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S K Quadri

Publications and source records attributed to S K Quadri.

At least 19 recordsLinked to original sources
PubMed1992

Interleukin-1 inhibits serotonin release from the hypothalamus in vitro.

During a 60-min incubation period, the in vitro release of serotonin (5-HT) from the hypothalami of control male rats decreased by 12.3 +/- 3.1%. In contrast, the presence of 25 ng of interleukin-1 beta (IL-1 beta) in the incubation medium more than doubled this decrease to 29.3 +/- 3.3% (P < 0.001), and the presence of 50 ng of IL-1 beta more than quadrupled this decrease to 53.7 +/- 7.4% (P < 0.001). The decrease produced by the higher dose of IL-1 beta was significantly greater than that produced by the lower dose (P < 0.01), indicating a dose response. During the next two 60-min periods when the hypothalami of the control as well as treatment groups were incubated without IL-beta, 5-HT release continued to decrease and then became stabilized in the control group. In contrast, 5-HT release in the treatment groups rebounded before becoming stabilized at levels that were not significantly different from those in the control group. It is concluded that IL-1 beta inhibits the release of serotonin from the hypothalamus in vitro.

Animals↗
PubMed1991

Interleukin-1 stimulates the release of dopamine and dihydroxyphenylacetic acid from the hypothalamus in vivo.

Push-pull perfusion technique was used to infuse IL-1 beta into and collect perfusate from the medial basal hypothalamus of freely moving male rats. Dopamine (DA) and its metabolite, dihydroxyphenylacetic acid (DOPAC), were measured in the perfusate using high performance liquid chromatography with electrochemical detection. In the control group, release rates of DA and DOPAC decreased and were 62% and 40%, respectively, below pretreatment levels after 325 min. In contrast, treatment with 50 ng of IL-1 beta produced substantial reductions in these decreases, and treatment with 100 ng of IL-1 beta produced increases of up to 118% and 89% in the release rates of DA and DOPAC, respectively. It is concluded that IL-1 beta affects the metabolism of catecholamines (and probably other neurotransmitters) in the brain, which, in turn, mediate its central and neuroendocrine actions.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1990

Interleukin-1 stimulates catecholamine release from the hypothalamus.

During a 60-min period, the in vitro release of norepinephrine (NE) from the hypothalami of male rats decreased by 28%. The presence of 50 or 100 ng of interleukin 1-beta (IL-1 beta) in the incubation medium prevented this decrease and raised the release by 17% or 45% respectively (P less than 0.05). The average release of dopamine (DA) decreased by 55% in the control group but 50 ng of IL-1 beta cut this decrease to 25%, and 100 ng of IL-1 beta not only completely prevented the decrease but raised the release by 44% (P less than 0.05). In a following 60-min period, when the hypothalami from the treatment groups were incubated without IL-1 beta, it resulted in sharp declines in the release of NE and DA, confirming that IL-1 beta was the stimulus for the increases in catecholamine release in the previous incubation period. It is concluded that IL-1 beta stimulates the release of catecholamines (and probably other neurotransmitters) in the brain which, in turn, mediate its central and neuroendocrine actions.

Animals↗
PubMed1990

Tyrosine hydroxylase messenger RNA in the hypothalamus, substantia nigra and adrenal medulla of old female rats.

The effects of aging in the female rat were analyzed in terms of tyrosine hydroxylase (TH) gene expression and serum prolactin levels. The number of tuberoinfundibular dopaminergic (TIDA) neurons and the concentration of TH mRNA per cell was greater in 16- to 18-month-old rats than in 25-month-old rats. The amount of TH immunostaining was more intense in the median eminence of the 18-month-old rats compared to either younger or older rats. Plasma prolactin levels were moderately elevated in 18-month-old rats compared to 4-month-old rats, and extremely elevated in 25-month-old rats due to the occurrence of pituitary prolactinomas. There were no detectable changes in TH mRNA levels in the substantia nigra with age, whereas adrenal TH mRNA increased with age. We propose that prolactin initially exerts a stimulatory effect on the TIDA neurons as the rat ages, but eventually causes a loss in neuronal number and neuronal function as the pituitary prolactinoma secretes increased amounts of prolactin.

Adrenal Medulla↗
PubMed1988

Effects of aging on the pituitary-thyroid axis in the dog.

The effects of advancing age on basal serum concentrations of thyroxine (T4) and thyrotropin (TSH), on T4 responses to TSH, and on TSH responses to thyrotropin-releasing hormone (TRH) were studied in beagle dogs. A total of 27 female dogs belonging to four age-groups were used: prepubertal (11.4 +/- 0.2 (SD) weeks), adult (2.1 +/- 0.3 years), middle-aged (6.5 +/- 0.2 years), and old (12.4 +/- 0.3 years). There was no significant difference between serum T4 concentrations of prepubertal (4.3 +/- 0.1 microgram/dl, mean +/- SE) and adult dogs (4.1 +/- 0.1 microgram/dl). Also, the decreases between adulthood and middle age (16.01%) and between middle age and old age (23.5%) were not significant, but serum T4 levels in the old dogs (2.6 +/- 0.2 micrograms/dl) were significantly (p less than 0.01) lower than those in the adult dogs. Serum cortisol levels showed a progressive increase with advancing age and were significantly higher in old animals (20.1 +/- 2.4 ng/ml) compared to those in the adults (13.4 +/- 1.2 ng/ml). There were no significant differences in serum TSH concentrations among the four age-groups. A single i.v. injection of TSH (0.15 IU/kg B.W.) raised serum T4 levels in the prepubertal animals by more than 45% in 1 h and by more than 100% in 2 h. T4 responses to TSH in the adult dogs were similar to those in the prepubertal dogs but were greatly delayed and subdued in the middle-aged and old animals. A single i.v. injection of TRH (5 micrograms/kg B.W.) increased serum TSH levels in the prepubertal animals by more than 120% in 15 min. These increases were less in the adult (74.8%) and middle-aged (21.3%) animals, and a significant increase (24.6%) in the old animals did not occur until 30 min after TRH treatment. This study demonstrates that, with advancing age, marked alterations occur in the regulation of the T4-TSH system in the dog.

Aging↗
PubMed1987

The effects of aging on the circadian rhythm of serum cortisol in the dog.

The purpose of this study was to determine if aging affects the circadian rhythm of serum cortisol. Female beagle dogs belonging to three age groups were used: adult (3.3 +/- 0.6 (SD) years), old (12.1 +/- 0.3 years), and puppies (8.4 +/- 0.2 weeks). Blood samples were collected by cephalic or jugular venipuncture at 3-h intervals during three 24-h periods and analyzed for total serum cortisol concentrations by radioimmunoassay. The circadian rhythm was present in the serum cortisol of adult animals, but no significant changes during a 24-h period could be detected in the old animals. No circadian rhythm in serum cortisol was present in the puppies. It is concluded that the circadian rhythm in plasma cortisol is disrupted in old animals and is not yet developed in puppies.

Aging↗
PubMed1987

Plasma thyroxine and cortisol under basal conditions and during cold stress in the aging dog.

The effects of aging on plasma concentration of thyroxine (T4) and cortisol and on responses of these hormones to low ambient temperatures were determined in the dog. Female beagle dogs were divided into three age groups: old, adult, and puppies. The mean (+/- SD) ages were 11.4 +/- 0.2 years, 3.0 +/- 0.4 years, and 7.6 +/- 0.2 weeks, respectively. All dogs came from a genetically homogeneous colony and were free from any disease. The adult and old dogs were used during anestrus. Based on four daily blood samples, the mean (+/- SE) T4 level in the old dogs (2.8 +/- 0.1 microgram/dl) was significantly (P less than 0.001) lower than that in the adults (4.2 +/- 0.2 micrograms/dl) and puppies (4.4 +/- 0.2 micrograms/dl). By contrast, mean plasma cortisol levels in the old dogs (21.1 +/- 3.1 ng/ml) and adults (15.4 +/- 2.4 ng/ml) were significantly higher than those in the puppies (7.2 +/- 1.1 ng/ml). No significant changes in plasma T4 and cortisol occurred in any of the three age groups at 22 degrees C or during exposure to 10 or 4 degrees C. Exposure to -5 degrees C, however, produced significant increases in T4 (greater than 130% by 5 hr) and cortisol (greater than 280% by 1 hr) in adult dogs. This temperature produced only a modest increase in T4 (70% by 3.5 hr) and no change in cortisol in the old dogs. The puppies showed no change in T4 and cortisol during exposure to -5 degrees C. The results demonstrate that with advancing age, plasma T4 and cortisol concentrations change in opposite directions, thus supporting the hypothesis of a negative relationship between these two hormones. These results also show that the responses of these hormones to the stress of cold decline during aging and are not yet developed in the very young.

Aging↗
PubMed1986

Premature mammary development in a heifer with abdominal mesothelioma.

A 13-month-old nonpregnant Holstein heifer had premature mammary gland development. A mesothelioma was found to involve the entire abdominal cavity, with 2 large tumorous masses adjacent to the right ovary and left kidney. Physiologic function of the ovary had been affected by the neoplasm.

Abdominal Neoplasms↗
PubMed1985

Inhibition of plasma prolactin in the rat by amantadine.

A single iv injection of 15 or 30 but not 7.5 mg/kg BW of an antiviral drug, amantadine, significantly (P less than 0.05) decreased plasma prolactin (PRL) concentrations in male rats. This effect was dose-dependent, with the highest dose producing a longer-lasting decrease in plasma PRL. The amantadine-induced decrease was unaffected by a simultaneous injection of 5-hydroxytryptophan (30 mg/kg BW) but was completely blocked by a simultaneous injection of haloperidol (0.05 mg/kg BW). It is concluded that this novel effect of amantadine on PRL is produced by an interaction with the dopaminergic system.

5-Hydroxytryptophan↗
PubMed1985

Effect of propiomazine on plasma prolactin in the rat: counteraction by L-dopa.

A single iv injection of 0.31, 0.62, 1.25, 2.5, 5, 10, or 20 mg/kg body wt of a phenothiazine derivative, propiomazine (PP), into male rats significantly (P less than 0.05) increased plasma prolactin concentrations. The higher doses (5, 10, and 20 mg/kg body wt) produced increases that were greater in both magnitude and duration than those produced by the lower doses. The higher doses of PP, along with the elevations in plasma prolactin, also produced concomitant decreases in plasma luteinizing hormone (LH) levels. Pretreatment with L-dopa (100 mg/kg body wt) completely blocked the PP-induced stimulation of prolactin release, indicating that antidopaminergic action of PP either at the hypothalamic or anterior pituitary level was responsible for its effects on the release of prolactin.

Animals↗
PubMed1978

Effects of centrally acting drugs on serum prolactin levels in rhesus monkeys.

Prolactin (Prl) responses to anesthetics, stress of immobilization, and agents that block adrenergic receptors were determined in 13 female rhesus monkeys. The local anesthetic (lidocaine HCl) had no effect, but the general anesthetics (ketamine HCl and sodium pentobarbital) significantly increased serum Prl levels in intact animals. There was no indication of a pentobarbital-induced inhibition of Prl secretion as reported for other species. A combination of halothane anesthesia and immobilization for 30 or 60 min produced significantly greater increases in Prl levels than immobilization alone for similar periods of time. Prl responses to blockers of adrenergic receptors varied in chair-adapted ovariectomized monkeys. The increase in serum Prl concentrations produced by the beta-receptor blocker propranolol was less marked than that induced by the alpha-receptor blockers phentolamine and phenoxybenzamine. Prl elevations of the highest magnitude and longest duration were produced by haloperidol, which blocks both adrenergic and dopaminergic receptors. Pretreatment of these animals with estradiol-17beta had no effect on Prl responses to phentolamine and haloperidol. These results indicate involvement of an adrenergic neurotransmitter system in the control of Prl secretion in primates.

Anesthetics↗
PubMed1977

Effects of estradiol-17beta on the induction of gonadotropin release by electrical stimulation of the hypothalamus in rhesus monkeys.

Serum LH and FSH were measured at 60, 30, and 0 min before, at 5, 15, and 30 min during, and at 10, 45, and 90 min after bilateral electrical stimulation (ES) of various hypothalamic regions in 12 unanesthetized ovariectomized rhesus monkeys. ES of the arcuate-ventromedial nuclei (medial basal hypothalamus; MBH) induced a prompt increase in serum LH that persisted throughout stimulation and returned to basal levels within 90 min thereafter. FSH was also released, but the release was slower and less dramatic than that of LH. Sham stimulation (0muA) caused no change in serum gonadotropins. The amount of LH released after MBH-ES depended upon current strength (1.0 mA greater than 0,5 or 0.7 mA). Three sequential 30-min MBH-ES trials at 90-min intervals induced comparable LH responses and 3 h of continuous MBH-ES maintained elevated serum LH levels throughout the stimulation period, suggesting that these stimulation period, suggesting that these stimulation parameters did not completely deplete pituitary stores of releasable LH. The character of the LH response was similar in individual monkeys through 3 to 24 trials during 4 to 18 months. Comparisons were made of the effects of estradiol-17beta (E2) treatment at different doses and for different intervals of time before MBH-ES. ES-induced LH release was not affected by low levels (25 and 55 pg/ml) ofE2 for 48 h, but was reduced by higher E2 concentrations (100 or 230 pg/ml). E2 concentrations of 100 pg/ml had no effect at 24 h, but reduced MBH-ES-activated LH release at 48 to 96 h; the degree of depression was time-related (48 h less than 72 h less than 96 h). ES of the preoptic-suprachiasmatic region (rostral hypothalamus; RH) in non-E2-treated monkeys also released LH, but this increase was less than after MBH-ES. FSH release was not measurable after RH-ES. In contrast to the depressed LH response to MBH-ES after 48 h of E2 (100 pg/ml), the response to RH-ES was not inhibited by this E2 regimen. These data suggest that ES of an area extending caudally from the rostral hypothalamus to the arcurate-median eminence region will evoke LH release in rhesus monkeys. This electrically induced gonadotropin release was affected by administration of physiological levels of E2 but the nature of effect depended on the specific region stimulated: distinct inhibition of the gonadotropic response to MBH-ES and slight facilitation of the response to RH-ES.

Animals↗
PubMed1977

Prolactin release following electrical stimulation of the brain in ovarectomized and ovariectomized estrogen-treated rhesus monkeys.

Selected areas in the medial basal (MBH) and rostral (RH) hypothalamus and in the amygdala (AMYG) of long-term ovariectomized rhesus monkeys were electrically stimulated for 30 min through permanently implanted bilateral stainless steel electrodes. Stimulation of an area in the MBH extending from the dorsal part of the ventromedial nucleus through the arcurate nucleus to the upper median eminence resulted in a 200 to 400% increase within 5 min in 8 monkeys. In one monkey the elevated serum prolactin levels persisted after termination of stimulation and in 2 monkeys prolactin remained unchanged during the 30-min stimulation but increased after stimulation was discontinued. Stimulation of the paraventricular-dorsomedial nuclear area in one monkey had no effect on prolactin release. Prolactin responses to stimulation in the RH varied. In 2 monkeys the electrode tips extended into the optic chiasm but part of the uninsulated tips remained in contact with the RH; only one of these monkeys released prolactin in response to stimulation. In 4 monkeys the electrode tips were located in the suprachiasmatic-anterior hypothalamus area. Serum prolactin increased by 200 to 300% in response to stimulation in 2 of these monkeys but increased only slightly in the remaining 2 monkeys. Prolactin responses to stimulation of the AMYG varied with the location of the electrodes. Stimulation in the corticomedial region produced no change in serum prolactin but stimulation in the basal or basolateral area produced marked elevations. An increase in circulating levels of estradiol-17beta (E2) to 100 pg/ml by SC implantation of E2 capsules 72 h before stimulation had no significant effect on basal prolactin levels, but markedly enhanced the prolactin release induced by stimulation in both the MBH and RH. Sham-stimulation did not affect serum prolactin. We conclude that prolactin release in rhesus monkeys can be triggered by electrical stimulation of selected hypothalamic and amygdaloid areas and that stimulation-induced prolactin release in the RH and MBH can be enhanced by E2 pretreatment.

Amygdala↗