mature female rats received streptozotocin (65 mg/kg) intravenously: a) prior to hypothalamic injury; b) 7 days following hypothalamic injury; or c) after the rats had already become obese following hypothalamic damage. Weight gain of lesioned rats was not impaired by hypophysectomy or adrenalectomy. Treatment of lesioned-hypophysectomized rats with growth hormone prevented most of the increase in weight. Cortisone treatment of adrenalectomized rats with lesions had no significant effect. Both lesioned and control rats lost weight following treatment with streptozotocin until supplemental insulin was given. Body weight of all anima...

Adrenergic and serotoninergic control of growth hormone secretion in adult male rats.

Abstract: Plasma radioimmunoassayable growth hormone (GH) levels measured in adult male rats anesthetized for 2 hr with urethane, were found to be lower and strikingly more uniform than those of animals decapitated while awake. Rats prepared in this manner, and bearing a cannula chronically implanted in a lateral ventricle of the brain, were used for the determination of the effect, on plasma GH levels, of the intraventricular administration of catecholamines, adrenergic receptor blockers, and serotonin (5- HT). While saline (10 μl/rat) or noradrenaline (1.0 μg/rat) did not induce any significant changes in plasma GH, dopamine (1.0 Mg/rat) significantly reduced plasma GH levels. This dopaminergic inhibition is apparently exerted through hypothalamic beta-adrenergic receptors, since it is abolished by the previous administration of propranolol (5O μg/rat), a specific beta-adrenergic blocker. The injections of 5-HT (1.0 μg/rat) were followed by a highly significant rise of plasma GH; this effect was abolished by the ...

The Effect of Stress and Nembutal on Plasma Levels of Gonadotropins and Prolactin in Ovariectomized Rats

Abstract: The stress of etherization and bleeding produced an elevation within 2 min in the plasma levels of prolactin, LH, and FSH in ovariectomized rats. Quantitatively the elevation was greatest in the case of prolactin, less for LH, and least for FSH. A second exposure to ether and bleeding one hour later produced a further elevation in prolactin and no further change in LH and FSH. The levels of prolactin and LH but not FSH had declined to control, nonstress (decapitated) levels within one hr. Nembutal blocked the stressinduced elevations of plasma prolactin and LH but did not affect the levels of FSH. The effect of Nembutal is thought to be on the CNS since the Nembutalized rats responded to hypothalamic extract or ovine LRF with dramatic elevations in plasma LH, indicating that the pituitary was still responsive to releasing factors. It is concluded that stress can induce a rapid release of pituitary FSH and LH as well as prolactin in the rat. (Endocrinology 90: 707, 1972)

Uptake of peroxidase from the third ventricle by ependymal cells of the median eminence.

Abstract: Peroxidase injected into the subarachnoid space in mice is absorbed by ependymal cells of the median eminence. The ependymal cells of the median eminence of the rat and Japanese quail absorb peroxidase injected into the third ventricle. The processes of these ependymal cells terminate at the capillaries of the primary plexus or those surrounding the ventromedial nucleus of the hypothalamus. In all three species, peroxidase is absorbed by the ependymal cells of the paraventricular organ and by those in close proximity to it. Some ependymal cells send processes to the capillaries in the lateral nucleus of the hypothalamus. These phenomena are discussed in relation to adenohypophysial function.

The Hormonal Control of the Amphibian Ovary

Abstract: synopsis. The ultimate control of amphibian gonadal function rests with environmen? tal factors mediated through the hypothalamus. It appears that control of ovarian growth resides in the infundibular region and ovulation in the preoptic area. For normal temporal relationships between oocyte growth and ovulation to occur, an intact hypothalamo-pituitary complex is necessary. It is uncertain whether the several types of pituitary basophils considered histologically as gonadotropin-producing cells are in fact producing separate LH- and FSH-like hormones. Perhaps the concensus indicates a single hormone has both vitellogenic and ovulatory functions. This hormone stimulates estrogen synthesis and secretion by the ovarian follicle cells, and this steroid causes oviduct growth and the hepatic biosynthesis of vitellogenin, the major yolk platelet precursor. Uptake of this lipoprotein from ihe circulation and its conversion to the components of the platelet is mediated by the gonadotropin, the presence of which results in the estaiblishment of a rapid micropinocytotic process at the level of the oocyte surface and of a mechanism for crystallization of the yolk. A sudden surge of pituitary hormone, when presented to fully grown oocytes leads to their maturation and ovulation, and to oviducal jelly release in some species. The active hormone is progestin in nature, again produced by the follicle cells. In this review the known factors involved in the hypothalamo-hypophysio-ovarian axis are discussed together with some consideration of outstanding problems and the possible relevance of oviparity and ovoviviparity in amphibians to the ovarian control found in viviparous species. Both the gametogenic and endocrine functions of the amphibian ovary are un? der pituitary control, but as in other lower vertebrate classes, the precise nature of this control, and the overriding regulation of ovarian cycles by the hypothalamus and central nervous system, leaves large areas where knowledge falls short of that for mammals. The fundamental features of reproduction in the female seem remark? ably uniform throughout the vertebrates although recourse to other contributions to this symposium will indicate inter-class differences in the emphasis placed on the various hormonal factors. Perhaps t'he most significant of these differences is the role of the estrogenic steroids in mediating the process of vitellogenesis. This process is, of course, of paramount importance in all oviparous species, and the gonadotropins fulfill their function of controlling ovarian growth by regulating estrogen synthesis

Abnormalities in the Release of TSH in Response to Thyrotropin-Releasing Hormone (TRH) in Patients with Disorders of the Pituitary, Hypothalamus and Basal Ganglia

Abstract: The availability of synthetic TRH has permitted studies of TSH release in various disorders of the hypothalamic-pituitary axis. Forty-five patients with disorders of the pituitary, hypothalamus or basal ganglia were studied. The TSH response to 400 μg intravenous TRH was normal in all but two of 19 acromegalics, normal or high in 6 patients with chromophobe adenomas, low or undetectable in 7 patients with panhypopituitarism, normal or low in 3 patients with galactorrhea and amenorrhea and in 5 with parkinsonism, and normal or markedly elevated in 3 patients with hypothalamic hypothyroidism. Unexpectedly, plasma GH also rose significantly after TRH administration in 10 of 11 untreated acromegalics with elevated fasting GH levels. These results demonstrate the usefulness of TRH in characterizing the location and extent of lesions in the hypothalamic-pituitary axis, and suggest those therapeutic measures, including the administration of certain releasing hormones, which may be employed to treat cert...

Acute and Chronic Effects of Hypothalamic Lesions on the Release of FSH, LH and Prolactin in Intact and Castrated Rats

Abstract: Plasma gonadotropins and prolactin were measured by radioimmunoassay before and after placement of direct current or radiofrequency lesions in the hypothalamus in intact and castrated rats of either sex. Following median eminence lesions, there was a rapid increase in the levels of plasma prolactin, LH and FSH. In general the response was greatest for LH, slightly less for prolactin and minimal for FSH. In the case of FSH and LH, this was followed by a decline to subnormal levels. The decline was much more pronounced in castrate than in intact animals. It is concluded that median eminence lesions may initially lead to release of stored releasing factors from the damaged tissues and that this is followed by a profound decrease in release of gonadotropins which is more pronounced for LH than for FSH. The initial rise in prolactin may be caused by release of prolactin—releasing factor. The maintained secretion of prolactin is presumably caused by withdrawal of tonic inhibitory hypothalamic influences. The el...

The role of monoamines in the control of gonadotropin and prolactin secretion.

Abstract: The efforts of the authors in the investigation of the role of monoamines in the control of gonadotrophin and prolactin secretion are reviewed with reference to other relevant studies. The approaches used in the authors investigations were varied. First the effects of monoamines on the release of hormones from pituitaries incubated in vitro and on the releasing factors from ventral hypothalamic fragments incubated in vitro were investigated. Secondly the effects of monoamines in vivo after intraventricular administration were studied. Finally the actions of drugs which selectively modify catecholamine and indoleamine synthesis in the hypothalamus were studied to analyze the effects of deficiency of excess of monoamines on gonadotrophin and prolactin release.

Effects of Estrogen on Plasma and Pituitary Gonadotropins and Prolactin, and on Hypothalamic Releasing and Inhibiting Factors

Abstract: Single subcutaneous injections of varying doses of estradiol benzoate (0.2–5 µg) in ovariectomized female rats were capable of lowering plasma FSH and LH and elevating plasma prolactin as determined by radioimmunoassay. The effects were demonstrable by 24 h and more marked at 48 h. Once an effect had been obtained, there was no clearly increased effect of higher doses of steroid. Pituitary content of FSH, LH, and prolactin increased significantly at 48 h with the 5 µg doses of estrogen, accompanied by an increase in anterior pituitary weight. Hypothalamic content of FSH-releasing factor (FRF) was reduced at 48 h only by the 1 µg dose of estradiol, whereas the content of LH-releasing factor (LRF) declined at 48 h only with the 0.2 and 0.5 µg doses. Prolactin-inhibiting factor (PIF) declined at 24 h after 0.5, 1, or 5 µg of estradiol and the level was still low at 48 h in the case of the 1 or 5 µg doses. The results are interpreted to mean that single injections of estradiol can inhibit release and synthesis of FSH and LH at least in part by a hypothalamic mechanism. With high doses, an elevation in stored hormone results in the pituitary, since synthesis of hormone is inhibited less than release. On the other hand, estrogen increases release and synthesis of prolactin and this effect is achieved, at least in part, by altered hypothalamic function.

Plasma Growth Hormone (GH) Response to Hypothalamic or Extrahypothalamic Electrical Stimulation

Abstract: Plasma growth hormone (GH) responses, as measured by radioimmunoassy, were determined in individual rats following electrical stimulation of various hypothalamic and extrahypothalamic sites. In the hypothalamus, positive GH responses (rise in plasma GH levels > 10 μg/ml within IS min) occurred only with stimulation of the ventromedial or arcuate nucleus. Effective extrahypothalamic stimulation sites included the hippocampus, basolateral amygdala and mesencephalic interpeduncular nucleus. Reserpine administration (5 mg/kg; 24 hr before stimulation) was effective in preventing GH release induced by hippocampal stimulation but had no effect on ventromedial—arcuate—induced GH release. These results suggest that GH release may be induced by electrical stimulation either of the “final common pathway” in the medial basal hypothalamus or of certain extrahypothalamic structures with known connections to this region. (Endocrinology 91: 107, 1972)