Showing papers on "Hypothalamus published in 1974"

Somatostatin: Hypothalamic Inhibitor of the Endocrine Pancreas

Abstract: Somatostatin, a hypothalamic peptide that inhibits the secretion of pituitary growth hormone, inhibits basal insulin secretion in fasted cats and rats. In fasted baboons both basal and arginine-stimulated secretion of insulin and glucagon are inhibited. Somatostatin appears to act directly on the endocrine pancreas. The action is dose-related, rapid in onset, and readily reversed.

Studies on the mechanism of the dopamine-mediated inhibition of prolactin secretion.

Abstract: A study of the in vitro effect of dopamine on the release of newly synthesized prolactin is reported. Pituitary glands of female rats were incubated with 4,5-3H-leucine and the radioactive prolactin present in the pituitary gland and that released into the incubation medium were measured. Incubation with 5 × l 10–7M dopamine caused an 85% decrease in prolactin release. Prior injection of the rats with perphenazine or haloperidol rendered the pituitary gland refractory to the in vitro inhibitory effect of dopamine. Although in vitro perphenazine and haloperidol had little or no effect on release of prolactin, 5 × 10–9M of these drugs directly blocked the in vitro action of dopamine on prolactin release. Phentolamine, an α-blocking agent, was partially able to block the inhibitory effect, of dopamine. Propranolol, however, was not effective. Apomorphine, an agent known to mimic the effects of dopamine, caused a significant decrease in the amount of radioactive and radioimmunoassayable prolactin released int...

Thyrotropin-releasing hormone (TRH): distribution in hypothalamic and extrahypothalamic brain tissues of mammalian and submammalian chordates

Abstract: A sensitive and specific radioimmunoassay for TRH is reported. Antibody was raised in a New Zealand white rabbit by immunization with TRH complexed to bovine thyroglobulin through bis-diazotized benzidine. The assay was capable of detecting below 7 pg of TRH in biological materials. Immunoreactive TRH was found in hypothalamic extracts from man, pig, rat, hamster, chicken, frog, snake, salmon, and in whole brain of the larval form of the primitive cyclostome lamprey, and in the head region of the protochordate amphioxus. The TRH levels in the frog hypothalamus were 1520–3620 pg/mg tissue, being 6–12 times the concentration detected in the rat hypothalamus. These findings indicate that TRH is distributed throughout the vertebrate kingdom, and has an ancient lineage. Immunoreactive (IR) TRH up to 764 pg/mg tissue was found in brain regions, other than hypothalamus, of the lower vertebrates, snake, frog, tadpole and salmon. Small but significant concentrations were also found in extrahypothalamic brain of th...

Thyrotropin-Releasing Hormone: Regional Distribution in Rat Brain

Abstract: A sensitive and specific radioimmnunoassay has been used to measure the distribution of thyrotropin-releasing hormone (TRH) in rat brain. All areas of brain tested, except cerebellum, contained readily measurable amounts of TRH. The hypothalamus contained only 31.2 percent of the total brain content of TRH. These results support recent suggestions of central actions for TRH in addition to its hypophysiotropic functions.

Thyrotropin-Releasing Hormone in Specific Nuclei of Rat Brain

Abstract: The regional distribution of thyrotropin-releasing hormone (TRH) in rat brain was studied. The greatest concentration of TRH was found in the median eminence. High concentrations were also found in several hypothalamic nuclei. Outside the hypothalamus, relatively large amounts of TRH were found in the septal and preoptic areas.

Distribution and concentration of TRH in the rat brain.

Abstract: Qualitative and quantitative criteria indicate that TRH is present in methanolic extracts prepared from all regions of the rat brain. The conclusion that TRH in the extracts of rat brain is the same as synthetic TRH is based on the following criteria: (a) immunoreactivity with a specific antiserum to synthetic TRH, (b) chromatographic properties on Sephadex G-10, (c) electrophoretic mobility on cellulose acetate, (d) susceptibility to degradation by plasma, and (e) capacity of the extracts to stimulate TSH release in vitro from anterior pituitary tissue. The greatest concentration of TRH, determined by radioirnmunoassay, was found in the hypothalamus, followed by the posterior pituitary gland, thalamus, brain stem, cerebrum, anterior pituitary gland, and cerebellum. The total quantity of TRH in the rat brain was 18.2 ng. Of this amount, 33.6% was present in the thalamus; 26.7% in the cerebrum; 18.8% in the hypothalamus; 18.6% in the brain stem; 1.6% in the cerebellum; 0.42% in the posterior pituitary glan...

Effects of Somatostatin on the Secretion of Thyrotropin and Prolactin

Abstract: Somatostatin, a tetradecapeptide isolated from ovine hypothalamic extracts on the basis of its ability to inhibit the spontaneous secretion of growth hormone (GH) by pituitary cell cultures, has been found to inhibit the stimulated secretion of thyrotropin (TSH) mediated by TRF(pGlu-His- Pro-NH2), 10 × [K†], or theophylline in vitro, while having no effect on the secretion of luteinizing hormone (LH) due to LRF. The spontaneous release of PRL in vitro is also inhibited by somatostatin but to a lesser extent than is the spontaneous secretion of GH. In vivo, the TRF-triggered secretion of TSH but not of PRL is suppressed by somatostatin in the estrogen-progesteronepretreated male rat. The injection of TRF leads to a greater rise in both plasma TSH and PRL in estrogen-progesterone-pretreated male rats than in untreated male rats. Somatostatin acts rapidly but reversibly to inhibit the secretion of TSH due to TRF in a dose-dependent manner. Thyroid hormones and somatostatin exhibit summation in their inhibiti...

Enhancement of cerebral noradrenaline turnover by thyrotropin-releasing hormone

Abstract: THYROTROPIN-RELEASING hormone (TRH) (pyroglutamyl-histidyl-proline-amide) has been reported to ameliorate mental depression1,2. The mechanism of action of the tripeptide in this condition is unknown. It may be connected with changes in the activity of noradrenergic or 5-hydroxytryptaminergic neurons which are thought to be involved in depressive states3,4. Therefore, we have investigated the action of TRH on the turnover of biogenic amines in rat brain.

A preview of growth hormone stimulation tests in children.

Abstract: No suggested screening test meets all of the criteria set for such a procedure. The minimum incidence of a positive response in normal children detected in a single blood sample after diethylstilbestrol, sleep or exercise is approximately 70%. This is higher than that observed when a single sample is obtained following oral glucose. While both sleep and exercise are physiologic stimuli, the former may be quite inconvenient unless an outpatient facility staffed with appropriate personnel is available. An exercise test employed in the office may well be the best screening procedure for the practicing physician. The optimal criteria for a definitive test of growth hormone function are also not met by any single stimulus. Insulin-induced hypoglycemia, arginine infusion, intramuscular glucagon and oral 1-DOPA are all useful procedures. None alone discriminate completely between the normal and the growth hormone-deficient child. Despite potential hazards, insulin-induced hypoglycemia remains the standard against which other stimuli are judged. Arginine and 1-DOPA appear to be equally effective. The literature contains insufficient data to allow adequate evaluation of intramuscular glucagon alone, and the results of combined propranolol-glucagon stimulation, while promising, require confirmation. Because of an inconstant and/or small magnitude of response leading to results which are difficult to interpret, the use of glucose, pyrogen, vasopressin and ACTH are not adequate tests of growth hormone function. Bovril® is a satisfactory stimulus for those children who will take it. Those factors which modify the growth hormone response must be considered in evaluating the results of stimulation tests. Blunted responses should be interpreted with extreme caution in the obese child. A fasting growth hormone concentration ≥ 7 ng/ml is presumptive evidence of intact growth hormone function regardless of the subsequent response to stimulation. It is essential that patients be euthyroid in order to interpret the results of growth hormone function tests. Physiologic glucocorticoid replacement therapy should not confuse the interpretation of results. Whether or not pretreatment with sex steroids is worthwhile in the routine evaluation of children for suspected growth hormone deficiency is an open question. Although it is agreed that the definitive diagnosis of growth hormone deficiency depends on the demonstration of failure to respond to two stimuli, which two are most satisfactory is not settled. The sequential administration of arginine and insulin on the same day appears to limit significantly the incidence of false-positive laboratory diagnoses of growth hormone deficiency. The significance of intermediate values in response to stimulation remains unclear. Caution should be exercised in assigning a child to the category of partial growth hormone deficiency. This question must be answered ultimately by the response to HGH therapy in the individual patient. Finally, several points should be kept in mind. All of the tests described depend on the detection and quantitation of immunologically active HGH and biological activity is not necessarily associated with the material(s) being measured. Since many of the stimuli used in the evaluation of growth hormone function are clearly pharmacologic, the physiological significance of the response to such stimuli must be interpreted with caution. The best current evidence suggests that all of the stimuli described act through an intact hypothalamus and pituitary. Differentiation between hypothalamic and pituitary sites of defective growth hormone function awaits the availability of growth hormone-releasing factor(s).

Gonadotrophin-releasing Hormone Therapy in Hypogonadal Males with Hypothalamic or Pituitary Dysfunction

Abstract: Subcutaneous self-administration of synthetic gonadotrophin-releasing hormone 500 μg eight-hourly for up to one year by 12 male patients (five prepubertal) with clinical hypogonadism due to hypothalamic or pituitary disease resulted in the synthesis and continued release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). There was a rise in circulating androgen levels in all patients. Improvements in pubertal ratings were seen in some prepubertal patients. Potency returned in the adults and spermatogenesis was induced and maintained in the four patients who had received treatment for more than four months, total counts reaching between 7·8 and 432 × 106 spermatozoa. A fall in the FSH response to the releasing hormone occurred during spermatogenesis though LH was little affected. During the initial weeks of therapy FSH secretion usually occurred before that of LH though LH secretion was greater as treatment continued. FSH secretion also persisted for longer when treatment was stopped.

Evidence for a direct effect of LRF and TRF on single unit activity in the rostral hypothalamus.

Abstract: MANY of the hormones produced by the pituitary and other endocrine glands influence the electrical activity of the brain (for recent references see Dyer1). There is now a growing awareness that some of the hypothalamic releasing factors, which regulate the secretion of hormones from the anterior pituitary gland, may themselves have a similar influence upon the central nervous system2–4. The amino acid sequences for both thyrotrophin releasing factor [TRF; (pyro) Glu-His-Pro (NH2)]5,6 and luteinising hormone releasing factor [LRF; (pyro) Glu-His-Trp-Ser-Tyr-Gly-Leu-Arg-Pro-Gly (NH2)]7 have been fully established and these polypeptides, produced synthetically and of high specific activity, are readily available. The experiments to be described were undertaken to establish whether LRF and/or TRF have a direct effect upon the electrical activity of neurones in the forebrain. Action potentials were recorded from single cells in the hypothalamus and cerebral cortex and LRF and TRF applied to them by microiontophoresis. The sensitivity of some of the neurones to oxytocin (a biologically active peptide of similar size) was also tested.

Deficits in instrumental responding after 6-hydroxydopamine lesions of the nigro-neostriatal dopaminergic projection

Abstract: Rats subjected to bilateral injections of 6-hydroxydopamine (8 μg) into the zona compacta of the substantia nigra completely failed to learn either a one-way active avoidance response or a simple approach response for food reinforcement. The neurotoxic lesions reduced striatal dopamine and tyrosine hydroxylase activity to less than 10 percent of control levels. A significant loss of hypothalamic norepinephrine was also produced by these lesions suggesting that this procedure also destroyed part of the ventral noradrenergic bundle. When bilateral lesions of the latter pathway were made caudal to the substantia nigra, so that similar losses were produced in hypothalamic norepinephrine levels without reducing striatal tyrosine hydroxylase activity, normal acquisition of both avoidance and appetitive responses were observed. In another experiment, almost complete retention of avoidance responding was obtained if the animals were overtrained on this response prior to the bilateral nigral lesions. These results suggest that the nigro-neostriatal dopaminergic projection may play an important role in the acquisition of learned instrumental responses.

Hypothalamic-Pituitary Function in Diverse Hyperprolactinemic States

Abstract: Prolactin secretion in normal adults is characterized by periods of episodic secretion which increase in magnitude during sleep. In this study, we report the 24-h mean prolactin concentrations, prolactin secretory patterns, and associated pituitary hormone function in nine patients (seven women and two men) with hyperprolactinemia of diverse etiologies. Four of the women and one of the men had clinically demonstrable pituitary tumors, one boy had a hypothalamic tumor, and the three other women had "functional" hyperprolactinemia. The 24-h mean prolactin concentrations derived from averaging the 20-min interval samples for 24 h ranged from 28.6 to 1,220 ng/ml. The plasma prolactin patterns in these patients showed persistence of episodic secretion in all and loss of the normal sleep-wake difference in plasma prolactin in seven of nine. Three of the patients with galactorrhea and comparable 24-h mean prolactin concentrations (58.3, 59.7, and 64.3 ng/ml) showed similar prolactin secretory patterns despite different etiologic mechanisms. Evaluation of the secretory patterns of luteinizing hormone (LH) in these patients showed loss of normal pulsatile LH release and a low 24-h mean LH concentration in the patient with the pituitary tumor, while the two patients without clinically demonstrable pituitary tumors ("post-pill" galactorrhea and "idiopathic" galactorrhea) showed normal LH secretory patterns and 24-h mean LH concentrations. The 24-h mean cortisol concentrations and secretory patterns were normal in five of the seven patients who had these parameters measured. The patient with the hypothalamic tumor had a low 24-h mean cortisol concentration and production rate and absent response to metyrapone. The patient with "idiopathic" galactorrhea had an elevated 24-h mean cortisol concentration but normal cortisol production rate and urinary 17-hydroxycorticoid excretion. Growth hormone secretion was abnormal in four of the patients (one with the hypothalamic tumor and three with pituitary tumors). Thyrotropin-releasing hormone (TRH) administration in four patients resulted in normal TSH release in two patients (one of whom developed galactorrhea after the test), an absent response in the patient with the hypothalamic tumor, and a blunted response in one of the women with a pituitary tumor. The two men had low 24-h mean plasma testosterone concentrations (69 and 30 ng/100 ml) and symptoms of impotence and loss of libido. Five of the women (four with pituitary tumors and one with Chiari-Frommel syndrome) had either low 24-h mean LH concentrations, abnormal LH secretory patterns, or both. These data indicate that patients with hyperprolactinemia encompassing a varied etiological range frequently show loss of the normal sleep-associated increase in prolactin secretion as well as abnormalities in the regulation of the other hypothalamic pituitary-regulated hormones. The finding that the abnormalities in LH, growth hormone, thyrotropin, and cortisol (adrenocorticotrophic) secretion were almost uniformly confined to the patients with the clinically demonstrable hypothalamic or pituitary tumors suggests that the size of the lesion is the critical factor.

Two pools of luteinizing hormone in the human pituitary: evidence from constant administration of luteinizing hormone-releasing hormone.

Abstract: The pituitary gonadotrophin response to constant intravenous infusions of hypothalamic luteinizing hormone-releasing hormone (LH-RH), 0.2 μg/min for 4 hr, was studied in 5 normal human men. Serum LH-RH levels were measured by radioimmunoassay to confirm the constancy of the infusions. Serum luteinizing hormone levels in response to the constant LH-RH administration revealed a biphasic pattern of elevation characterized by early and late peaks. This pattern of release is similar to that of other hormones stored in granules and suggests the existence of two pools of luteinizing hormone in the human pituitary, one requiring longer LH-RH stimulation for release than the other. In contrast, serum follicle-stimulating hormone values revealed a gradual rise during the entire infusion.

Localization of gonadotropin-releasing hormone (Gn-RH) in the hypothalamus of the mouse by immunoperoxidase technique.

Abstract: The localization of gonadotropinreleasing hormone (Gn-RH) in the hypothalamus of male and female mice was investigated. Serial paraffin sections were prepared. Rabbit antiserum to synthetic Gn-RH was used as the first reactant in the immunoperoxidase bridge technique. Final reaction products with 3,3' diaminobenzidine were seen by light microscopy. Addition of Gn-RH to the first antibody blocked the staining of immunoreactive tissue Gn-RH. In the hypothalamus of both sexes, the immunoperoxidase technique localized Gn-RH in the perikarya of some arcuate neurons, and throughout the course of numerous tanycytes of the median eminence. Gn-RH staining was also found associated with the organum vasculosum of the lamina terminalis in one of the brains. The releasing hormone was found neither in axons of arcuate neurons nor in other neurons of the hypothalamus. These results suggest that Gn-RH may be synthesized in arcuate neurons, and that tanycytes may provide a major pathway for the secretion of this releasing...

Effects of hypothalamic deafferentation on the pulsatile rhythm in plasma concentrations of luteinizing hormone in ovariectomized rats.

Abstract: Plasma LH concentrations were measured by radioimmunoassay in blood collected at 10-min intervals through atrial cannulas implanted in long-term ovariectomized rats. Regular fluctuating levels of the hormone were recorded in which plasma LH concentration rose rapidly to a peak every 20–40 min. Interruption of the anterior nerve projections to the medial basal hypothalamus (MBH) by deafferentation with a small stereotaxic knife rendered rats acyclic and resulted in a persistently cornified vaginal epithelium (constant estrus). Although these neural afferents were necessary for an ovulatory discharge of LH, the anterior deafferentation procedure did not block either the post-castration rise in plasma LH or the pulsatile discharge of hormone in the same rats when they were ovariectomized 4–6 weeks after deafferentation.Similarly, an extended frontal or an anterior-lateral cut resulted in constant estrus and permitted the pulsatile circulating levels of LH after ovariectomy. Posterior-lateral deafferentation ...

Oestrogen effects on brain and pituitary enzyme activities

Abstract: — Ovariectomized female rats were treated daily with oestradiol-17β benzoate for intervals up to one week and enzyme activities were measured in the pituitary and various brain regions. Brain regions were selected for study on the basis of their previously demonstrated content of putative oestradiol receptor sites. (1) Pituitary showed oestrogen-dependent increases in glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH) and lactic dehydrogenase (LDH), and no change in NADP+-dependent isocitric dehydrogenase (ICDH), NADP+-dependent malic dehydrogenase (MDH) or hexokinase (HK). MDH and ICDH were elevated in whole hypothalamus. Enzyme activities did not change significantly in whole amygdala, cerebral cortex, or hippocampus. (2) Sub-regions of the preoptic area, hypothalamus and amygdala were dissected to obtain more highly concentrated populations of cells containing putative oestrogen receptor sites. In the basomedial sub-region of hypothalamus, activities of MDH, ICDH and G6PDH were elevated by oestrogen treatment. In the corticomedial sub-region of amygdala, MDH and ICDH were elevated by oestrogen treatment. No change was observed in any of the six enzymes in medial preoptic area. (3) Increases in enzyme activities were related to the total in vivo dose of oestradiol benzoate given. (4) Hypophysectomy or adrenalectomy did not prevent the enzymatic responses to oestrogen. (S) Oestrogen added directly to the enzyme incubation medium did not change enzyme activities. (6) Weight loss in ovariectomized rats due to reduced food intake did not increase enzyme activities. (7) In the pituitary, good correlation was obtained between the known receptor binding properties of various oestrogenic and non-oestrogenic steroids and the elevation in G6PDH activity. The results indicate that oestradiol acts directly to cause changes in activities of some brain and pituitary enzymes. The possibility is discussed that these changes may result from oestrogen interaction with putative receptor sites found in pituitary and certain brain regions.

Luteinizing Hormone-Releasing Hormone (LH-RH) Content of the Hypothalamic Nuclei in Rat

Abstract: The luteinizing hormone-releasing hormone (LH-RH) content of 16 separate hypothalamic nuclei and of the median eminence have been determined by radioimmunoassay in the rat. High concentrations of LH-RH were measured in the median eminence and in the arcuate nucleus. Other nuclei of the hypothalamus, as well as the medial preoptic nucleus, contained little or no LH-RH. The amount of LH-RH stored in the median eminence is about twice that found in the arcuate nucleus, but the concentration in the median eminence is 7.7 times higher than in the arcuate nucleus. Within the arcuate nucleus 73% of the LH-RH is present in the middle part (NA III) of the nucleus. (Endocrinology 95: 554, 1974)

Biogenic amines and control of melanophore stimulating hormone release.

Abstract: Release of melanophore stimulating hormone (MSH) from the vertebrate pars intermedia is under inhibitory control by the hypothalamus. Removal of the rat pituitary or the neurointermediate lobe of the frog (Rana pipiens) to in vitro incubation medium results in rapid uninhibited release of MSH. This secretion is inhibited by norepinephrine, epinephrine, phenylephrine, and dopamine, and the inhibition is antagonized by α-adrenergic receptor blocking agents. Isoproterenol stimulation of MSH secretion from isolated glands is blocked by pro-pranolol, a β-adrenergic receptor antagonist. These results implicate dopaminergic or classical α-adrenergic receptors (or both) in inhibition of MSH release by catecholamines, and implicate β-adrenergic receptors in stimulation of MSH release by the bioamines.

Modulation of corticotrophin-releasing factor release from hypothalamic synaptosomes.

Abstract: NERVE endings (synaptosomes) isolated from the mammalian hypothalamus contain the hypophysiotrophic hormones which regulate adenohypophysial function. Edwardson et al. have shown1 that release of these neurosecretory substances can be elicited from incubated hypothalamic synaptosomes by electrical or potassium stimulation and the release mechanism has been shown2 to be calcium dependent. We report here that steroid hormones administered both in vivo and in vitro and neurotransmitter substances given in vitro modulate the release of corticotrophin-releasing factor (CRF) from synaptosomes prepared from rat and sheep hypothalamus.

Autoradiographic localization of 3H-estradiol or its metabolites in the central nervous system of the developing rat.

Abstract: The cellular and subcellular localization of radioactivity in the brain of 2-day-old female rats was investigated by dry-mount and thaw-mount autoradiography 2 hr after SC injection of 1.0 µg of 2,4,6,7 3H estradiol-17β per 10 g body wt. A specific topographic pattern of nuclear concentration of estrogen was obtained similar to that of the adult rat in specific neurons of the basal hypothalamus, preoptic region and amygdala, thus providing the first in vivo evidence for estrogen receptors in the central nervous system (CNS) ofthe developing rat during the “critical period” of brain organization. In competition experiments, nuclear concentration of radioactivity was inhibited in all areas studied with estradiol, while no inhibition wasobtained with 5α-dihydrotestosterone. Testosterone clearlyinhibited the nuclear concentrationof radioactivity in all areas studied except the nucleus preopticus medialis in which either noinhibition or only a partial inhibition occurred. The implications of this selective com...

A microinjection study of the control of antidiuretic hormone release by the supraoptic nucleus of the hypothalamus in the cat.

Abstract: 1. The release of antidiuretic hormone (ADH) has been studied in the chloralose anaesthetized cat after microinjection of various agents directly into the brain, in particular the supraoptic nucleus of the hypothalamus (SON). The concentration of ADH in jugular venous blood was determined using the waterloaded, alcohol anaesthetized rat assay. The position of the microinjection cannula was located post mortem in stained brain sections. 2. Nicotine, noradrenaline (NA) and hypertonic saline caused release of ADH, whereas microinjections of isotonic saline did not affect the blood level of the hormone. 3. Nicotine administered to other sites in the central nervous system ( C.N.S.) could also cause ADH release. Hypertonic saline proved to be an ineffective stimulus at all the tested sites outside the supraoptic region. 4. The ganglion-blocking agents hexamethonium and pempidine inhibited the releasing action of nicotine at the SON in most of the experiments. These blocking drugs had no effect on osmotic release. When administered alone, both hexamethonium and pempidine had variable, but analogous effects on the hormone output. 5. The α-adrenoreceptor blocking drug, phentolamine, stimulated ADH release, but the β-receptor blocking drug, propranolol, had no such effect. Both drugs appeared to have inhibitory action on noradrenergic release of ADH, but neither had a consistent effect on the osmotic release of the hormone.

The isolated organ-cultured supraoptic nucleus as a neuropharmacological test system

Abstract: Supraoptic nucleus tissue from neonatal puppies was dissected, minced and explanted into an organ culture medium. After 2 to 3 weeks of organ culture, explants were transferred into a small superfusion chamber and cell membrane potentials recorded from nerve cells by making microelectrode penetrations of these cells. Supraoptic nucleus neurons were not spontaneously active. They could be excited to initiate spiking activity by glutamate and by nicotine in a concentration-dependent fashion. Excited cells could be inhibited by exposure to γ-aminobutyric acid, to beta adrenergic agonists and probably by activating muscarinic receptors. The inimihitory effects of γ-aminobutyric acid and of norepinephrine may depend on different ionic mechanisms, since they result in different changes in the spike configuration. The explants contain measurable vasopressin, but the vasopressin is not released into the medium in measurable quantities. It is concluded that the organ-cultured supraoptic nucleus can be used to study membrane effects of drugs and other agents that influence vasopressin secretion.

Effect of blockade of dopaminergic receptors on prolactin and LH release: median eminence and pituitary sites of action.

Abstract: Pimozide, a dopamine receptor blocker, was injected SC or implanted into the hypothalamus or adenohypophysis of ovariectomized rats to determine its effect on the release of LH and prolactin. Following SC injection of the drug, there was a gradual rise in plasma prolactin which became significant at 30 min after injection, and was maintained for 78 hr. This was accompanied by a gradual fall in LH which achieved significance at 2–4 hr after injection, and was maintained for54 hr. Implantation of Pimozide into the median eminence-arcuate region evoked a gradual consistent increase in prolactin which became significant at 1 hr, and was accompanied by a small decline in plasma LH at 4 hr. Much smaller increases in plasma prolactin followed implantation of the drug into the adenohypophysis and these implantations were not associated with any alterations in plasma LH. It is suggested that dopamine exerts an inhibitory control over prolactin release from the adenohypophysis by inhibiting the release of prolactin...