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Biomedical subjects

S M McCann

Publications and source records attributed to S M McCann.

At least 199 records · Page 11Linked to original sources
PubMed1987

Alpha-melanocyte stimulating hormone discloses a stimulatory effect of beta-endorphin on somatostatin release.

The influence of alpha-melanocyte stimulating hormone (alpha-MSH) and beta-endorphin (beta-END) on the secretion of somatostatin (SRIF) from the median eminence (ME) was studied using an in vitro incubation system. The MEs from adult male rats were first preincubated at 37 degrees C for 30 min with constant shaking in 0.4 ml of Krebs-Ringer bicarbonate-glucose buffer (pH 7.4) containing bacitracin in an atmosphere of 95% O2/5% CO2. Medium was discarded and replaced by medium containing different doses of alpha-MSH, beta-END, or a fixed dose of alpha-MSH (10(-7) M or 10(-9) M) plus beta-END at various concentrations. By themselves alpha-MSH and beta-END did not alter basal SRIF release, but in the presence of alpha-MSH (10(-7) M) beta-END stimulated somatostatin release. This effect was significant at concentrations of beta-END of 10(-8) M and higher. The permissive effect of alpha-MSH was observed at a concentration as low as 10(-9) M, but in this case the stimulatory effect of beta-END became evident only at higher doses tested (10(-7) M). It is suggested that alpha-MSH and beta-END participate in the modulation of SRIF release. By themselves beta-END and alpha-MSH did not affect basal release of SRIF but in the presence of alpha-MSH, beta-END had a stimulatory effect on SRIF release. The mechanism for this interaction is unknown. The results are consistent with the possibility that beta-END neurons have stimulatory and inhibitory effects on SRIF release and that alpha-MSH, by blocking the inhibitory components, discloses the stimulatory effect of beta-END on SRIF release.

Adrenocorticotropic Hormone↗
PubMed1987

Arginine vasopressin as a thyrotropin-releasing hormone.

Although hypothyroidism (with concomitant increased levels of thyroid-stimulating hormone) has been associated with elevated plasma vasopressin, the role that vasopressin plays in controlling thyroid-stimulating hormone secretion from the adenohypophysis is not understood. In two in vitro pituitary cell systems, vasopressin caused a specific and dose-related release of thyroid-stimulating hormone from cells that was equal in potency to that elicited by thyrotropin-releasing hormone, the primary acknowledged regulator of thyroid-stimulating hormone release. When injected into the hypothalamus, however, vasopressin specifically inhibited the release of thyroid-stimulating hormone. Thus, vasopressin may exert differential regulatory effects on thyroid-stimulating hormone secretion in the hypothalamus and pituitary gland.

Animals↗
PubMed1987

The effects of the cholecystokinin antagonist, proglumide, on prolactin secretion in the rat.

Since cholecystokinin produced important effects on prolactin secretion following its intraventricular injection in ovariectomized rats, we have evaluated the effects of the cholecystokinin antagonist, proglumide, to assess the physiologic significance of CCK in the control of prolactin release. Conscious rats of either sex were used following implantation of third ventricular and/or intravenous cannulae for the administration of proglumide. Blood samples were drawn from conscious animals at various times after injection of the compound. Intraventricular injection of 1 or 10 micrograms of proglumide produced a dramatic decline in plasma prolactin levels in either castrate or intact male rats. Similar results were found following the intravenous injection of 10 or 100 micrograms of the drug. These results contrasted sharply with the findings in ovariectomized females in which the intraventricular injection of the same two doses of proglumide used in males produced a dose-related elevation of prolactin which was opposite to the delayed lowering of prolactin following the intravenous injection of the same doses of the compound used in males. These results indicate that proglumide can lower prolactin in male rats and suggests a physiologically significant role of CCK in the control of prolactin secretion in the male. There appears to be a sex difference in the response since the results contrasted sharply in ovariectomized female rats. The results in the females are puzzling and it is apparent that further studies are needed to determine whether or not CCK has a physiologically significant role to play in prolactin secretion in the female. Since previous results have shown that CCK has no effect on the release of prolactin by the pituitary directly these interactions are presumably taking place in the hypothalamus.

Animals↗
PubMed1987

Central action of interleukin-1 in altering the release of TSH, growth hormone, and prolactin in the male rat.

In order to determine the possible effects of interleukin-1 on the release of pituitary hormones by direct action on the brain, the peptide was injected into the third brain ventricle of conscious, unrestrained male rats and the effects on hormone release were compared with effects on rectal temperature. The procedure of blood sampling and intraventricular injection resulted in a significant decline in body temperature and a decrease in plasma growth hormone without alteration in the plasma level of thyroid stimulating hormone (TSH) and prolactin. Interleukin-1 injected intraventricularly at a dose of 5 ng (0.3 pmol) prevented the decline in body temperature that occurred in the saline-injected controls and resulted in a significant elevation of plasma growth hormone levels that became apparent within 15 min of injection, as well as a highly variable but significant elevation of plasma prolactin and a significant decline in plasma TSH that was observed at 30 min. The results were similar when areas under the release curves for the various hormones were calculated. On the other hand, the higher dose of 25 ng (1.5 pmole) of interleukin-1, although producing a frank pyrexia, was associated with smaller changes in hormone values, which were no longer significant for any of the three hormones. The results indicate that interleukin-1 can act in minute doses, presumably on structures near the third ventricle, to stimulate growth hormone and prolactin release and to inhibit TSH release. Apparently when frank febrile responses occur, these hormonal responses are muted for reasons that are yet to be determined. In view of the minute doses injected we favor a hypothalamic site for these effects.

Animals↗
PubMed1987

Lesions of the sexually dimorphic nucleus of the preoptic area: effects upon LH, FSH and prolactin in rats.

Bilateral lesions were placed in the sexually dimorphic nucleus of the preoptic area (SDN-POA) in castrated adult male rats in an attempt to determine a physiologic role for this nucleus. These lesions significantly attenuated the increase in plasma FSH and LH due to simultaneous castration at 24 hr, and at 7 and 14 days following surgery, and significantly decreased the levels of plasma prolactin on comparison with pre-operative values and those of castrated controls. When rats were castrated and lesions placed at 14 days following castration, plasma levels of FSH, LH and prolactin were significantly decreased at 24 hr and at 7 days following surgery. Lesions which were placed lateral or caudal to the SDN-POA simulated the effects of lesions placed within the SDN-POA upon plasma LH, FSH and prolactin, with lateral lesions being most effective. However, lesions which were placed dorsal or rostral to the SDN-POA had no effect. The results of these studies suggest that the SDN-POA may be involved in the regulation of LH, FSH, and prolactin release.

Animals↗
PubMed1987

Factors controlling adrenal weight and corticosterone secretion in male rats as revealed by median eminence lesions and pharmacological alteration of prolactin secretion.

To determine whether or not prolactin, as well as ACTH, was involved in the control of adrenal weight and steroid release, lesions in the median eminence which had previously resulted in impaired steroid release and atrophy of the adrenal were placed in animals in which the plasma prolactin was allowed to rise as a result of the lesions or prevented from rising by the administration of the dopamine agonist, CB-154. As previously reported, as the severity of diabetes insipidus (DI) increased as a result of interruption of the supraoptico-hypophyseal tract, adrenal weight declined reaching a nadir at water intakes of approximately 100-150 ml/day. This was followed by a reversal of this trend and an increase in adrenal weight as water intakes increased further. These effects were not modified by CB-154 which was effective to lower the elevated prolactin levels in the animals. In general, adrenal weight correlated with levels of plasma corticosterone and progesterone. The ability of the animals to undergo compensatory adrenal hypertrophy was also impaired by median eminence lesions in the presence or absence of CB-154. Exceptional animals were encountered in which adrenal weight was high and yet plasma corticosterone was low. Treatment of hypophysectomized animals with long-acting ACTH plus maintenance doses of triiodothyronine prevented the adrenal atrophy characteristic of the hypophysectomized animal, thus confirming that ACTH is the most important hormone in the control of adrenal weight.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1987

Delta sleep inducing peptide (DSIP) stimulates the release of LH but not FSH via a hypothalamic site of action in the rat.

Long term ovariectomized (OVX) Sprague-Dawley rats were injected intraventricularly (3rd ventricle) with 5 micrograms (2 microliter) of DSIP. This caused a significant elevation (p = 0.01) of LH levels within 30 min. The values remained elevated for 2 hr; however, FSH levels remained unchanged. The minimal effective dose of DSIP to evoke this effect was 1 microgram. If plasma PH was lowered by pretreatment of the animals with estradiol, the 5 micrograms dose evoked an even greater effect to elevate LH significantly at 30 and 60 min following its intraventricular injection. To determine the site of action of DSIP, dispersed, overnight cultured pituitary cells from OVX rats were incubated with varying concentrations (10(-7) to 10(-12) M) of DSIP in an in vitro system. There was no response to DSIP from the cells in the above system. To evaluate its possible action on the hypothalamus, median eminence (ME) fragments from male rats were incubated in vitro with DSIP in varying concentrations from 10(-7) to 10(-10) M. There was a significant (p less than 0.001) increase in LHRH released from the ME at a concentration of DSIP of 10(-7) M. A sleep-related increase in LH release is seen during puberty in man. It is possible that DSIP released within the hypothalamus may play a physiological role in sleep-related LH release.

Animals↗
PubMed1987

Purification of FSH-releasing factor: its dissimilarity from LHRH of mammalian, avian, and piscian origin.

Sheep stalk median eminence fragments were lyophylized, extracted and filtered through a column of Sephadex G-25. The fractions were then assayed for the presence of LHRH by radioimmunoassay (RIA) and bioassayed for FSH and LH-releasing activity following their IV injection into ovariectomized, estrogen progesterone-blocked rats. The radioimmunoassayable LHRH emerged from the column at the same position from which it emerged many years before when LH was measured by bioassay. This same region also contained the LH-releasing activity as measured by bioassay. FSH-releasing activity was present in two tubes just preceding the emergence of the bio- and immunoassayable LHRH. The activity was highly significant and there was no LH-releasing activity in the fractions. They contained much less LHRH as determined by RIA than is sufficient to evoke LH release in this assay. The FSH-releasing activity was recovered in the same fractions in which it was found many years ago with this same assay but with measurement of plasma FSH by bio-rather than immunoassay as employed here. A dose-related release of LH was obtained by injection of LHRH in this assay but there was no significant FSH release even with a dose of 27 ng of LHRH per rat. To determine if one of the LHRHs of lower forms might be FSH-RF, Chicken I and II LHRH and Salmon LHRH were also assayed for FSH- and LH-releasing activity. Each of these peptide possessed LH-releasing activity, albeit much less than that of the mammalian peptide but had no FSH-releasing activity whatsoever.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Beta-adrenergic blockers decrease levels of luteinizing hormone in plasma of orchidectomized rats.

The beta-adrenergic antagonists, propranolol and bornaprolol (FM-24), at greater than 2 mg/kg (as [-] form) significantly depressed plasma levels of luteinizing hormone (LH) in orchidectomized rats. This occurred in the absence of consistently significant changes in interpulse intervals or amplitudes of pulsatile LH release. Nadirs of plasma LH decreased significantly even at low blocker doses, with a clear dose dependence for both drugs. The highly significant decrease of plasma LH induced by blocker dosages causing greater than 93% inhibition of beta-adrenergic binding in the anterior pituitary gland was shown to occur without significant changes in binding of specific ligands at pituitary dopamine receptors and hypothalamic alpha 1-adrenergic receptors. The above evidence indicates that beta-blockers may lower LH release in vivo at the level of pituitary beta-adrenergic receptors.

Adrenergic beta-Antagonists↗
PubMed1987

Detrimental effects of short-term ethanol exposure on reproductive function in the female rat.

To more completely assess the means by which alcohol impairs the female reproductive cycle in rats, we have measured hypothalamic luteinizing hormone-releasing hormone (LHRH), pituitary LHRH receptor content, and the serum levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin (Prl), and progesterone (P). After two successive cycles, the animals began receiving either an alcohol or a isocaloric control liquid diet regimen beginning on the first day of diestrus, with continued monitoring of the estrous cycle throughout the experiment. An additional set of controls consisted of animals maintained on lab chow and water provided ad libitum. Our results indicate that those animals receiving the control diets showed uninterrupted estrous patterns, whereas those animals receiving the alcohol diet remained in diestrus. Additionally, the alcohol-treated animals showed an increase (p less than 0.05) in LHRH content, with a concomitant decrease (p less than 0.01) in serum LH, and an increase (p less than 0.01) in serum Prl. No significant differences were detected in serum FSH levels or pituitary LHRH receptor content. No differences were detected in serum P levels. These results indicate that short-term alcohol administration disrupts the female reproductive cycle, causing persistent diestrus, and support our hypothesis that the alcohol-induced depression in serum LH levels is due to a diminished release rate of hypothalamic LHRH.

Animals↗
PubMed1987

The role of brain peptides in neuroimmunomodulation.

Since neuroimmunomodulation is brought about in part, at least, by secretion of pituitary hormones involved in stress and immune responses, we review briefly the hypothalamic control of the release of ACTH, growth hormone, and prolactin. The release of ACTH is controlled particularly by corticotropin-releasing factor (CRF), but vasopressin has intrinsic releasing activity and potentiates the action of CRF at both hypothalamic and pituitary levels. Oxytocin may even potentiate the action of CRF, but has little, if any, ACTH-releasing activity by itself. In addition, epinephrine may augment responses to the CRFs. In contrast, growth hormone is under dual control by growth-hormone-releasing factor (GRF) and somatostatin, and prolactin is under multifactorial control by a series of inhibitors and stimulators. Dopamine is accepted as a physiological prolactin-inhibiting factor (PIF), but probably GABA and possibly acetylcholine as well are PIFs. There is good evidence for a peptide PIF as well. There are a number of prolactin-releasing factors (PRFs) which include oxytocin, vasoactive intestinal polypeptide, PHI and TRH. Several other peptides can also release prolactin, including angiotensin II. In response to stress there is a complex interaction of peptides intrahypothalamically. CRF augments its own release by an ultra short-loop positive feedback, and there is negative ultra short-loop feedback of GRF and somatostatin. Vasopressin appears to augment CRF release as well as to act directly on the pituitary, and there are complex interactions of various peptides to influence prolactin and GH release.

Adjuvants, Immunologic↗
PubMed1987

Delta sleep inducing peptide inhibits somatostatin release via a dopaminergic mechanism.

Delta sleep inducing peptide (DSIP) has been localized in the rat hypothalamus. The effect of DSIP on somatostatin (SRIF) release from the median eminence of the hypothalamus was evaluated in male and female rats in an in vitro incubation system. DSIP inhibited SRIF release in a dose-dependent manner. The median eminences from females were less sensitive to the inhibitory action of DSIP than those of males; however, in both sexes the maximum effect was observed at a concentration of 10(-8) M DSIP. This effect was blocked by addition of pimozide at a concentration of 10(-6) M. Pimozide alone had no effect on SRIF release. These findings lead to the conclusion that DSIP inhibits SRIF release via a dopaminergic mechanism.

Animals↗
PubMed1987

Effects of delta-9-tetrahydrocannabinol on the hypothalamic-pituitary control of luteinizing hormone and follicle-stimulating hormone secretion in adult male rats.

The main psychoactive component of marihuana, delta-9-tetrahydrocannabinol (THC) was injected into the 3rd cerebral ventricle. A single dose of THC (2 microliter of 10(-6) M) decreased serum LH temporarily but did not alter serum follicle-stimulating hormone (FSH) levels. The mediobasal hypothalamic (MBH) luteinizing hormone-releasing hormone (LHRH) content was elevated by 30 min after the injection. The elevation persisted for 1 h. Then, the LHRH content returned towards the preinjection level. In contrast, the LHRH in the organum vasculosum of the lamina terminalis did not change after a single dose of THC. The results indicate that THC alters pituitary LH release by inhibiting the release of LHRH which then increases in the MBH by continued synthesis or transport from rostral areas. In addition, the data support the existence of an FSH releasing factor, the release of which is not suppressed by this dose of THC. THC did not alter the release, storage or responsiveness to LHRH of cultured anterior pituitary cells, which further supports the view that its principal site of action is on the hypothalamus.

Animals↗
PubMed1987

Evidence that growth hormone-releasing factor stimulates somatostatin release in vitro via beta-endorphin.

Previous results indicate that GH-releasing factor (GRF) induces a dose-related stimulation of somatostatin (SRIF) release from median eminence fragments incubated in vitro. In the present investigation we examined whether this action was mediated by other neurotransmitters or neuromodulators. Studies using receptor blockers for dopamine (pimozide), alpha-adrenergic receptors (phentolamine), and muscarinic cholinergic receptors (atropine) revealed that these receptor blockers, at a dose of 10(-6) M, which was capable of blocking the response to the relevant transmitter in previous studies, had no effect on basal release of SRIF in the static incubation system and failed to modify the response to GRF (10(-10) M). On the other hand, the opiate receptor blocker naloxone at a dose of 10(-6) M, although failing to alter basal release, completely blocked the response to 10(-10) M GRF. To determine the opioid peptide involved in mediating the SRIF release induced by GRF, highly specific antibodies directed against beta-endorphin were added to the in vitro incubation system. These antibodies significantly depressed basal release SRIF and completely blocked the response to 10(-10) M GRF. Incubations in the presence of normal rabbit serum or highly specific antiserum directed against alpha MSH had no effect on either basal release of SRIF or that induced by GRF. These results suggest that in this incubation system there is a beta-endorphin tone which is partially responsible for the basal release of SRIF and that the stimulation of SRIF release induced by GRF is mediated via beta-endorphin terminals, which presumably synapse on the terminals of the somatostatinergic neurons in the median eminence fragment.

Animals↗
PubMed1986

The influence of suckling on the hypothalamic and pituitary secretion of immunoreactive alpha-melanocyte stimulating hormone.

The effect of suckling on the secretion of alpha-melanocyte stimulating hormone (alpha-MSH) from the hypothalamus and pituitary was determined by a specific radioimmunoassay. There was an increase in the neurointermediate lobe (NIL) content of alpha-MSH 1 h after the onset of suckling. The values were restored to control levels within 3 h. The anterior lobe content of alpha-MSH was not affected by suckling. Plasma alpha-MSH levels were also unaffected by suckling, indicating that suckling probably affects the synthesis of NIL alpha-MSH, and not its release. Suckling lowered the alpha-MSH content in the mediobasal hypothalamus of lactating rats, and had no effect on the median eminence content of this peptide. In vitro, hypothalami from lactating rats released more alpha-MSH than hypothalami of random cycling females under basal, and stimulated (56 mM potassium) conditions. These results suggest that hypothalamic alpha-MSH may play a role in mediating some of the hormonal changes occurring during lactation.

Animals↗
PubMed1986

Effects of unilateral decortication on beta-adrenergic receptors in the remaining cortex and in the hypothalamus of female rats.

Many experiments have been performed to evaluate the physiological role of catecholaminergic mechanisms in gonadotropin release. The purpose of the present study was to determine the concentration of beta-adrenoreceptors in the remaining (right) cerebral cortex and in right and left hypothalamic halves of hemi-decorticated female rats which exhibited elevated plasma gonadotropin levels as observed previously. The density of beta-receptors was measured using a high-affinity beta-adrenergic ligand, iodocyanopindolol (ICYP). Scatchard estimates were obtained for maximum binding (Bmax fmol/mg of tissues) from pooled cerebral cortical and hypothalamic tissue of animals under several experimental conditions after hemi-decortication and sham operation. There was an increase in beta-adrenoreceptor density in the remaining (right) cerebral cortex at all times examined in hemi-decorticate in comparison with the sham-operated animals (7 days, +10.9%; 21 days, +8.4%; 90 days, +22%; and 90 days plus ovariectomy, +34.8%). The number of beta-adrenoreceptors in the right hypothalamic half in hemi-decorticates decreased at 21 days (-42.20%) and then increased at 90 days (+76.63%) and 90 days plus ovariectomy (+51.75%) when compared with the left hypothalamic half. At the same time there were no significant changes in the sham-operated animals when comparing the receptor density in the right and left hypothalamic halves, respectively. Thus, our results suggest a direct or indirect adrenergic pathway by which the left cortex can influence the right cortex and a crossed pathway to the contralateral hypothalamus changing adrenergic activity which can alter the beta-adrenergic receptor binding capacity in the hypothalamus.

Animals↗