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Biomedical subjects

D K Sarkar

Publications and source records attributed to D K Sarkar.

At least 73 records · Page 4Linked to original sources
PubMed1986

Loss of estradiol-positive feedback action on LH release during prepubertal period in rats treated postnatally with an opiate antagonist.

The purpose of this study was to determine the role of endogenous opioid peptides in the differentiation of the neuroendocrine brain that leads to estradiol-dependent LH release in female but not in male rats. Newborn intact or gonadectomized rats were given an opiate antagonist, naltrexone, with or without an opiate agonist, morphine, or saline alone during the critical period of the sexual differentiation of the brain (days 1-10). These animals were weaned on day 21 and injected with estradiol benzoate (EB) in oil or oil alone twice, 48 h apart, and the action of EB on plasma and pituitary levels of LH was studied. The release of LH during the prepubertal period was increased following EB treatment both in intact females and gonadectomized males and females, but not in intact male rats. Naltrexone treatment during the neonatal period prevented the EB-induced LH release in both intact and gonadectomized rats. Morphine blocked the inhibitory effect of naltrexone on LH release. Naltrexone treatment did not directly affect pituitary LH storage, but prevented EB-induced depletion of pituitary LH pools; morphine blocked this action of naltrexone. Hence, the inhibitory effect of naltrexone on LH release appeared to result from an alteration of the central mechanism responsible for EB-induced LH secretion. These results suggest a possible involvement of endogenous opioid peptides in the neuroendocrine brain differentiation that results in LH release after EB treatment during the prepubertal period in rats.

Animals↗
PubMed1986

Gonadotropin-releasing hormone-like immunoreactivity in rat placenta.

The concentration of gonadotropin-releasing hormone (GnRH) in the placenta, maternal plasma and fetal hypothalamus was measured in rats during days 13-21 of gestation. A substantial amount of GnRH was detectable in the extract of placenta and maternal plasma samples collected between days 13 and 21 and in the extract of fetal hypothalamus collected between days 19 and 21 of pregnancy. The GnRH level in the placenta and fetal hypothalamus, but not in plasma, fluctuated significantly during pregnancy. The level of GnRH gradually decreased in the placenta but increased in the fetal hypothalamus as the pregnancy proceeded. After gel filtration of placental extract, GnRH eluted in the same position as synthetic GnRH and hypothalamic GnRH. Dilution of placental extracts produced a displacement curve parallel to that of GnRH and hypothalamic extracts. These results indicate that GnRH is present in the placenta and that placental GnRH may have a role in the maintenance of pregnancy in rats.

Animals↗
PubMed1986

Persistence of low hypothalamic dopaminergic activity after removal of chronic estrogen treatment.

The purpose of this study was to determine whether inhibition of tuberoinfundibular dopaminergic (TIDA) neuron function which occurs during chronic estrogen administration persists after removal of the estrogen. Ovariectomized (OVX) Fischer 344 (F344) rats were implanted for 4 weeks with a Silastic capsule containing estradiol-17 beta (E2) and controls with an empty capsule for 4 weeks. Other rats which received E2 for 4 weeks had the capsule removed and experiments performed 4 weeks later. At the end of 4 weeks of E2 treatment, anterior pituitary (AP) weight was increased sixfold, serum prolactin (PRL) 65-fold, and AP DNA content fivefold over OVX control rats. Four weeks after removal of E2, AP weight, serum PRL, and AP DNA content declined, but remained significantly above OVX control values. At the end of 4 weeks of E2 treatment and after E2 withdrawal, release of [3H]dopamine (DA) from median eminence (ME) tissue superfused in vitro was lower than from ME of OVX control rats although [3H]DA accumulation was not significantly different among the treatment groups. Administration of apomorphine (APO), a dopamine agonist, significantly reduced plasma prolactin levels in OVX control rats, in rats at the end of 4 weeks E2 treatment, and in rats after 4 weeks of E2 withdrawal. Injection of haloperidol (HALO) produced similar increases in plasma PRL/estimated PRL-cell DNA in OVX controls, at the end of E2 treatment or after E2 withdrawal. However, injection of morphine (MOR), a drug which increases the release of PRL by inhibiting hypothalamic dopaminergic activity, resulted in a rise in plasma PRL/estimated PRL-cell DNA in OVX control rats that was significantly greater compared to rats at the end of E2 treatment or after E2 withdrawal. Since rats treated with E2 released less [3H]DA from ME tissue in vitro, and were less responsive to MOR, it can be that animals treated for 4 weeks with E2 show a decreased ability to release DA from TIDA neurons which persists even after termination of E2 treatment. These results suggest that chronic high circulating E2 levels result in a depression of TIDA neuronal activity which is sustained after E2 is removed.

Animals↗
PubMed1985

Relation of gonadal hormones to differential LH response to naloxone in prepubertal male and female rats.

Naloxone (NAL) has been shown to induce LH release in female but not in male rats 10-25 days of age. The purpose of this study was to examine the role of neonatal gonadal hormones on NAL-induced LH release in male and female rats 15, 25, and 35 days of age. On each of these days rats received a s.c. injection of either NAL (5 mg/kg) or physiological saline, and blood was collected 30 min later by decapitation. At 15 days of age, NAL induced LH release in intact and ovariectomized (OVX) female rats, and in male rats castrated (CAST) on the 1st day of life (neonate CAST males). Injection of 10 micrograms estradiol benzoate (EB) 24 h prior to NAL administration blocked NAL-induced LH release in these rats. NAL had no effect on LH release in 15- or 25-day-old intact and CAST male rats or in female rats given 2 mg testosterone propionate at 3 days of age (androgenized female rats). At 35 days of age, NAL induced LH release in intact, OVX, and OVX-EB treated female rats, and in neonate CAST and neonate CAST-EB treated male rats. NAL had no effect on serum LH levels in androgenized female rats. NAL induced LH release in intact and CAST 35-day-old male rats, but pretreatment with estrogen prevented NAL from eliciting LH release. These results indicate that neonatal exposure to androgen is responsible for the sex difference in the LH response to NAL observed in prepubertal male and female rats before 30 days of age.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Changes in beta-endorphin-like immunoreactivity in pituitary portal blood during the estrous cycle and after ovariectomy in rats.

beta-Endorphin-like immunoreactivity (beta-EP-LI) was measured by RIA in plasma collected from pituitary portal vessels of rats at various times in the estrous cycle and after ovariectomy. There were no appreciable differences between the mean beta-EP-LI concentration either in the afternoon (1500-1700 h) of estrus (4.1 +/- 1.5 ng/ml) or on diestrous days 1 (4.1 +/- 1.3 ng/ml) or 2 (5.4 +/- 1.5 ng/ml). The concentration increased slightly (6.7 +/- 1.3 ng/ml) but not significantly in the early afternoon (1400-1500 h) of proestrus. The concentration of beta-EP-LI then fell to 0.5 +/- 0.1 ng/ml at 1700-1800 h on proestrus, a level significantly lower than at any other time of the cycle. Portal plasma beta-EP-LI was also low (1.9 +/- 0.5 ng/ml) in animals ovariectomized for 3 weeks. After gel filtration of the portal plasma extracts, most of the beta-EP-LI eluted in the same position as synthetic beta-EP. Dilution of portal plasma produced a displacement curve parallel to that of beta-EP and hypothalamic extract. These results indicate that the secretion of hypothalamic beta-EP into the blood of pituitary portal vessels changes during the estrous cycle, possibly due to cyclic changes in sex steroids.

Animals↗
PubMed1985

Hyperprolactinemia decreases the luteinizing hormone-releasing hormone concentration in pituitary portal plasma: a possible role for beta-endorphin as a mediator.

Hyperprolactinemia can reduce the LH secretion in rats, but the mechanism of the effect of PRL is not clear. We have investigated the actions of PRL on the secretion of LHRH and LH and the interaction among PRL, beta-endorphin (beta-EP), and LHRH. The effects of PRL on LHRH and LH secretion were studied in ovariectomized female rats after transplanting four anterior pituitaries to the right kidney capsule of each ovariectomized rat for 2-3 weeks. The level of PRL in rats with pituitary transplants was approximately 5 times higher than that in control rats. The concentration of LHRH in pituitary portal plasma of hyperprolactinemic rats was approximately 4 times lower than that in control rats. Hyperprolactinemic animals also showed lower plasma LH levels than the controls. Since beta-EP inhibits the secretion of LHRH, we have tested whether the reduced secretion of LHRH in hyperprolactinemic ovariectomized rats is associated with an increase in beta-EP activity. This was studied by measuring the concentration of beta-EP in pituitary portal plasma and the response of LHRH and LH to the opiate antagonist naloxone. The level of beta-EP-like immunoreactivity in pituitary portal plasma was significantly higher in hyperprolactinemic rats than in control animals. Naloxone (10 mg/kg, sc) increased both LHRH and LH concentrations in hyperprolactinemic rats, but not in control rats. The present results demonstrate that hyperprolactinemia can reduce LHRH release and suggest a possible involvement of beta-EP in the PRL inhibitory action on LHRH.

Animals↗
PubMed1984

Inhibition by estrogen of autofeedback regulation of prolactin secretion.

The effect of estradiol-17 beta (E2) on autofeedback regulation of prolactin (PRL) secretion was tested in ovariectomized rats after s.c. implantation of an (E2)-containing or empty silastic capsule, followed by i.v. injection of bovine PRL (b-PRL) or bovine serum albumin (BSA; 500 micrograms/100 g B.W.). Implantation of an E2 capsule (day 0), 2.5 mm or 5.0 mm in length, produced plasma E2 concentrations of 79 +/- 6 (9) and 140 +/- 8 pg/ml (8), respectively. Assay of PRL in plasma samples collected at 1 h intervals between 1100-1800 h on days 3, 4 and 5, after E2 capsule implantation showed a daily afternoon PRL surge. Empty capsule-treated rats did not show any afternoon PRL surge. Injection of b-PRL, but not BSA, at 1200 h on day 3 reduced basal PRL release both on days 3 and 4 in empty capsule-treated rats. In ovariectomized rats treated with a smaller E2 capsule (2.5 mm), b-PRL injection at 1200 h on day 3 reduced the amplitude of the afternoon surge of PRL and the total amount of PRL released on day 4. b-PRL, however, was ineffective in reducing PRL release in rats bearing the large E2 capsule (5.0 mm). These results suggest that high E2 levels in the blood can block the negative feedback action of PRL on PRL release.

Animals↗
PubMed1984

Reduced tuberoinfundibular dopaminergic neuronal function in rats with in situ prolactin-secreting pituitary tumors.

Tuberoinfundibular dopaminergic (TIDA) neuronal function in rats with spontaneous or estrogen-induced prolactin- (PRL-)secreting pituitary tumors (prolactinomas) was studied by assaying dopamine (DA) concentration in pituitary stalk blood and electrically induced release of 3H-DA from the median eminence in vitro. Old rats with spontaneous prolactinomas showed enlarged and hemorrhagic pituitaries and elevated serum PRL levels. These rats had reduced DA in pituitary stalk blood, showed significantly lower response to the DA-releasing drug, nomifensine, and exhibited reduced electrically induced 3H-DA release from the median eminence in vitro, when compared to corresponding values in young and old rats without prolactinomas. The dopamine agonist piribedil failed to reduce electrically induced 3H-DA release by the superfused median eminence from old rats with prolactinomas, but not from old and young rats without prolactinomas. Old rats without prolactinomas also showed higher serum PRL values and pituitary weight than young rats without prolactinomas. However, stalk blood DA values before and after nomifensine, electrically induced 3H-DA release by the median eminence in vitro, and inhibition by piribedil of 3H-DA release in vitro were significantly lower in old rats without prolactinomas than in young rats without prolactinomas. Estrogen treatment of young ovariectomized rats for 5 months produced enlarged and hemorrhagic pituitaries and elevated serum PRL values, but reduced the content of stalk blood DA and electrically induced release of 3H-DA by the median eminence in vitro as compared with values in untreated young ovariectomized control rats. Estrogen-treated rats also showed no response to piribedil on in vitro 3H-DA release.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Cyclic variation of oxytocin in the blood of pituitary portal vessels of rats.

The release of oxytocin (OT) into pituitary portal blood during the estrous cycle was studied in female rats under Althesin anesthesia. On each afternoon of the 4-day estrous cycle, animals were anesthetized with Althesin, and pituitary portal blood samples were collected. The concentration of OT in portal plasma collected between 14.00 and 16.00 h of proestrus (1,079 +/- 185 pg/ml) was significantly higher than that at any other time studied. There were no appreciable differences between the mean OT concentration on the days of estrus (198 +/- 29 pg/ml), metestrus (283 +/- 55 pg/ml), and diestrus (267 +/- 49 pg/ml). The concentration of OT in pituitary portal plasma was also greater than that in blood withdrawn from the external jugular vein (less than 41-67 pg/ml). Comparison of the portal plasma OT with peripheral plasma prolactin in Althesin-anesthetized rats indicated an association between the release of these hormones during the estrous cycle.

Animals↗
PubMed1984

Decline of tuberoinfundibular dopaminergic function resulting from chronic hyperprolactinemia in rats.

The effect of hyperprolactinemia on tuberoinfundibular dopaminergic (TIDA) neurons was studied after sc transplantation of a PRL-secreting pituitary tumor (MtT.W15) to young female rats. TIDA activity was determined by measuring the concentration of dopamine (DA) in pituitary stalk portal blood, the uptake and release of [3H]DA by the median eminence in vitro, and the presynaptic DA receptor activity. Eight weeks after transplantation of the tumor, serum PRL increased to approximately 100 times higher values than those in nontumor-bearing animals. Both the DA concentration and the content in pituitary stalk blood collected from rats bearing tumors for 6 weeks were significantly lower than those in nontumor-bearing rats. Injection of a DA uptake blocker, nomifensine, significantly increased stalk blood DA in nontumor-bearing rats, but did not increase DA release in tumor-bearing rats. The uptake of [3H]DA in vitro by the median eminence of rats bearing pituitary tumors for 8 weeks was lower than that in control rats. Basal and electrically induced release of [3H]DA from the median eminence in vitro from rats with tumors for 8 weeks were also significantly lower than in rats without tumors. Piribedil, a DA receptor agonist, reduced stimulated release of [3H]DA in vitro from the median eminence of rats without tumors, presumably by activating presynaptic DA receptors. However, piribedil had no effect on release of [3H]DA from the median eminence of rats with tumors. These results indicate that chronic elevation of PRL can produce a decline in TIDA function.

Animals↗
PubMed1983

Uptake and release of [3H]dopamine by the median eminence: evidence for presynaptic dopaminergic receptors and for dopaminergic feedback inhibition.

The accumulation and release of [3H]dopamine by the median eminence in vitro was studied after treatments with different pharmacological agents, to determine whether such a procedure would be useful for measuring neuronal activity in the tuberoinfundibular dopaminergic system. The accumulation of [3H]dopamine was temperature, time, and sodium dependent, and reduced by unlabelled dopamine and by a potent dopamine uptake blocker, nomifensine. The outflow of tritium was studied after blocking the oxidative deamination of dopamine by nialamide. The outflow of tritium was elicited consistently by biphasic square wave electrical pulses and by high molarity potassium ions. The response to electrical stimulation was dependent largely on calcium and partially on sodium. The response to high molarity potassium ions was reduced in the absence of calcium ions. The response to electrical stimulation was increased by nomifensine and by a dopaminergic antagonist, haloperidol, and was reduced by dopamine and by a dopaminergic agonist, piribedil. The inhibitory action of dopamine was antagonized by haloperidol. These results indicate the existence of uptake and release mechanisms in the tuberoinfundibular dopamine neurons, and suggest that dopamine may inhibit its own release via dopaminergic receptors. This in vitro method may be useful for measuring dopamine uptake and release by tuberoinfundibular dopaminergic neurons.

Animals↗
PubMed1983

Failure of prolactin short loop feedback mechanism to operate in old as compared to young female rats.

The short loop feedback effect of PRL was studied in young (4-5 months of age) and old (24-26 months of age) ovariectomized rats after a single iv injection of bovine PRL (bPRL, 500 micrograms/100 g BW) or BSA (500 micrograms/100 g BW). Blood samples were collected via intraatrial cannula every 20 min for assay of PRL. Plasma PRL levels in both young and old ovariectomized rats were pulsatile in nature, and showed approximately one PRL pulse per hour. The magnitude of the PRL peaks and concentrations of plasma PRL, but not the number of PRL peaks, were significantly greater in the old than in the young rats. The effect of bPRL on in situ PRL release was studied after verifying that bPRL does not cross-react with rat PRL RIA, but does significantly increase the release of [3H] dopamine from the median eminence in vitro. This latter effect was dose dependent. In young rats, a single injection of bPRL minimally reduced the concentration of plasma PRL between 100 min and 5 h, but by 22-25 h it decreased plasma PRL to approximately one third of preinjection levels. The magnitude of the PRL pulses, but not the pulse frequency was significantly reduced after administration of bPRL treatment to young rats. Treatment with BSA did not alter the concentration of plasma PRL or the magnitude and frequency of the PRL pulses in young rats. In old rats, plasma PRL concentrations and the frequency and magnitude of the PRL pulses were not significantly decreased after injection of either bPRL or BSA. Thus, the feedback inhibition of PRL on PRL release may not be operative in old rats. The loss of the short loop feedback inhibition of PRL is believed to be due to the reduction in hypothalamic dopaminergic activity previously reported by our and other laboratories in old rats.

Aging↗
PubMed1982

Sex difference in response to alphaxalone anaesthesia may be oestrogen dependent.

The steroid anaesthetic Althesin (Glaxo), which is a mixture of two C21 steroids, alphaxalone (3 alpha-hydroxy-5 alpha-pregnane-11, 20-dione--the active compound) and alphadolone acetate (21-acetoxy-3 alpha-hydroxy-5 alpha-pregnane-11, 20-dione), has been especially useful for the study of forebrain-autonomic and neuroendocrine functions. As determined by the loss of the righting reflex, Child et al. found no sex difference in the anaesthetic dose of Althesin administered intravenously (i.v.). However, in our neuroendocrine studies in which the anaesthetic was administered intraperitoneally (i.p.) and at dosage sufficient to produce surgical anaesthesia and analgesia, we observed a sex difference in the efficacy of Althesin. This may explain the difficulties that have been encountered in obtaining adequate anaesthesia (blockade of the somatomotor response to pain) with Althesin. Here we report, using cortical electroencephalography, that Althesin is a more potent anaesthetic than either sodium pentobarbitone or urethane, and that anaesthesia in the male rat requires about four times more Althesin (administered i.p.) than in the female. This sex difference is age dependent, can be abolished by administering oestrogen to the male, does not depend on sexual differentiation of the brain, and cannot be attributed to a sex difference in the metabolic clearance rate of alphaxolone. These results, taken together with those of Richards and Hesketh, suggest that the effect of alphaxalone may be mediated by interactions with synaptic membranes that are more specific than simply a generalized change in membrane structure, and that these interactions are affected by sex steroids.

Age Factors↗
PubMed1981

Effect of manipulating central catecholamines on puberty and the surge of luteinizing hormone and gonadotropin releasing hormone induced by pregnant mare serum gonadotropin in female rats.

We have investigated the effect of manipulating central catecholamines on the timing of puberty (as assessed by vaginal opening) in female rats and the surge of luteinizing hormone (LH) and gonadotropin releasing hormone (GnRH) induced by pregnant mare serum gonadotropin (PMSG) in immature female rats. Manipulation of the catecholamines was carried out with either 6-hydroxydopamine (6-OHDA) administered with or without either desipramine (DMI) or pargyline, or alpha-methyl-p-tyrosine (alpha-MPT). The neonatal administration of 6-OHDA delayed puberty, an effect which was potentiated by pretreatment with DMI and was associated with a reduction in the rate of body growth. Catecholamine fluorescence in animals aged 60--65 days that had been treated with DMI followed by 6-OHDA was diminished only in the caudatus--putamen; treatment with 6-OHDA alone resulted in diminished fluorescence in the hypothalamus and in the intermediate but not the external layer of the median eminence. The neonatal administration of alpha-MPT had no significant effect on either the growth rate or the timing of puberty. Regular oestrous cycle occurred after puberty in animals treated with either 6-OHDA or alpha-MPT. The PMSG-induced LH surge was significantly enhanced by 6-OHDA (administered i.v.) plus DMI, and reduced by 6-OHDA injected in to the lateral ventricle (v). The inhibitory effect of 6-OHDA (v) was reduced by DMI, but in animals given 6-OHDA (i.v.) after pargyline there was a marked reduction in the height of the LH surge. There was a good correlation between the changes in the concentrations of LH in peripheral plasma and the concentrations of GnRH in pituitary stalk plasma in that the PMSG-induced surge of GnRH was significantly increased by 6-OHDA (i.v.) plus DMI and reduced by 6-OHDA (v). In animals treated with 6-OHDA (i.v. plus DMI catecholamine fluorescence was reduced only in the external layer of the median eminence, while after 6-OHDA (v) plus DMI degeneration was seen in the medial forebrain bundle. These results demonstrate a marked difference between the long-term and acute effects of 6-OHDA on the gonadotropin control system. Neonatal treatment with 6-OHDA plus DMI significantly delays puberty and the rate of body growth, but does not affect cyclical gonadotropin release and has no persistent effect on the hypothalamic catecholaminergic systems. The acute administration of 6-OHDA, depending upon the route of administration and whether it is given after DMI, can either potentiate or inhibit the PMSG-induced surge of GnRH and consequently LH by mechanisms which involve destruction, respectively, of either dopaminergic terminals in the median eminence or catecholaminergic fibres in the dorsal hypothalamus.

Animals↗