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Biomedical subjects

E Vijayan

Publications and source records attributed to E Vijayan.

At least 37 records · Page 2Linked to original sources
PubMed1986

The effects of the cholecystokinin antagonist, proglumide, on gonadotropin release in the rat.

Since cholecystokinin had manifest effects on anterior pituitary hormone 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 gonadotropin secretion. 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 the injection of the compound. In castrate female rats proglumide produced a small but significant increase in plasma LH whether administered by the intravenous or intraventricular route at the lower dose of 10 or 2 micrograms, respectively. The higher doses of 10 micrograms injected intraventricularly or 100 micrograms, injected intravenously failed to affect LH levels in these animals. In contrast there was a much larger increase in plasma LH in castrate males following intraventricular or intravenous injection of the lower doses of proglumide. Even after the higher doses, there was a slight increase in levels of LH by either route of injection. The results indicate that in the castrate animal proglumide can elevate LH levels by either route of injection but that the response is greater in castrate males than females. The reduction in response with the higher doses may reflect an agonist activity of proglumide. By contrast proglumide had no effect on plasma FSH except for a slight elevation observed following the intravenous or intraventricular injection of the lower doses of the compound in castrate males. The results favor a physiologically significant role of CCK in control of LH release in the rat.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Neurotensin enhances estradiol induced DNA synthesis in immature rat uterus.

Systemic administration of Neurotensin, a tridecapeptide, in immature rats treated with estradiol benzoate significantly enhances uterine DNA synthesis as reflected by the incorporation of 3H-thymidine. The peptide may have a direct action on the uterus. Substance P, a related peptide, had no effect on uterine DNA synthesis.

Animals↗
PubMed1985

Recent developments in female contraception: LHRH.

During the last few years new approaches to female contraception based on LHRH and its analogs have been developed. The physiological significance of pulsatile LHRH release and its stimulation of the pituitary has been elucidated by recent studies in rhesus monkey. Immunization against LHRH results in complete inhibition of reproductive function in animals and may find as a useful method of long-term fertility control in domestic animals. Clinical studies have utilized this knowledge to treat infertile hypogonadal women with chronic intermittent low-dose of LHRH. The superactive stimulatory LHRH analogs, used to treat infertility, paradoxically proved to have antifertility effects. They induce desensitization of the processes responsible for gonadotropic and gonadal hormone secretion, mediated by specific LHRH receptors in the pituitary and gonad. While contraceptive effectiveness of luteolytic approach remains to be proven, inhibition of ovulation by intranasal LHRH analog administration or continuous LHRH infusion by programmed minipumps seem to provide safe and effective contraception in women.

Amenorrhea↗
PubMed1984

Hypothalamic tyrosine hydroxylase activity, plasma gonadotropin and prolactin levels after aminooxyacetic acid in ovariectomized rats.

Plasma concentrations of gonadotropin, prolactin and hypothalamic tyrosine hydroxylase (TH) activity were measured in ovariectomized rats treated with aminooxyacetic acid (AOAA), a drug which elevates brain GABA levels. Hypothalamic TH activity was significantly increased with a significant decrease in prolactin (Prl) release. Plasma levels of gonadotropins were not modified by AOAA. These results support an inhibitory action of GABA on Prl release possibly mediated through hypothalamic dopamine.

Acetates↗
PubMed1984

Gamma aminobutyric acid (GABA), a modulator of anterior pituitary hormone secretion by hypothalamic and pituitary action.

We have evaluated the role of GABA in the control of anterior pituitary (AP) hormone secretion by injecting it into the third ventricle of ovariectomized, ovariectomized-steroid primed and male rats. Specificity of the effects was determined by injecting the GABA blocker, bicuculline. The action of GABA directly on the pituitary was evaluated in vitro. The results indicate that intraventricular GABA can stimulate LH, growth hormone (GH) and, at high doses, prolactin (Prl) release, whereas low doses inhibit Prl and al doses inhibit TSH release. All of these actions are blocked by bicuculline. Intraventricular GABA administration is followed by an elevation of hypothalamic norepinephrine (NE) and median eminence dopamine (DA) levels and AP DA levels, which indicates that the compound stimulates both NE and DA release. The actions on GH and LH appear to proceed independently of DA, since the DA receptor blocker, pimozide, did not interfere with these effects, whereas the action to elevate Prl and to lower TSH was blocked by DA receptor blockade. Anterior pituitary hormone release by AP's incubated with GABA in vitro was unaltered except for an inhibition of Prl release by very high GABA doses, which could be blocked by bicuculline. Intravenous injection of bicuculline to assess the physiological significance of GABA in control of AP hormone secretion revealed no effect on FSH but a delayed rise in LH, an initial rise in Prl, followed by a fall, a tendency for GH values to rise and dramatic fall in TSH levels. These results suggest the possibility that GABA plays a physiological role in the control of AP hormone secretion, mainly via a hypothalamic action.

Animals↗
PubMed1984

Hypothalamic tyrosine hydroxylase activity and plasma gonadotropin and prolactin levels in ovariectomized-steroid treated rats.

Plasma gonadotropin, prolactin levels and hypothalamic tyrosine hydroxylase (TH) activity were evaluated in ovariectomized (OVX) estradiol benzoate (EB) or progesterone (P) treated rats. Single injection of 10 micrograms or daily injection of 5 micrograms EB/rat for 7 days significantly lowered gonadotropin levels in OVX animals and elevated PRL levels. Single injection of 2 mg or daily injection of 200 micrograms P/rat for 7 days increased gonadotropin and PRL levels. Hypothalamic TH activity was significantly elevated by estradiol. Single injection of 2 mg P suppressed TH activity in contrast to the elevation in enzyme activity following chronic treatment. These results indicate that hypothalamic noradrenergic as well as dopaminergic neurons participate in the stimulatory or inhibitory feedback effects of ovarian hormones on gonadotropin and PRL secretion.

Animals↗
PubMed1984

Involvement of catecholamines and glutamate in GABAergic mechanism regulatory to luteinizing hormone and prolactin secretion.

There is some evidence that a population of estrogen-receptive neurons exists in the preoptic/anterior hypothalamic area which uses gamma-aminobutyric acid (GABA) as neurotransmitter and which is involved in mediating the negative feedback of estrogens on pituitary luteinizing hormone (LH) secretion. These neurons are proposed to be presynaptic inhibitors to norepinephrine (NE) release thereby inhibiting the stimulatory effect of NE on LHRH neurons. Muscimol, a potent GABA agonist, inhibits pituitary LH release in ovariectomized rats after intraventricular injection of 5 nmol. This treatment significantly increased prolactin levels. Catecholamine turnover rates in micropunches of various hypothalamic and mesolimbic structures following intraventricular treatment with muscimol were determined using the method of blocking the activity of tyrosine hydroxylase by alpha-methyl-p-tyrosine. Muscimol did not affect catecholamine, GABA and glutamate concentrations. Turnover rates of NE were significantly reduced in the medial preoptic/anterior hypothalamic area. In this structure as well as in the nucleus accumbens and in the anterior mediobasal hypothalamus turnover rates of dopamine (DA) were also reduced whereas DA turnover in mediocortical amygdalae was increased by muscimol. The selective reduction of NE turnover following muscimol may be explained by a direct or indirect action of the GABA-eric drug on NE axon terminals. The reduced NE and DA turnover in the medial preoptic area may be causally related to reduced serum LH levels whereas the reduced hypothalamic DA turnover may explain increased blood prolactin levels.

Animals↗
PubMed1983

Involvement of preoptic-anterior hypothalamic GABA neurons in the regulation of pituitary LH and prolactin release.

The effects of intraventricular injections of the highly specific gamma-amino-butyric acid (GABA) agonist muscimol (5 nmol/animal) on blood LH and prolactin levels were measured in ovariectomized (ovx) and in ovx estrogen-progesterone (OEP) primed rats. While the drug stimulated pituitary prolactin release in both experimental groups, pituitary LH release was significantly inhibited in the ovx animals. Muscimol was without any effect on LH levels in ovx-OEP primed rats. Bilateral implantation of tubes containing a muscimol-mannitol mixture into the medial preoptic/anterior hypothalamic (MPO/AH) area abolished pulsatile LH release whereas blood prolactin values were elevated. The intraventricular injection of GABA (8 mumol) also reduced LH and increased prolactin levels in the blood. Measurements of catecholamine turnover rates in the MPO/AH and in the mediobasal hypothalamus (MBH) yielded reduced preoptic but unchanged hypothalamic norepinephrine (NE) and stimulated hypothalamic dopamine (DA) turnover. In view of the well known stimulatory involvement of the NE system in the mechanism of pulsatile LH release and the inhibitory effect of GABA and its agonist muscimol on pulsatile LH release, it is suggested that GABA inhibits NE release in the MPO/AH by the mechanism of presynaptic inhibition. The observation that muscimol is unable to suppress LH release in vox OEP-primed rats may indicate that those estrogen receptive neurons in the MPO/AH which mediate the negative feedback action of the steroid may use GABA as neurotransmitter and that they are the neurons which inhibit NE release. The inhibitory effect of locally implanted muscimol into the MPO/AH also supports this hypothesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Plasma gonadotropin, prolactin levels and hypothalamic tyrosine hydroxylase activity following intraventricular bombesin and secretin in ovariectomized conscious rats.

Plasma gonadotropins, prolactin and hypothalamic tyrosine hydroxylase (TH) activity were evaluated at 15 and 30 min after third ventricular injection of bombesin at doses of 100 or 1000 ng and secretin at doses of 1000 and 5000 ng in ovariectomized (OVX) unanesthetized rats. Bombesin had no effect on plasma gonadotropin levels. Intraventricular injection of either 100 or 1000 ng dose of bombesin significantly suppressed prolactin levels with parallel elevation in hypothalamic TH activity and there appears to be no dose response relationship. Secretin at 1000 ng dose, significantly lowered plasma LH and PRL levels and elevated hypothalamic TH activity whereas a 5000 ng dose increased PRL concentrations but had no effect on gonadotropin levels and hypothalamic TH activity. Bombesin appears to be a potent inhibitor of PRL release in OVX, conscious rats and this effect may be mediated via hypothalamic dopamine. Lower dose of secretin appears to inhibit PRL release by possibly activating the hypothalamic dopaminergic system, while at higher dose peripheral activation results in enhanced prolactin release.

Animals↗
PubMed1983

Postnatal treatment of human seminal plasma inhibin: gonadotropin and prolactin levels during the onset of puberty in the rat.

Plasma gonadotrophin and prolactin levels, pituitary and accessory sex organ weights were evaluated on day 40 in rats of either sex treated with human seminal plasma (HSP) inhibin on day 7, 15, 21 and 30 postnatally. HSP inhibin suppressed both FSH and LH but without any effect on plasma PRL levels. The weights of pituitary and accessory sex organs were significantly suppressed. These results indicate a role for inhibin in the postnatal gonadotrophin release and a possible direct action on the accessory reproductive organs in the rat.

Animals↗
PubMed1983

Effects of arginine vasotocin on levels of plasma gonadotropins and prolactin in ovariectomized conscious rats.

Arginine vasotocin was injected into the third ventricle or intravenously in conscious, ovariectomized rats and its effect on gonadotropin and prolactin release evaluated. The peptide lowered plasma levels of both LH and prolactin in doses of 40 or 100 ng given intraventricularly. The higher dose was slightly more effective than the lower dose. Intravenous injection of a 1-microgram dose of vasotocin failed to alter plasma LH in the ovariectomized animals; however, a 5-micrograms dose induced a slight depression apparent at only 60 min following injection. Intravenous injection of 1 microgram produced a significant lowering of plasma prolactin, whereas a dramatic lowering followed the injection of the higher dose. Plasma FSH was unaffected in these experiments. Incubation of dispersed anterior pituitary cells from ovariectomized rats with various doses of vasotocin revealed no effect of the peptide on the release of FSH, LH, or prolactin. It also did not alter the response to LHRH, but it partially blocked the action of dopamine to inhibit prolactin release. The data indicate that quite low doses of arginine vasotocin act within the brain to inhibit LH and prolactin secretion in ovariectomized, conscious animals.

Animals↗
PubMed1982

Demonstration of tyrosinase in the vitiligo skin of human beings by a sensitive fluorometric method as well as by 14C(U)-L-tyrosine incorporation into melanin.

Tyrosinase activity (Monophenol, dihydroxyphenylalanine: oxygen oxidoreductase EC 1.14.18.1) in vitiligo and normal epidermal homogenates of skin from human beings was measured by estimating beta 3,4-dihydroxyphenylalanine (dopa) by a highly sensitive fluorometric method described in this paper. The tyrosine activity in the vitiligo skin was about 4 to 37% of corresponding normal skin. The activity of tyrosinase in normal human skin from different individuals and from different regions of the body was in the range of 4 to 140 picomoles of beta 3,4-dihydroxyphenylalanine formed per min/mg protein of epidermal homogenate. The enzyme from vitiligo and normal skin was severely inhibited by substance(s) of low molecular weight. The enzyme exhibits a lag of about 4 hr in the absence of added beta 3,4-dihydroxyphenylalanine and 1 hr in presence of 5 microM dopa. Tyrosinase from the normal and vitiligo skin was inhibited by excess concentration of tyrosine. The homogenates from vitiligo skin could synthesize melanin from C14(U)-L-Tyrosine. The rate of tyrosine incorporation into melanin by the epidermal homogenates is increased by 3,4-dihydroxyphenylalanine (dopa) disproportionate to its effect on tyrosinase activity. Based on the data presented in this paper it is concluded that melanocytes are present in the vitiligo skin. A tentative hypothesis is put forward to explain the lack of melanin synthesis by the vitiligo skin under in vivo conditions, although melanocytes are present.

Cadaver↗
PubMed1982

The effects of neurotensin on anterior pituitary hormone secretion.

The present experiments were conducted to determine the effects of neurotensin on secretion of a variety of anterior pituitary hormones. Conscious rats with indwelling cannulae in the third ventricle and external jugular vein were used and the effects on plasma hormone levels measured by radioimmunoassay. Neurotensin was found to decrease plasma prolactin levels in ovariectomized females, normal males, and males in which prolactin levels had been elevated by ether or by a combination of fluoxetine and 5-hydroxytryptaphane. The prolactin-lowering effect was blocked by alpha-methyl-tyrosine to inhibit catecholamine synthesis and by the specific dopamine receptor blocker, spiroperidol. In ovariectomized females, neurotensin was also capable of suppressing LH and elevating growth hormone following its intraventricular injection. Intravenous injection of the peptide elevated prolactin but had no effect on the release of the other pituitary hormones. When hemipituitaries of ovariectomized rats were incubated in vitro, neurotensin elevated prolactin and TSH release into the medium. The minimal effective dose to elevate prolactin and TSH release was 50 ng/ml. Release of gonadotropins and growth hormone was unaffected. It is concluded that neurotensin inhibits prolactin release by a CNS, presumably hypothalamic action, to stimulate the tuberoinfundibular dopaminergic neurons. The dopamine released then inhibits prolactin release either by a direct action on the pituitary or by release of another prolactin-inhibiting factor. In addition, the peptide has a direct prolactin-releasing action on the pituitary. Neurotensin can inhibit LH and stimulate growth hormone presumably by a hypothalamic action since there was no effect on the release of these pituitary hormones by glands incubated in vitro. Although the peptide had no effect on TSH release following its intraventricular injection, it stimulated prolactin release by pituitaries incubated in vitro. The physiological significance of these results is not yet established; however, the presence of the peptide in regions concerned with pituitary control suggests that it may play a physiological role.

5-Hydroxytryptophan↗
PubMed1982

Gastrointestinal hormones: central nervous system localization and sites of neuroendocrine actions.

It was established that VIP (vasoactive intestinal peptide), secretin, CCK (cholecystokinin), gastrin and motilin can be localized to the CNS by immunologic means. Whether or not these immuno-crossreactivities represent peptides identical to those in the g.i. tracts remains to be established. The neuronal localization of these five peptides in the gut predicted, however, their presence in neurons of the CNS. Furthermore, their presence within the hypothalamus and pituitary suggested physiological roles for these hormones in anterior pituitary function. We have now demonstrated the direct actions of VIP, secretin, gastrin and motilin on pituitary hormone release in vitro. Perhaps more importantly, we have described a hypothalamic site of action of VIP, secretin, CCK and gastrin to alter hormone release in vitro. Our data, taken in concert with those of other groups, suggest a modulatory role for the g.i. hormones and indicate the possible symphonic control by many hormones and transmitter candidates of distinct secretory events in the pituitary. Indeed, these data indicate the complexity underlying the finally tuned hypothalamus-pituitary-target tissue axis.

Animals↗