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Esther L Sabban - One of the best experts on this subject based on the ideXlab platform.
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regulation of angiotensin ii type 2 receptor gene expression in the adrenal medulla by acute and repeated Immobilization Stress
Journal of Endocrinology, 2012Co-Authors: Regina Nostramo, Lidia I Serova, Richard Kvetnansky, Andrej Tillinger, Juan M Saavedra, Ashok Kumar, Varunkumar Pandey, Esther L SabbanAbstract:While the Renin-Angiotensin System is important for adrenomedullary responses to Stress, the involvement of specific angiotensin II receptor subtypes is unclear. We examined gene expression changes of angiotensin II type 1A (AT1A) and type 2 (AT2) receptors in rat adrenal medulla in response to Immobilization Stress (IMO). AT2 receptor mRNA levels decreased immediately after a single 2 h IMO. Repeated IMO also decreased AT2 receptor mRNA levels, but the decline was more transient. AT1A receptor mRNA levels were unaltered with either single or repeated IMO, although binding was increased following repeated IMO. These effects of Stress on angiotensin II receptor expression may alter catecholamine biosynthesis, as tyrosine hydroxylase and dopamine beta-hydroxylase mRNA levels in PC12 cells are decreased with angiotensin II treatment in the presence of ZD7155 (AT1 receptor antagonist), or with {"type":"entrez-protein","attrs":{"text":"CGP42112","term_id":"874777115","term_text":"CGP42112"}}CGP42112 (AT2 receptor agonist) treatment. Involvement of Stress-triggered activation of the hypothalamic-pituitary-adrenocortical (HPA) or sympatho-adrenal axis in AT2 receptor downregulation was examined. Cultured cells treated with the synthetic glucocorticoid dexamethasone displayed a transcriptionally-mediated decrease in AT2 receptor mRNA levels. However, glucocorticoids are not required for the immediate Stress-triggered decrease in AT2 receptor gene expression, as demonstrated in corticotropin-releasing hormone knockout (CRH KO) mice and hypophysectomized rats, although they can regulate basal gene expression. cAMP and pituitary adenylate cyclase-activating polypeptide (PACAP) also reduced AT2 receptor gene expression and may mediate this response. Overall, the effects of Stress on adrenomedullary AT1A and AT2 receptor expression may contribute to allostatic changes, such as regulation of catecholamine biosynthesis.
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Immobilization Stress elevates tryptophan hydroxylase mrna and protein in the rat raphe nuclei
Biological Psychiatry, 2004Co-Authors: Firas Chamas, Mark D Underwood, Victoria Arango, Lidia I Serova, Suham Kassir, John J Mann, Esther L SabbanAbstract:Abstract Background Stress triggers adaptive and maladaptive changes in the central nervous system, including activation of the hypothalamic–pituitary–adrenal axis, and can trigger mood disorders and posttraumatic Stress disorder. We examined the effect of Immobilization Stress (IMO) on gene expression of tryptophan hydroxylase (TPH), the rate-limiting enzyme in serotonin biosynthesis, and the role of cortisol in that response. Methods Regular and adrenalectomized Sprague-Dawley rats were exposed to various repetitions of IMO. Tryptophan hydroxylase messenger ribonucleic acid (mRNA) was determined by competitive reverse transcriptase polymerase chain reaction, and TPH protein was examined by immunoblot and immunocytochemistry. Results Elevation of TPH mRNA by IMO was tissue-specific and dose-dependent. A single IMO elicited a threefold rise in TPH mRNA in median raphe nucleus (MRN), but repeated (3×) IMOs were needed for similar response in dorsal raphe nucleus (DRN). Repeated daily IMO, up to 7 days, triggered a robust induction (6–10-fold) in TPH mRNA, accompanied by corresponding rise in TPH protein levels in raphe nuclei but not in the pineal gland. The rise in TPH immunoreactivity was widespread throughout the DRN and MRN. Bilateral adrenalectomy did not prevent the IMO-triggered increase in TPH immunoreactive protein in the raphe nuclei. Conclusions This study reveals adrenal glucocorticoid–independent induction of TPH gene expression in raphe nuclei in response to Immobilization Stress.
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increase in rat adrenal phenylethanolamine n methyltransferase mrna level caused by Immobilization Stress depends on intact pituitary adrenocortical axis
Journal of Neurochemistry, 2002Co-Authors: Esther L Sabban, Emil Viskupic, Richard Kvetnansky, Koki Fukuhara, Virginia K Weise, Irwin J Kopin, Joan P SchwartzAbstract:: The effects of a single and of repeated Immobilization Stress on the expression of the final enzyme involved in epinephrine biosynthesis, phenylethanolamine N-methyltransferase (PNMT), are described. A single Immobilization (whether lasting 5 or 120 min) caused a severalfold increase of the adrenal PNMT mRNA level as measured 2 h after the beginning of the procedure. This elevation was of a transient nature, peaked 3–6 h after the 2-h Immobilization, and returned to control values by 12 h after the Stress. When the animals were immobilized for 2 h/day for seven consecutive days, an increase in content of PNMT mRNA of a similar magnitude was observed, which persisted for at least 2 days after the seventh Immobilization. The Immobilization-induced increase was completely abolished in hypophysectomized animals, whereas adrenal denervation failed to prevent it. These data suggest that the Immobilization-induced increase in adrenal PNMT mRNA level depends primarily on pituitary-adrenocortical regulation.
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tryptophan hydroxylase mrna levels are elevated by repeated Immobilization Stress in rat raphe nuclei but not in pineal gland
Neuroscience Letters, 1999Co-Authors: Firas Chamas, Lidia I Serova, Esther L SabbanAbstract:Abstract Repeated Stress triggers a wide range of adaptive changes in the central nervous system including the elevation of serotonin (5-HT) metabolism and an increased susceptibility to affective disorders. To begin to examine whether these changes are mediated by alterations in gene expression for tryptophan hydroxylase (TPH), the rate-limiting enzyme in 5-HT biosynthesis, we quantitated its mRNA levels by competitive reverse transcription-polymerase chain reaction (RT-PCR). Repeated Immobilization Stress (2 h, 7 days) elicited a six- or ten-fold rise in TPH mRNA in median raphe nucleus (MRN) and dorsal raphe nucleus (DRN), respectively, without significantly altering TPH mRNA levels in the pineal gland. In contrast, there was little change in mRNA levels for GTP cyclohydrolase I (GTPCH), the rate limiting enzyme in synthesis of the tetrahydrobiopterin (BH4), the obligate cofactor for TPH. This is the first study to reveal Stress-elicited activation of TPH gene expression.
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tyrosine hydroxylase mrna levels in locus ceruleus of rats during adaptation to long term Immobilization Stress exposure
Molecular and Chemical Neuropathology, 1998Co-Authors: M Rusnak, Esther L Sabban, Stefan Zorad, Patricia Buckendahl, Richard KvetňanskýAbstract:The major central norepinephrinergic nucleus, locus ceruleus (LC), is thought to participate in modulation of such brain areas as cerebral cortex, septum, hippocampus, thalamus, hypothalamus, and cerebellum in animals facing various physiological challenges, including Stress. Exposure of experimental animals to different Stressors causes an increase in LC activity and gene expression of tyrosine hydroxylase (TH), the rate-limiting enzyme in catecholamine biosynthesis. The aim of this work was to investigate the effect of a single and repeated (7 time) or long-term repeated (42 times) daily Immobilization Stress (IMMO) on TH mRNA levels in LC of laboratory rats byin situ hybridization method. A single IMMO caused significant elevation of LC TH mRNA levels in comparison to unStressed controls. This was found immediately and at 3 and 6 h after IMMO, and progressively increased up to 24 h after the first IMMO terminated. Further exposure to IMMO did not cause additional increases in LC TH mRNA levels, which stayed significantly elevated in comparison to unStressed rats. In animals that underwent IMMO for 42 times, the LC TH gene expression, 24 h after the last Stress exposure, was significantly lower when compared to that of singly or seven times Stressed rats. Thus, our results indicate a possible adaptation of catecholamine-synthesizing system at the level of TH gene expression in LC of rats exposed to long-term repeated IMMO.
Teresa A Milner - One of the best experts on this subject based on the ideXlab platform.
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chronic Immobilization Stress primes the hippocampal opioid system for oxycodone associated learning in female but not male rats
Synapse, 2019Co-Authors: Batsheva Reich, Bruce S Mcewen, Yan Zhou, Ellen Goldstein, Sudarshan S Srivats, Natalina H Contoreggi, Joshua F Kogan, Mary Jeanne Kreek, Teresa A MilnerAbstract:In adult female, but not male, Sprague Dawley rats, chronic Immobilization Stress (CIS) increases mossy fiber (MF) Leu-Enkephalin levels and redistributes delta- and mu-opioid receptors (DORs and MORs) in hippocampal CA3 pyramidal cells and GABAergic interneurons to promote excitation and learning processes following subsequent opioid exposure. Here, we demonstrate that CIS females, but not males, acquire conditioned place preference (CPP) to oxycodone and that CIS "primes" the hippocampal opioid system in females for oxycodone-associated learning. In CA3b, oxycodone-injected (Oxy) CIS females relative to saline-injected (Sal) CIS females exhibited an increase in the cytoplasmic and total densities of DORs in pyramidal cell dendrites so that they were similar to Sal- and Oxy-CIS males. Consistent with our earlier studies, Sal- and Oxy-CIS females but not CIS males had elevated DOR densities in MF-CA3 dendritic spines, which we have previously shown are important for opioid-mediated long-term potentiation. In the dentate gyrus, Oxy-CIS females had more DOR-labeled interneurons than Sal-CIS females. Moreover, Sal- and Oxy-CIS females compared to both groups of CIS males had elevated levels of DORs and MORs in GABAergic interneuron dendrites, suggesting capacity for greater synthesis or storage of these receptors in circuits important for opioid-mediated disinhibition. However, more plasmalemmal MORs were on large parvalbumin-containing dendrites of Oxy-CIS males compared to Sal-CIS males, suggesting a limited ability for increased granule cell disinhibition. These results suggest that low levels of DORs in MF-CA3 synapses and hilar GABAergic interneurons may contribute to the attenuation of oxycodone CPP in males exposed to CIS.
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sex differences in the subcellular distribution of corticotropin releasing factor receptor 1 in the rat hippocampus following chronic Immobilization Stress
Neuroscience, 2018Co-Authors: Helena R Mcalinn, Elizabeth M Waters, Bruce S Mcewen, Batsheva Reich, Natalina H Contoreggi, Teresa A Milner, Renata Poulton Kamakura, Andreina G DyerAbstract:Abstract Corticotropin-releasing factor receptors (CRFR1) contribute to Stress-induced adaptations in hippocampal structure and function that can affect learning and memory processes. Our prior studies showed that female rats with elevated estrogens compared to males have more plasmalemmal CRFR1 in CA1 pyramidal cells, suggesting a greater sensitivity to Stress. Here, we examined the distribution of hippocampal CRFR1 following chronic Immobilization Stress (CIS) in female and male rats using immuno-electron microscopy. Without Stress, total CRFR1 dendritic levels were higher in females in CA1 and in males in the hilus; moreover, plasmalemmal CRFR1 was elevated in pyramidal cell dendrites in CA1 in females and in CA3 in males. Following CIS, near-plasmalemmal CRFR1 increased in CA1 pyramidal cell dendrites in males but not to levels of control or CIS females. In CA3 and the hilus, CIS decreased cytoplasmic and total CRFR1 in dendrites in males only. These results suggest that in naive rats, CRF could induce a greater activation of CA1 pyramidal cells in females than males. Moreover, after CIS, which leads to even greater sex differences in CRFR1 by trafficking it to different subcellular compartments, CRF could enhance activation of CA1 pyramidal cells in males but to a lesser extent than either unStressed or CIS females. Additionally, CA3 pyramidal cells and inhibitory interneurons in males have heightened sensitivity to CRF, regardless of Stress state. These sex differences in CRFR1 distribution and trafficking in the hippocampus may contribute to reported sex differences in hippocampus-dependent learning processes in baseline conditions and following chronic Stress.
Richard Kvetnansky - One of the best experts on this subject based on the ideXlab platform.
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repeated Immobilization Stress increases expression of β3 adrenoceptor in the left ventricle and atrium of the rat heart
Stress and Health, 2014Co-Authors: Richard Kvetnansky, Marcela Laukova, Andrej Tillinger, Martina Novakova, Olga Krizanova, Jaromir MyslivecekAbstract:Stress is a contributor of many cardiovascular diseases. Positive inotropic and chronotropic effects of catecholamines are regulated via β-adrenergic receptors (ARs). Many reports exist concerning changes of cardiac β1- and β2-ARs in Stress, but only a few deal with modulation of cardiac β3-AR. Our aim was to analyze the expression and binding sites of β1-, β2- and β3-ARs and adenylyl cyclase activity in the left ventricle, and β3-AR expression and binding in the left atrium of rats exposed to acute and chronic Immobilization Stress (IMO). The concentration of noradrenaline in the ventricle decreased, while adrenaline increased, especially after repeated IMO. The mRNA and protein levels, and binding sites of β3-subtype significantly rose following chronic IMO, while all parameters for β2-AR dropped after single and repeated exposure. Similarly, the mRNA levels and binding sites for β3-subtype increased in the left atrium as a consequence of chronic IMO. The rise in β3-subtypes and a drop in β2-subtypes resulted in inhibition of adenylyl cyclase activity within the left ventricle. Taken together, among other factors, up-regulation of β3-AR could represent an adaptation mechanism, which might be related to altered physiological function of the left ventricle and atrium during prolonged emotional Stress and might serve cardioprotective function during catecholamine overload. Copyright © 2013 John Wiley & Sons, Ltd.
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regulation of angiotensin ii type 2 receptor gene expression in the adrenal medulla by acute and repeated Immobilization Stress
Journal of Endocrinology, 2012Co-Authors: Regina Nostramo, Lidia I Serova, Richard Kvetnansky, Andrej Tillinger, Juan M Saavedra, Ashok Kumar, Varunkumar Pandey, Esther L SabbanAbstract:While the Renin-Angiotensin System is important for adrenomedullary responses to Stress, the involvement of specific angiotensin II receptor subtypes is unclear. We examined gene expression changes of angiotensin II type 1A (AT1A) and type 2 (AT2) receptors in rat adrenal medulla in response to Immobilization Stress (IMO). AT2 receptor mRNA levels decreased immediately after a single 2 h IMO. Repeated IMO also decreased AT2 receptor mRNA levels, but the decline was more transient. AT1A receptor mRNA levels were unaltered with either single or repeated IMO, although binding was increased following repeated IMO. These effects of Stress on angiotensin II receptor expression may alter catecholamine biosynthesis, as tyrosine hydroxylase and dopamine beta-hydroxylase mRNA levels in PC12 cells are decreased with angiotensin II treatment in the presence of ZD7155 (AT1 receptor antagonist), or with {"type":"entrez-protein","attrs":{"text":"CGP42112","term_id":"874777115","term_text":"CGP42112"}}CGP42112 (AT2 receptor agonist) treatment. Involvement of Stress-triggered activation of the hypothalamic-pituitary-adrenocortical (HPA) or sympatho-adrenal axis in AT2 receptor downregulation was examined. Cultured cells treated with the synthetic glucocorticoid dexamethasone displayed a transcriptionally-mediated decrease in AT2 receptor mRNA levels. However, glucocorticoids are not required for the immediate Stress-triggered decrease in AT2 receptor gene expression, as demonstrated in corticotropin-releasing hormone knockout (CRH KO) mice and hypophysectomized rats, although they can regulate basal gene expression. cAMP and pituitary adenylate cyclase-activating polypeptide (PACAP) also reduced AT2 receptor gene expression and may mediate this response. Overall, the effects of Stress on adrenomedullary AT1A and AT2 receptor expression may contribute to allostatic changes, such as regulation of catecholamine biosynthesis.
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increase in rat adrenal phenylethanolamine n methyltransferase mrna level caused by Immobilization Stress depends on intact pituitary adrenocortical axis
Journal of Neurochemistry, 2002Co-Authors: Esther L Sabban, Emil Viskupic, Richard Kvetnansky, Koki Fukuhara, Virginia K Weise, Irwin J Kopin, Joan P SchwartzAbstract:: The effects of a single and of repeated Immobilization Stress on the expression of the final enzyme involved in epinephrine biosynthesis, phenylethanolamine N-methyltransferase (PNMT), are described. A single Immobilization (whether lasting 5 or 120 min) caused a severalfold increase of the adrenal PNMT mRNA level as measured 2 h after the beginning of the procedure. This elevation was of a transient nature, peaked 3–6 h after the 2-h Immobilization, and returned to control values by 12 h after the Stress. When the animals were immobilized for 2 h/day for seven consecutive days, an increase in content of PNMT mRNA of a similar magnitude was observed, which persisted for at least 2 days after the seventh Immobilization. The Immobilization-induced increase was completely abolished in hypophysectomized animals, whereas adrenal denervation failed to prevent it. These data suggest that the Immobilization-induced increase in adrenal PNMT mRNA level depends primarily on pituitary-adrenocortical regulation.
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endogenous glucocorticoids restrain catecholamine synthesis and release at rest and during Immobilization Stress in rats
Endocrinology, 1993Co-Authors: Richard Kvetnansky, Koki Fukuhara, Karel Pacak, Giovanni Cizza, David S Goldstein, Irwin J KopinAbstract:Cardiovascular and metabolic adjustments during Stress involve participation of the sympatho-adrenal and hypothalamic-pituitary-adrenocortical systems, which interact at several levels. The present study investigated the effects of removal of endogenous glucocorticoids on indices of norepinephrine release and metabolism and of catecholamine biosynthesis in sympathetic nerves, at baseline and in response to Immobilization Stress (IMMO) in rats. Plasma levels of the catecholamine precursor dihydroxyphenylalanine, norepinephrine (NE), the NE metabolites dihydroxyphenylglycol and methoxyhydroxyphenylglycol, dopamine, and the dopamine metabolites dihydroxyphenylacetic acid and homovanillic acid were measured in adrenalectomized, adrenal-medullectomized, or sham-operated conscious rats, with or without glucocorticoid treatment (25 mg/kg.24 h cortisol for 7 days by osmotic minipumps), at rest and after 5, 20, 60, and 120 min of IMMO. Adrenalectomy eliminated plasma levels of epinephrine and corticosterone and au...
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Immobilization Stress rapidly decreases hypothalamic corticotropin releasing hormone secretion in vitro in the male 344 n fischer rat
Life Sciences, 1993Co-Authors: Giovanni Cizza, George P Chrousos, Richard Kvetnansky, Maria E Tartaglia, Marc R Blackman, Philip W GoldAbstract:Abstract Corticotropin-Releasing-Hormone (CRH) is the principal secretagogue for plasma ACTH and corticosterone secretion and plays an important role in coordinating a variety of physiological and behavioral responses to Stress. To explore whether there is a rapid change in the secretory response of the hypothalamic CRH neuron during acute Stress, we report here a study of the effects of KCl and norepinephrine (NE) on CRH release in vitro from rat hypothalami explanted after 5, 30, 60, and 120 minutes of Immobilization. We also measured the plasma levels of ACTH, β-endorphin, corticosterone, prolactin, GH, and TSH at these intervals. As the duration of Immobilization increased, KCl and NE-induced CRH release in vitro progressively fell. After reaching a maximal rise after 30 minutes of Immobilization, plasma ACTH, β-endorphin, and prolactin progressively fell in plasma, whereas corticosterone remained elevated up to 120 minutes; TSH and GH secretion rapidly declined and remained suppressed. Taken together, these data suggest that during Immobilization Stress, the responsiveness of the hypothalamic CRH neuron rapidly falls, owing either to CRH depletion and/or desensitization to NE, and this is paralleled by a concomitant decrease in pituitary-adrenal responsiveness.
Lidia I Serova - One of the best experts on this subject based on the ideXlab platform.
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regulation of angiotensin ii type 2 receptor gene expression in the adrenal medulla by acute and repeated Immobilization Stress
Journal of Endocrinology, 2012Co-Authors: Regina Nostramo, Lidia I Serova, Richard Kvetnansky, Andrej Tillinger, Juan M Saavedra, Ashok Kumar, Varunkumar Pandey, Esther L SabbanAbstract:While the Renin-Angiotensin System is important for adrenomedullary responses to Stress, the involvement of specific angiotensin II receptor subtypes is unclear. We examined gene expression changes of angiotensin II type 1A (AT1A) and type 2 (AT2) receptors in rat adrenal medulla in response to Immobilization Stress (IMO). AT2 receptor mRNA levels decreased immediately after a single 2 h IMO. Repeated IMO also decreased AT2 receptor mRNA levels, but the decline was more transient. AT1A receptor mRNA levels were unaltered with either single or repeated IMO, although binding was increased following repeated IMO. These effects of Stress on angiotensin II receptor expression may alter catecholamine biosynthesis, as tyrosine hydroxylase and dopamine beta-hydroxylase mRNA levels in PC12 cells are decreased with angiotensin II treatment in the presence of ZD7155 (AT1 receptor antagonist), or with {"type":"entrez-protein","attrs":{"text":"CGP42112","term_id":"874777115","term_text":"CGP42112"}}CGP42112 (AT2 receptor agonist) treatment. Involvement of Stress-triggered activation of the hypothalamic-pituitary-adrenocortical (HPA) or sympatho-adrenal axis in AT2 receptor downregulation was examined. Cultured cells treated with the synthetic glucocorticoid dexamethasone displayed a transcriptionally-mediated decrease in AT2 receptor mRNA levels. However, glucocorticoids are not required for the immediate Stress-triggered decrease in AT2 receptor gene expression, as demonstrated in corticotropin-releasing hormone knockout (CRH KO) mice and hypophysectomized rats, although they can regulate basal gene expression. cAMP and pituitary adenylate cyclase-activating polypeptide (PACAP) also reduced AT2 receptor gene expression and may mediate this response. Overall, the effects of Stress on adrenomedullary AT1A and AT2 receptor expression may contribute to allostatic changes, such as regulation of catecholamine biosynthesis.
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Immobilization Stress elevates tryptophan hydroxylase mrna and protein in the rat raphe nuclei
Biological Psychiatry, 2004Co-Authors: Firas Chamas, Mark D Underwood, Victoria Arango, Lidia I Serova, Suham Kassir, John J Mann, Esther L SabbanAbstract:Abstract Background Stress triggers adaptive and maladaptive changes in the central nervous system, including activation of the hypothalamic–pituitary–adrenal axis, and can trigger mood disorders and posttraumatic Stress disorder. We examined the effect of Immobilization Stress (IMO) on gene expression of tryptophan hydroxylase (TPH), the rate-limiting enzyme in serotonin biosynthesis, and the role of cortisol in that response. Methods Regular and adrenalectomized Sprague-Dawley rats were exposed to various repetitions of IMO. Tryptophan hydroxylase messenger ribonucleic acid (mRNA) was determined by competitive reverse transcriptase polymerase chain reaction, and TPH protein was examined by immunoblot and immunocytochemistry. Results Elevation of TPH mRNA by IMO was tissue-specific and dose-dependent. A single IMO elicited a threefold rise in TPH mRNA in median raphe nucleus (MRN), but repeated (3×) IMOs were needed for similar response in dorsal raphe nucleus (DRN). Repeated daily IMO, up to 7 days, triggered a robust induction (6–10-fold) in TPH mRNA, accompanied by corresponding rise in TPH protein levels in raphe nuclei but not in the pineal gland. The rise in TPH immunoreactivity was widespread throughout the DRN and MRN. Bilateral adrenalectomy did not prevent the IMO-triggered increase in TPH immunoreactive protein in the raphe nuclei. Conclusions This study reveals adrenal glucocorticoid–independent induction of TPH gene expression in raphe nuclei in response to Immobilization Stress.
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tryptophan hydroxylase mrna levels are elevated by repeated Immobilization Stress in rat raphe nuclei but not in pineal gland
Neuroscience Letters, 1999Co-Authors: Firas Chamas, Lidia I Serova, Esther L SabbanAbstract:Abstract Repeated Stress triggers a wide range of adaptive changes in the central nervous system including the elevation of serotonin (5-HT) metabolism and an increased susceptibility to affective disorders. To begin to examine whether these changes are mediated by alterations in gene expression for tryptophan hydroxylase (TPH), the rate-limiting enzyme in 5-HT biosynthesis, we quantitated its mRNA levels by competitive reverse transcription-polymerase chain reaction (RT-PCR). Repeated Immobilization Stress (2 h, 7 days) elicited a six- or ten-fold rise in TPH mRNA in median raphe nucleus (MRN) and dorsal raphe nucleus (DRN), respectively, without significantly altering TPH mRNA levels in the pineal gland. In contrast, there was little change in mRNA levels for GTP cyclohydrolase I (GTPCH), the rate limiting enzyme in synthesis of the tetrahydrobiopterin (BH4), the obligate cofactor for TPH. This is the first study to reveal Stress-elicited activation of TPH gene expression.
Firas Chamas - One of the best experts on this subject based on the ideXlab platform.
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Immobilization Stress elevates tryptophan hydroxylase mrna and protein in the rat raphe nuclei
Biological Psychiatry, 2004Co-Authors: Firas Chamas, Mark D Underwood, Victoria Arango, Lidia I Serova, Suham Kassir, John J Mann, Esther L SabbanAbstract:Abstract Background Stress triggers adaptive and maladaptive changes in the central nervous system, including activation of the hypothalamic–pituitary–adrenal axis, and can trigger mood disorders and posttraumatic Stress disorder. We examined the effect of Immobilization Stress (IMO) on gene expression of tryptophan hydroxylase (TPH), the rate-limiting enzyme in serotonin biosynthesis, and the role of cortisol in that response. Methods Regular and adrenalectomized Sprague-Dawley rats were exposed to various repetitions of IMO. Tryptophan hydroxylase messenger ribonucleic acid (mRNA) was determined by competitive reverse transcriptase polymerase chain reaction, and TPH protein was examined by immunoblot and immunocytochemistry. Results Elevation of TPH mRNA by IMO was tissue-specific and dose-dependent. A single IMO elicited a threefold rise in TPH mRNA in median raphe nucleus (MRN), but repeated (3×) IMOs were needed for similar response in dorsal raphe nucleus (DRN). Repeated daily IMO, up to 7 days, triggered a robust induction (6–10-fold) in TPH mRNA, accompanied by corresponding rise in TPH protein levels in raphe nuclei but not in the pineal gland. The rise in TPH immunoreactivity was widespread throughout the DRN and MRN. Bilateral adrenalectomy did not prevent the IMO-triggered increase in TPH immunoreactive protein in the raphe nuclei. Conclusions This study reveals adrenal glucocorticoid–independent induction of TPH gene expression in raphe nuclei in response to Immobilization Stress.
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tryptophan hydroxylase mrna levels are elevated by repeated Immobilization Stress in rat raphe nuclei but not in pineal gland
Neuroscience Letters, 1999Co-Authors: Firas Chamas, Lidia I Serova, Esther L SabbanAbstract:Abstract Repeated Stress triggers a wide range of adaptive changes in the central nervous system including the elevation of serotonin (5-HT) metabolism and an increased susceptibility to affective disorders. To begin to examine whether these changes are mediated by alterations in gene expression for tryptophan hydroxylase (TPH), the rate-limiting enzyme in 5-HT biosynthesis, we quantitated its mRNA levels by competitive reverse transcription-polymerase chain reaction (RT-PCR). Repeated Immobilization Stress (2 h, 7 days) elicited a six- or ten-fold rise in TPH mRNA in median raphe nucleus (MRN) and dorsal raphe nucleus (DRN), respectively, without significantly altering TPH mRNA levels in the pineal gland. In contrast, there was little change in mRNA levels for GTP cyclohydrolase I (GTPCH), the rate limiting enzyme in synthesis of the tetrahydrobiopterin (BH4), the obligate cofactor for TPH. This is the first study to reveal Stress-elicited activation of TPH gene expression.
