S K Quadri

Michigan State University, East Lansing, MI, United States

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Publications (39)74.82 Total impact

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    ABSTRACT: The direct effects of L-deprenyl, a monoamine oxidase inhibitor, on the hypothalamus of male Sprague-Dawley rats was investigated by measuring the efflux of norepinephrine (NE), dopamine (DA), serotonin (5-HT), dihydroxyphenylacetic acid (DOPAC), and 5-hydroxyindoleacetic acid (5-HIAA) using a combination of high performance liquid chromatography with electrochemical detection and an in vitro incubation system. After measuring basal efflux by incubating the hypothalami with Krebs-Ringers Henseleit (KRH) alone during the first incubation period, hypothalami were incubated either with the medium, KRH alone (0 mM), or KRH containing 0.1, 1, and 10 mM L-deprenyl. During the third incubation period, hypothalami were again incubated with KRH alone to measure the residual effects if any. During the final incubation period, the hypothalami were stimulated with high K(+) KRH. Deprenyl produced a dose-dependent increase in the efflux of NE, DA, and 5-HT from the hypothalami. Neurotransmitter efflux returned to pretreatment levels when L-deprenyl was removed from the medium. In contrast to NE, DA, and 5-HT, the efflux of the metabolites DOPAC and 5-HIAA was inhibited in a dose-dependent fashion after incubation with L-deprenyl. Results from this study demonstrate that L-deprenyl is capable of stimulating the efflux of neurotransmitters in vitro by a direct action on the hypothalamus.
    Brain Research Bulletin 05/2001; 54(6):675-80. · 2.94 Impact Factor
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    ABSTRACT: The purpose of this study was to investigate the age-related changes in the responsiveness of tuberoinfundibular dopamine (TIDA) neurones to chronic hypoprolactinemia induced by treatment with bromocriptine, a dopamine receptor agonist. In one experiment, TIDA neuronal activity after acute hypoprolactinemia or exogenous prolactin was monitored by measuring tyrosine hydroxylase (TH) activity in the stalk median eminence of middle-aged cycling female rats (10-12 months), old constant oestrous rats (18-20 months) and old pseudopregnant rats (22-24 months). In another experiment, middle-aged cycling (10-12 months) rats were treated with bromocriptine for 6 or 12 months. TH activity was measured in the stalk median eminence, TH mRNA levels were measured in the arcuate nucleus and dopamine concentrations were measured in the arcuate nucleus and median eminence. Responsiveness of TIDA neurones to exogenous prolactin and to the withdrawal of bromocriptine in these rats was also tested. While the TIDA neurones in all three age groups responded to acute hypoprolactinemia by showing a reduction in TH activity, older rats failed to respond to exogenous prolactin administration. In contrast, chronic hypoprolactinemia for 12 months enabled the rats to retain TIDA neuronal responsiveness to exogenous prolactin. It also decreased TIDA neuronal function as measured by dopamine concentrations in the median eminence, TH activity in the stalk median eminence and TH mRNA in the arcuate nucleus of ageing rats. The restoration of the responsiveness of these neurones to prolactin stimulation in older rats demonstrates for the first time that hypoprolactinemia produced by chronic bromocriptine treatment indeed provides a neuroprotective effect on TIDA neurones. These results indicate that maintaining a low level of neuronal activity by lowering prolactin levels may be a contributing factor in retaining the plasticity of TIDA neurones.
    Journal of Neuroendocrinology 04/2001; 13(3):261-9. · 3.51 Impact Factor
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    ABSTRACT: Lipopolysaccharide (LPS) is known to produce a number of central and neuroendocrine effects but the mechanisms involved are still unclear. This study was done to investigate the possibility that LPS-induced fever and activation of central monoamines are mediated through the vagus. Adult male rats were subjected to sub-diaphragmatic vagotomy (SDV), or sham operation and treated with saline or LPS in saline (10 microg/kg bw) 2 h later. Rectal temperature was monitored at half-hourly intervals for 5 h after which the animals were sacrificed and monoamine concentrations in hypothalamic nuclei were measured using HPLC-EC. SDV delayed the rise in rectal temperature induced by LPS by 1 h when compared to Sham animals. It also increased the concentrations of monoamines in the paraventricular nucleus of both Sham and SDV rats. This indicates that routes other than the vagus probably mediate LPS' actions on the central nervous system.
    Neuroscience Letters 05/2000; 284(3):159-62. · 2.03 Impact Factor
  • S ThyagaRajan, S K Quadri
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    ABSTRACT: In vivo release of catecholamines in the medial basal hypothalamus (MBH) by L-deprenyl, a monoamine oxidase-B (MAO-B) inhibitor, was measured in young male Sprague-Dawley rats with stereotaxically implanted push-pull cannulae in the MBH and perfused with 0 (control), 1.5, 2.5 or 10.0 microg deprenyl in 20 microl of saline. Perfusate samples were collected at 20-min intervals and analyzed for norepinephrine (NE) and dopamine (DA) by high performance liquid chromatography (HPLC)-EC. NE release in the MBH was enhanced following perfusion with 2.5 and 10.0 microg deprenyl while DA release was augmented after infusion of 10.0 microg of deprenyl. There were no significant alterations in the release of NE and DA in the control and 1.5 microg deprenyl groups. These results suggest that deprenyl-induced in vivo release of catecholamines in the MBH may be involved in the reversal of some of the reproductive aging processes.
    Neuroscience Letters 08/1999; 270(2):79-82. · 2.03 Impact Factor
  • S ThyagaRajan, S K Quadri
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    ABSTRACT: Previously, we have reported that L-deprenyl decreased the incidence of mammary tumors and pituitary tumors in old acyclic rats. The objective of the present study was to investigate the effects of L-deprenyl, a monoamine oxidase-B (MAO-B) inhibitor, treatment on the development and growth of tumors and on the metabolism of catecholamines and indoleamine in the medial basal hypothalamus (MBH) and the striatum (ST) of rats bearing 7,12-dimethylbenzanthracene (DMBA)-induced mammary tumors. Female Sprague-Dawley rats with DMBA-induced mammary tumors were injected (sc) daily with 0.25 mg or 5.0 mg of deprenyl/kg BW or the vehicle (saline; control) for 12 wk. Tumor diameter, tumor number, body weight, and feed intake were measured every week of the treatment period. Serum PRL and the concentrations of catecholamines, indoleamine, and their metabolites were measured by RIA and HPLC, respectively. Treatment with 5.0 mg deprenyl decreased the tumor diameter, tumor number, and serum prolactin (PRL) level. Although the body weight increased in all three groups, the body weight gain in the 5.0 mg group was smaller than that in the control and 0.25 mg groups. Deprenyl treatment had no effect on feed intake. The concentrations of dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were decreased in the MBH and the ST, and the concentration of 5-hydroxyindoleacetic acid (5-HIAA) was decreased in the MBH of deprenyl-treated rats. Treatment with 5.0 mg deprenyl enhanced the concentrations of norepinephrine (NE) and serotonin (5-HT) in the MBH and in the ST, and the concentration of dopamine (DA) in the MBH. These results suggest that the suppression of the development and growth of DMBA-induced mammary tumors by chronic deprenyl treatment may be mediated through alterations in the synthesis and metabolism of catecholamines and indoleamine in the MBH and inhibition of PRL secretion.
    Endocrine 07/1999; 10(3):225-32. · 2.25 Impact Factor
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    ABSTRACT: Lipopolysaccharide (LPS) is known to produce several central and neuroendocrine effects and some of these effects are believed to be mediated through cytokines and other proteins. One such protein, leptin, produced by adipose tissue has been shown to cause anorexia, a central effect associated with LPS treatment. This raised the possibility that LPS-induced effects on feeding behavior may be mediated through leptin. This study was done to investigate the effects of systemic administration of LPS on plasma leptin levels in rats and the possible involvement of interleukin-1 (IL-1) in this mechanism. Adult male rats were implanted with indwelling jugular catheters and after collecting two pretreatment blood samples, the animals were injected (i.p.) with saline, 5 microg, 10 microg, or 25 microg/kg BW of LPS, or treated with 25 microg of soluble IL-1 receptor (sIL-1R) 5 min before and 90 min after 25 microg/kg BW of LPS. Posttreatment blood samples were collected at 30 min intervals for a period of 6 h. Plasma leptin concentrations were measured by radioimmunoassay. Treatment with saline did not produce any change in plasma leptin levels. In contrast, each of the three doses of LPS produced a dose-dependent increase in plasma leptin levels within 120 min. Leptin levels remained elevated for the next 4 h. Treatment with sIL-1 R completely blocked the LPS-induced increase in leptin levels, indicating that this effect is in fact mediated through IL-1. These results indicate that leptin could be a possible mediator of LPS-induced effects on feeding.
    Endocrine 07/1999; 10(3):291-5. · 2.25 Impact Factor
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    ABSTRACT: The purpose of this study was to examine the specificity in the effects of lipopolysaccharide (LPS) on monoamine concentrations in different areas of the brain and the involvement of interleukin-1 (IL-1) in the LPS-induced effects. Adult male rats were injected i.p. with saline, 10 micrograms/kg body weight of LPS, or treated with 250 micrograms of IL-1 receptor antagonist (IL-1ra) 5 min before and 2 h after LPS. Several brain areas including the hippocampus (HI), caudate putamen (CP), the hypothalamic paraventricular nucleus (PVN), arcuate nucleus (AN), median eminence (ME) and the medial preoptic area (MPA) were microdissected and analyzed for neurotransmitter concentrations by HPLC-EC. LPS treatment produced marked increases in the concentrations of norepinephrine (NE), dopamine (DA), serotonin (5-HT) and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the PVN. In the AN, it increased DA concentrations and was without any effect on the MPA, ME, CP and HI. Treatment with IL-1ra in combination with LPS completely blocked the LPS-induced effects. It is concluded that LPS produces highly specific changes in monamine metabolism in the hypothalamus and that these effects are mediated at least in part by IL-1beta.
    Brain Research 05/1999; 824(2):232-7. · 2.88 Impact Factor
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    ABSTRACT: The purpose of this study was to examine the specificity in the effects of lipopolysaccharide (LPS) on monoamine concentrations in different areas of the brain and the involvement of interleukin-1 (IL-1) in the LPS-induced effects. Adult male rats were injected i.p. with saline, 10 μg/kg body weight of LPS, or treated with 250 μg of IL-1 receptor antagonist (IL-1ra) 5 min before and 2 h after LPS. Several brain areas including the hippocampus (HI), caudate putamen (CP), the hypothalamic paraventricular nucleus (PVN), arcuate nucleus (AN), median eminence (ME) and the medial preoptic area (MPA) were microdissected and analyzed for neurotransmitter concentrations by HPLC-EC. LPS treatment produced marked increases in the concentrations of norepinephrine (NE), dopamine (DA), serotonin (5-HT) and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the PVN. In the AN, it increased DA concentrations and was without any effect on the MPA, ME, CP and HI. Treatment with IL-1ra in combination with LPS completely blocked the LPS-induced effects. It is concluded that LPS produces highly specific changes in monamine metabolism in the hypothalamus and that these effects are mediated at least in part by IL-1β.
    Brain Research - BRAIN RES. 01/1999; 824(2):232-237.
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    ABSTRACT: The purpose of this study was to examine specificity in the effects of interleukin-1beta (IL-1beta) on monoamines in various areas of the hypothalamus. Adult male rats were injected i.p. with saline or 2.5 or 5.0 microg of IL-1beta or were pretreated with 500 microg of IL-1 receptor antagonist (IL-1ra) followed 5 min later by 5 microg of IL-1beta. The paraventricular nucleus (PVN), arcuate nucleus (AN), median eminence (ME), and medial preoptic area (MPA) were microdissected and analyzed for neurotransmitter concentrations by high-performance liquid chromatography with electrochemical detection (HPLC-EC). In the PVN, IL treatment produced significant increases in the concentrations of norepinephrine (NE), dopamine (DA), DA metabolite dihydroxyphenylacetic acid (DOPAC), serotonin (5-HT), and its metabolite 5-hydroxyindoleacetic acid (5-HIAA). IL-1 treatment increased the concentrations of NE and DA in the AN but only of NE in the ME, and it was without any effect in the MPA. Pretreatment with IL-1ra completely blocked the IL-1 effects. It is concluded that IL-1 induces highly specific changes in monoamine metabolism in the hypothalamus, and the nature of these changes depends on specific hypothalamic nuclei.
    Brain Research Bulletin 10/1998; 47(1):29-34. · 2.94 Impact Factor
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    ABSTRACT: Serotonin is known to stimulate prolactin secretion by decreasing tyrosine hydroxylase (TH) activity in the tuberoinfundibular dopaminergic (TIDA) neurons. However, the effects of aging on the responsiveness of TIDA neurons to serotonin are not known. An effective way to increase serotonergic activity is to administer 5-hydroxytryptophan (5-HTP), a serotonin precursor. The present study was done to investigate the effects of 5-HTP on TIDA neuronal activity in aging animals. Middle-aged (10-12 mo), old (18-20 mo), and very old (22-24 mo) female Sprague-Dawley rats were bilaterally ovariectomized. Ten days later, they were injected iv with 50 mg/kg body wt of 5-HTP or the vehicle for 5-HTP (PBS-HCI). Twenty minutes later, m-hydroxybenzylhydrazine (NSD), a DOPA decarboxylase inhibitor, was administered. Ten minutes later, the animals were killed, and tyrosine hydroxylase (TH) activity was determined by measuring L-DOPA accumulation in the stalk median eminence by HPLC-EC. In all three groups, administration of 5-HTP increased serum prolactin levels significantly. In control middle-aged rats, TH activity (L-DOPA pg/ microg protein) was 33.0+/-5.6. Treatment with 5-HTP decreased TH activity by 60%. Similarly, 5-HTP treatment decreased TH activity by 52 and 56% in 18- to 20- and 22- to 24-mo-old rats, respectively, compared to the control rats. The magnitudes of the 5-HTP-induced decreases in TH activities in middle-aged, old, and very old rats were not different from each other. These results indicate that TIDA neuronal responsiveness to serotonin does not change with age and that 5-HTP is capable of stimulating PRL release even in very old rats.
    Endocrine 09/1998; 9(1):33-7. · 2.25 Impact Factor
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    ABSTRACT: Prolactin (PRL) secretion is under the inhibitory regulation of the tuberoinfundibular dopaminergic (TIDA) system. Short-term elevation in PRL levels has been shown to increase the activity of TIDA neurons, however, the responsiveness of TIDA neurons to chronically elevated serum PRL levels is controversial. The purpose of this study was to investigate the effects of prolonged elevations of serum PRL on TIDA neuronal activity. Female Sprague-Dawley rats (2-3 months old) were ovariectomized and implanted (s.c.) with haloperidol (HAL), a dopamine receptor antagonist for 6 or 9 months to produce hyperprolactinemia. Ovariectomized, sham-implanted rats were used as controls. Other groups of intact rats were implanted with HAL or sham-implanted for 9 months and then were implanted with PRL-producing MMQ cells for 6 weeks to further increase circulating PRL levels. TIDA neuronal activity was measured in terms of tyrosine hydroxylase (TH) activity in the stalk-median eminence and was correlated with changes in serum PRL levels. After 6 months of treatment, TH activity in HAL-treated rats was 130% higher than that in the control rats. After 9 months of treatment, TH activity in HAL-treated rats was 81% higher than that in control rats. This increase was significantly less than the increase that occurred after 6 months of treatment. Nine months of HAL-induced hyperprolactinemia followed by implantation of PRL-producing MMQ cells, which resulted in very high levels of PRL, did not increase TH activity in the stalk-median eminence. These results demonstrate that hyperprolactinemia over a prolonged period reduces the responsiveness of TIDA neurons, and these effects vary depending on the duration and intensity of hyperprolactinemia.
    Proceedings of The Society for Experimental Biology and Medicine 04/1998; 217(4):461-5.
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    ABSTRACT: The purpose of this study was to examine specificity in the effects of interleukin-1β (IL-1β) on monoamines in various areas of the hypothalamus. Adult male rats were injected i.p. with saline or 2.5 or 5.0 μg of IL-1β or were pretreated with 500 μg of IL-1 receptor antagonist (IL-1ra) followed 5 min later by 5 μg of IL-1β. The paraventricular nucleus (PVN), arcuate nucleus (AN), median eminence (ME), and medial preoptic area (MPA) were microdissected and analyzed for neurotransmitter concentrations by high-performance liquid chromatography with electrochemical detection (HPLC-EC). In the PVN, IL treatment produced significant increases in the concentrations of norepinephrine (NE), dopamine (DA), DA metabolite dihydroxyphenylacetic acid (DOPAC), serotonin (5-HT), and its metabolite 5-hydroxyindoleacetic acid (5-HIAA). IL-1 treatment increased the concentrations of NE and DA in the AN but only of NE in the ME, and it was without any effect in the MPA. Pretreatment with IL-1ra completely blocked the IL-1 effects. It is concluded that IL-1 induces highly specific changes in monoamine metabolism in the hypothalamus, and the nature of these changes depends on specific hypothalamic nuclei.
    Fuel and Energy Abstracts 01/1998; 47(1):29-34.
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    ABSTRACT: The tuberoinfundibular dopaminergic (TIDA) system is known to inhibit prolactin (PRL) secretion. In young animals this system responds to acute elevations in serum PRL by increasing its activity. However, this responsiveness is lost in aging rats with chronically high serum PRL levels. The purpose of this study was to induce hyperprolactinemia in rats for extended periods of time and examine its effects on dopaminergic systems in the brain. Hyperprolactinemia was induced by treatment with haloperidol, a dopamine receptor antagonist, and Palkovits' microdissection technique in combination with high-performance liquid chromatography was used to measure neurotransmitter concentrations in several areas of the brain. After 6 months of hyperprolactinemia, dopamine (DA) concentrations in the median eminence (ME) increased by 84% over the control group. Nine months of hyperprolactinemia produced a 50% increase in DA concentrations in the ME over the control group. However, DA response was lost if a 9-month long haloperidol-induced hyperprolactinemia was followed by a 1 1/2 month-long extremely high increase in serum PRL levels produced by implantation of MMQ cells under the kidney capsule. There was no change in the levels of DA, norepinephrine (NE), serotonin (5-HT), or their metabolites in the arcuate nucleus (AN), medial preoptic area (MPA), caudate putamen (CP), substantia nigra (SN), and zona incerta (ZI), except for a decrease in 5-hydroxyindoleacetic acid (5-HIAA) in the AN after 6-months of hyperprolactinemia and an increase in DA concentrations in the AN after 9-months of hyperprolactinemia. These results demonstrate that hyperprolactinemia specifically affects TIDA neurons and these effects vary, depending on the duration and intensity of hyperprolactinemia. The age-related decrease in hypothalamic dopamine function may be associated with increases in PRL secretion.
    Brain Research Bulletin 02/1997; 42(6):435-41. · 2.94 Impact Factor
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    ABSTRACT: HPLC and Palkovits' microdissection technique were used to measure activities of two catecholamine-synthesizing enzymes, tyrosine hydroxylase (TH) and dopa decarboxylase (DD), in the medial preoptic area (MPA) and arcuate nucleus (AN), both of which are involved in LH regulation. The measurements were made during an 8-h period at 1200, 1400, 1600, 1800, and 2000 h on the days of proestrus and diestrus in young (4-5-month-old) rats. Similar measurements were made at 1400, 1600, 1800, and 2000 h in middle-aged (8-10-month-old) proestrous rats and in 18-22-month-old persistently diestrous rats. For each hour (1200, 1400, etc.), five to seven rats were used. In the young proestrous rats, TH activity in the MPA increased progressively to maximum levels at 1800 h, which is approximately the time when the proestrous surge of LH is known to occur. In contrast, in the young diestrous rats, in which serum LH is known to remain stable, TH activity remained unchanged throughout the afternoon. As in the young proestrous rats, in the middle-aged proestrous rats TH activity reached a peak at 1800 h followed by a precipitous decline at 2000 h. As in the young diestrous rats, in the old persistently diestrous rats no changes in TH activity were observed. The profiles of TH activity in the AN of the four groups were essentially similar to those in the MPA. The cyclic changes in TH activity observed in this study provide a basis for the reported cyclic changes in NE activity, which, in turn, are believed to be responsible for cyclic changes in LH release. The marked deficiency and absence of changes in TH activity in the acyclic old animals corresponded to the reported marked decrease and absence of fluctuations in catecholamine activity in old age. A correlation between DD activities and catecholamine activities was not obvious, most probably due to the large number of compounds that are known to be substrates for this enzyme.
    Brain Research Bulletin 02/1997; 42(4):265-71. · 2.94 Impact Factor
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    ABSTRACT: The direct effects of deprenyl on the pituitary were investigated by measuring the release of luteinizing hormone (LH) from the pituitary glands of male Sprague-Dawley rats in vitro. Basal release of LH was determined by incubating the pituitaries in Krebs-Ringer Henseleit (KRH) solution with 0, 0.1, 1, or 10 mM of deprenyl for 1 h. In the control group, LH release was not different in pre- and posttreatment periods. In contrast, in the 10 mM group, LH release increased by 436% (p<0.01). Incubation of pituitaries with 0.1 or 1 mM deprenyl did not alter LH release. It is concluded that deprenyl a monoamine oxidase inhibitor, can also act directly on the pituitary.
    Life Sciences 01/1997; 61(18):1783-8. · 2.56 Impact Factor
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    ABSTRACT: The direct effects of deprenyl on the pituitary were investigated by measuring the release of luteinizing hormone (LH) from the pituitary glands of male Sprague-Dawley rats in vitro. Basal release of LH was determined by incubating the pituitaries in Krebs-Ringer Henseleit (KRH) solution with 0, 0.1, 1, or 10 mM of deprenyl for 1 h. In the control group, LH release was not different in pre- and posttreatment periods. In contrast, in the 10 mM group, LH release increased by 436% (p
    Life Sciences - LIFE SCI. 01/1997; 61(18):1783-1788.
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    ABSTRACT: HPLC and Palkovits' microdissection technique were used to measure activities of two catecholamine-synthesizing enzymes, tyrosine hydroxylase (TH) and dopa decarboxylase (DD), in the medial preoptic area (MPA) and arcuate nucleus (AN), both of which are involved in LH regulation. The measurements were made during an 8-h period at 1200, 1400, 1600, 1800, and 2000 h on the days of proestrus and diestrus in young (4–5-month-old) rats. Similar measurements were made at 1400, 1600, 1800, and 2000 h in middle-aged (8–10-month-old) proestrous rats and in 18–22-month-old persistently diestrous rats. For each hour (1200, 1400, etc.), five to seven rats were used. In the young proestrous rats, TH activity in the MPA increased progressively to maximum levels at 1800 h, which is approximately the time when the proestrous surge of LH is known to occur. In contrast, in the young diestrous rats, in which serum LH is known to remain stable, TH activity remained unchanged throughout the afternoon. As in the young proestrous rats, in the middle-aged proestrous rats TH activity reached a peak at 1800 h followed by a precipitous decline at 2000 h. As in the young diestrous rats, in the old persistently diestrous rats no changes in TH activity were observed. The profiles of TH activity in the AN of the four groups were essentially similar to those in the MPA. The cyclic changes in TH activity observed in this study provide a basis for the reported cyclic changes in NE activity, which, in turn, are believed to be responsible for cyclic changes in LH release. The marked deficiency and absence of changes in TH activity in the acyclic old animals corresponded to the reported marked decrease and absence of fluctuations in catecholamine activity in old age. A correlation between DD activities and catecholamine activities was not obvious, most probably due to the large number of compounds that are known to be substrates for this enzyme.
    Brain Research Bulletin - BRAIN RES BULL. 01/1997; 42(4):265-271.
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    ABSTRACT: Push-pull perfusion and HPLC were used to measure the release of norepinephrine (NE) and dopamine (DA) in the medial basal hypothalamus of young (4-5 months old), middle-aged (8-10 months old), and old (22-24 months old) rats. In the young animals, the afternoon of proestrus was characterized by a gradual increase in NE release and a simultaneous gradual decrease in DA release. The peak in NE release and the nadir in DA release occurred at about the time when the proestrous surges in serum LH and PRL are known to occur. No changes in NE and DA releases occurred in the afternoon of diestrus when serum LH and PRL are known to remain stable. In the middle-aged proestrous animals, the patterns of NE and DA releases were similar to those in the young proestrous animals, but the peak in NE release was attenuated and did not reach statistical significance. This corresponded with the reported attenuation in the LH surge in middle age. In the old persistently diestrous animals, NE and DA were released at constant rates, which correlated with the well-documented constant levels of serum LH and PRL in old age. These data provide an explanation for the simultaneous proestrous surges of LH and PRL and lead us to conclude that NE plays a facilitatory role in the LH surge, while DA, through its inhibitory action, regulates the PRL surge.(ABSTRACT TRUNCATED AT 250 WORDS)
    Brain Research 09/1995; 689(1):122-8. · 2.88 Impact Factor
  • Source
    S Thyagarajan, J Meites, S K Quadri
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    ABSTRACT: The purpose of this study was to investigate the effects of long term treatment with deprenyl, a monoamine oxidase-B inhibitor, on estrous cyclicity, serum PRL, incidence of mammary and pituitary tumors, and monoamine metabolism in the medial basal hypothalamus (MBH) and striatum (ST) of old female rats. Acyclic female Sprague-Dawley rats (15-16 months old) were treated sc with 0, 0.25, or 2.5 mg deprenyl/kg BW.day for more than 8 months. Body weight and food intake were measured every week, and the estrous cycles and development of mammary tumors were monitored throughout the treatment period. At the end of the treatment period, the concentrations of catecholamines, serotonin, and their metabolites in the MBH and ST were determined by HPLC with electrochemical detection. The wet weights of the pituitary, heart, liver, lung, kidney, adrenals, uterus, and ovaries were recorded. Trunk blood was collected for measurement of serum PRL concentrations by RIA. Deprenyl treatment temporarily reestablished estrous cycles in most of the rats. The incidence of pituitary and mammary tumors was markedly reduced in the deprenyl-treated rats compared with that in the saline-treated control rats. Deprenyl had no significant effect on the weights of internal organs. The high dose of deprenyl (2.5 mg/kg) decreased serum PRL concentrations significantly. There were no significant differences in body weight or food intake between the control and deprenyl-treated groups. Deprenyl decreased the concentrations of the monoamine metabolites, dihydroxyphenylacetic acid, homovanillic acid, and 5-hydroxyindoleacetic acid, in both the MBH and ST. It had no effect on the concentrations of norepinephrine and dopamine in the MBH, but significantly increased norepinephrine concentrations in the ST and serotonin concentrations in both the MBH and ST (P < 0.05). It is concluded that deprenyl treatment exerted these effects via suppression of monoamine metabolism.
    Endocrinology 04/1995; 136(3):1103-10. · 4.72 Impact Factor
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    ABSTRACT: High-performance liquid chromatography with electrochemical detection (HPLC-EC) and Palkovits' microdissection technique were used to measure norepinephrine (NE) concentrations in the medial preoptic area (MPA) and arcuate nucleus (AN) during various stages of the estrous cycle. NE was measured seven times at 2-h intervals between 1000 h and 2200 h on the days of proestrus and diestrus in young (4-month-old) rats and four times at 2-h intervals between 1400 h and 2000 h in old (20-22-month-old) persistently diestrous rats. On the day of proestrus in young animals, NE increased progressively from low levels at 1000 h to peak levels at 2000 h, followed by a sharp decline at 2200 h. In contrast, no changes in NE occurred on the day of diestrus. Unlike the young proestrous rats, but similar to the young diestrous rats, no changes in NE concentrations either in the MPA or in the AN occurred in the old persistently diestrous rats. These data demonstrate that NE concentrations in the MPA and AN change during the estrous cycle. We believe the increase in NE on the afternoon of proestrus is related to the surge in serum luteinizing hormone (LH) that occurs simultaneously in this stage of the estrous cycle. The lack of change in NE concentrations in the young diestrous and persistently diestrous old animals is consistent with the well-established absence of changes in serum LH in these animals.
    Brain Research Bulletin 02/1995; 38(6):561-4. · 2.94 Impact Factor

Publication Stats

536 Citations
74.82 Total Impact Points

Institutions

  • 2001
    • Michigan State University
      • College of Veterinary Medicine
      East Lansing, MI, United States
  • 1997–2001
    • University of Kansas
      • Department of Molecular and Integrative Physiology
      Kansas City, KS, United States
  • 1985–2001
    • Kansas State University
      • • Department of Diagnostic Medicine/Pathobiology
      • • Department of Anatomy and Physiology
      Kansas, United States