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Toshiie Sakata - One of the best experts on this subject based on the ideXlab platform.
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Neuronal glucoprivation enhances hypothalamic histamine turnover in rats.
Journal of neurochemistry, 2002Co-Authors: Akihiko Oohara, Mamoru Kurokawa, Hironobu Yoshimatsu, Ryozo Oishi, Kiyomi Saeki, Toshiie SakataAbstract:: Histamine (HA) turnover in the rat hypothalamus following insufficient energy supply due to glucoprivation was examined after administration of insulin or 2-deoxy-d-glucose (2-DG). HA turnover was assessed by accumulation of Tele-Methylhistamine (t-MH), a major metabolite of brain HA, following administration of pargyline. Intraperitoneal injection of 1, 2, and 4 U/kg of insulin, which had no influence on steady-state levels of HA and t-MH, increased pargyline-induced accumulation of t-MH. Accumulation of t-MH due to pargyline was inversely related to the concomitant plasma glucose concentration after different doses of insulin. The level of t-MH accumulated by pargyline did not change compared with that of controls, when a euglycemic condition was maintained or insulin at a dose of 6 mU per rat was infused into the third cerebroventricle. Intracerebroventricular infusion of 24 µmol per rat of 2-DG, which had no influence on steady-state levels of HA and t-MH, increased the level of t-MH enhanced by pargyline. The results indicate that an increase in hypothalamic HA turnover in response to glucoprivation may be involved in homeostatic regulation of energy metabolism in the brain.
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Prostaglandin E2 mediates activation of hypothalamic histamine by interleukin-1beta in rats.
Experimental Biology and Medicine, 1999Co-Authors: Masahiro Kang, Mamoru Kurokawa, Ryuichi Ogawa, Hironobu Yoshimatsu, Toshiie SakataAbstract:The present study was designed to investigate the effects of peripheral interleukin-1beta (IL-1beta) on hypothalamic histamine (HA) systems. Intraperitoneal injection of IL-1beta increased the turnover rate of hypothalamic HA, which was assessed by accumulation of Tele-Methylhistamine after pargyline treatment. IL-1beta increased the activities of both histidine decarboxylase (HDC), an HA synthesizing enzyme, and HA-N-methyltransferase (HMT), an HA catabolizing enzyme. Pretreatment with indomethacin completely blocked the effects induced by IL-1beta on hypothalamic HA. Infusion of prostaglandin E2 (PGE2) into the third cerebroventricle increased the hypothalamic HA turnover rate, and simultaneously activated both HDC and HMT dose-dependently, but intravenous infusion of PGE2 had no effect on the dynamics of hypothalamic HA turnover. These results indicate that hypothalamic PGE2 activated by peripheral administration of IL-1beta, but not by peripheral PGE2, may enhance synthesis and release of hypothalamic HA by activation of HDC, and may facilitate degradation of extracellular histamine by activation of HMT.
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Prostaglandin E2 Mediates Activation of Hypothalamic Histamine by Interleukin‐1β in Rats
Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York N.Y.), 1999Co-Authors: Masahiro Kang, Mamoru Kurokawa, Ryuichi Ogawa, Hironobu Yoshimatsu, Toshiie SakataAbstract:The present study was designed to investigate the effects of peripheral interleukin-1β (IL-1β) on hypothalamic histamine (HA) systems. Intraperitoneal injection of IL-1β increased the turnover rate of hypothalamic HA, which was assessed by accumulation of Tele-Methylhistamine after pargyline treatment. IL-1β increased the activities of both histidine decarboxylase (HDC), an HA synthesizing enzyme, and HA-N-methyltransferase (HMT), an HA catabolizing enzyme. Pretreatment with indomethacin completely blocked the effects induced by IL-1β on hypothalamic HA. Infusion of prostaglandin E2 (PGE2) into the third cerebroventricle increased the hypothalamic HA turnover rate, and simultaneously activated both HDC and HMT dose-dependently, but intravenous infusion of PGE2 had no effect on the dynamics of hypothalamic HA turnover. These results indicate that hypothalamic PGE2 activated by peripheral administration of IL-1β, but not by peripheral PGE2, may enhance synthesis and release of hypothalamic HA by activation of HDC, and may facilitate degradation of extracellular histamine by activation of HMT.
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A physiological role of brain histamine during energy deficiency
Brain research bulletin, 1994Co-Authors: Toshiie Sakata, Mamoru Kurokawa, Akihiko Oohara, Hironobu YoshimatsuAbstract:Abstract Histaminergic activation in the rat hypothalamus was investigated under a deficit in energy supply. Fasting of rats for 24 h increased hypothalamic histamine (HA) content. Intraperitoneal (IP) injection of insulin (2 U/kg) increased pargyline-induced accumulation of Tele-Methylhistamine (t-MH) leaving steady-state HA and t-MH levels unaffected, which implies enhancement of HA turnover rate. The insulin infusion induced hypoglycemia both in rats with and without pargyline pretreatment. Infusion of 2-deoxy- D -glucose (2-DG) into the third cerebroventricle also produced an increase in pargyline-induced accumulation of t-MH and no change in steady-state HA and t-MH levels. The 2-DG infusion induced hyperglycemia. Hypothalamic glycogen content decreased after 24 h starvation, but this decrease was prevented by depletion of HA by α-fluoromethylhistidine. Absolute glycogen contents in the cortex were lower than those in the hypothalamus, and were not affected by fasting or depletion of HA. The results indicate that activation of hypothalamic HA in response to glucoprivation may modulate homeostatic control of energy supply in the brain.
Pekka T Mannisto - One of the best experts on this subject based on the ideXlab platform.
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Brain histamine and histamine H3 receptors following repeated L-histidine administration in rats.
Life sciences, 2003Co-Authors: V. Lozeva, Juhani Tarhanen, Pekka T Mannisto, Martti Attila, Leena TuomistoAbstract:Abstract In order to assess the importance of the chronic increase in precursor availability on central histaminergic mechanisms in rats, nine male Wistar rats received l -histidine orally at a dose of 1000 mg/kg, twice daily (07.00 h and 19.00 h) for 1 week; 9 rats were used as controls. Brain tissue histamine and Tele -Methylhistamine levels, as well as plasma histamine concentration were assayed. Binding properties and regional distribution of the autoregulatory histamine H 3 receptors in brain were studied with [ 3 H]-R-α-Methylhistamine receptor binding and autoradiography. In l -histidine loaded rats, tissue histamine levels in cortex, hypothalamus, and rest of the brain were significantly increased by 40%–70%. Histamine concentrations in cerebellum and plasma, and Tele -Methylhistamine concentrations in cortex and hypothalamus did not change. The binding properties of H 3 receptors in cortex were not altered. However, there were changes in the regional distribution of [ 3 H]-R-α-Methylhistamine binding sites, suggestive of a region-selective up-/down-regulation of histamine H 3 receptors or their receptor sub-types. These results imply that following repeated l -histidine administration in the rat (1) there is enhanced synthesis of brain histamine not reflected in its functional release; (2) the excess of histamine is sequestered and stored rather than being metabolized; (3) histamine H 3 receptor binding properties are not altered, whereas receptor density is changed in selected regions. In conclusion, these results demonstrate that the neuronal mechanisms controlling histamine synthesis, storage, and release are adaptable and allow the sequestration of the excess of histamine in order to prevent excessively high neuronal activity.
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an acute i c v infusion of leptin has no effect on hypothalamic histamine and Tele Methylhistamine contents in wistar rats
European Journal of Pharmacology, 2000Co-Authors: Anne Lecklin, Pekka Hermonen, Juhani Tarhanen, Pekka T MannistoAbstract:The actions of intracerebroventricularly (i.c.v.) infused leptin on food intake, body weight and hypothalamic contents of histamine and Tele-Methylhistamine, the main histamine metabolite in the mammalian brain, were studied in male Wistar rats. The effect of the histamine H1 receptor blockade on leptin-induced anorexia was also examined. It was found that leptin at the dose of 10 μg i.c.v. reduced 24-h food intake by 48% as compared with the controls (P<0.01). This leptin dose reduced feeding during 2–4 consecutive days. In spite of the marked changes in food consumption and body weight gain, leptin did not alter the hypothalamic contents of histamine and Tele-Methylhistamine. Furthermore, the blockade of histamine H1 receptors by mepyramine did not attenuate the effect of leptin on feeding and body weight. The findings indicate that centrally administered leptin suppresses feeding and promotes weight loss through mechanisms that do not require the direct participation of the brain histaminergic neuron system.
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An acute i.c.v. infusion of leptin has no effect on hypothalamic histamine and Tele-Methylhistamine contents in Wistar rats.
European journal of pharmacology, 2000Co-Authors: Anne Lecklin, Pekka Hermonen, Juhani Tarhanen, Pekka T MannistoAbstract:The actions of intracerebroventricularly (i.c.v.) infused leptin on food intake, body weight and hypothalamic contents of histamine and Tele-Methylhistamine, the main histamine metabolite in the mammalian brain, were studied in male Wistar rats. The effect of the histamine H1 receptor blockade on leptin-induced anorexia was also examined. It was found that leptin at the dose of 10 μg i.c.v. reduced 24-h food intake by 48% as compared with the controls (P
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Hypothalamic histamine, growth rate, plasma prolactin and growth hormone levels in rats with long-term portacaval anastomosis.
Inflammation research : official journal of the European Histamine Research Society ... [et al.], 1999Co-Authors: V. Lozeva, Pekka T Mannisto, E. Anttila, Raimo K. Tuominen, Mikko Hippeläinen, Leena TuomistoAbstract:Objective and Design: Histamine can modulate feeding behaviour and hormone release; therefore we examined the hypothalamic histamine system, the growth pattern and the serum levels of prolactin and growth hormone in rats with portacaval anastomosis (PCA).¶Material: The growth rate of 30 PCA- and 30 sham-operated male Han:Wistar rats was monitored for 6 months. Thirteen sham and 9 PCA rats were used for biochemical studies.¶Methods: Histamine was assayed by HPLC, Tele-Methylhistamine by GC-MS, prolactin and growth hormone by RIA. Student's t-test was used to compare the groups.¶Results: Six months after surgery, the PCA rats exhibited marked growth retardation (weight gain of 20 g vs. 140 g for the sham rats; p < 0.001), increased plasma levels of prolactin (9.7 ± 2.4 vs. 3.6 ± 0.6; p < 0.01) and unaltered growth hormone levels (6.2 ± 0.5 vs. 8.1 ± 1.0). A six-fold elevation of histamine concentration (29.5 ± 3.9 vs. 4.8 ± 0.4; p < 0.001) and a two-fold increase of Tele-Methylhistamine levels (1.8 ± 0.1 vs. 0.8 ± 0.02; p < 0.001) were found in hypothalamus.¶Conclusion: We suggest that increased histaminergic activity in the hypothalamus may be involved in the development of growth retardation and in the enhanced basal secretion of prolactin in male rats with long-term PCA.
Leena Tuomisto - One of the best experts on this subject based on the ideXlab platform.
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increased concentrations of histamine and its metabolite Tele Methylhistamine and down regulation of histamine h3 receptor sites in autopsied brain tissue from cirrhotic patients who died in hepatic coma
Journal of Hepatology, 2003Co-Authors: Violina Lozeva, Juhani Tarhanen, Leena Tuomisto, Roger F ButterworthAbstract:Abstract Background/Aims : Hepatic encephalopathy (HE) is a serious neuropsychiatric complication of chronic liver disease. To determine whether changes in the central histaminergic system are a feature of human HE, we studied histamine, Tele -Methylhistamine, and presynaptic autoregulatory H 3 receptors in cerebral cortex and caudate–putamen obtained at autopsy from six cirrhotic patients and six appropriately matched controls. Methods : Histamine was assayed by HPLC; Tele -Methylhistamine by GC-MS. H 3 receptors were studied by in vitro receptor binding using [ 3 H]R-α-Methylhistamine as ligand. Results : In HE patients, there was a significant fourfold increase of histamine in caudate–putamen and a significant increase in all cortical regions studied. Tele -Methyhistamine was also increased and the densities of histamine H 3 receptor sites were significantly decreased in patient material. Conclusions : These findings are consistent with activation of the histaminergic system in HE. Given that histamine participates in the regulation of arousal and circadian rhythmicity, they indicate that induction of central histamine mechanisms may contribute to the development of neuropsychiatric symptoms, such as sleep disturbances and altered circadian rhythms in chronic HE and suggest that pharmacological manipulation of the histaminergic system could be beneficial in the treatment of HE in chronic liver failure.
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Brain histamine and histamine H3 receptors following repeated L-histidine administration in rats.
Life sciences, 2003Co-Authors: V. Lozeva, Juhani Tarhanen, Pekka T Mannisto, Martti Attila, Leena TuomistoAbstract:Abstract In order to assess the importance of the chronic increase in precursor availability on central histaminergic mechanisms in rats, nine male Wistar rats received l -histidine orally at a dose of 1000 mg/kg, twice daily (07.00 h and 19.00 h) for 1 week; 9 rats were used as controls. Brain tissue histamine and Tele -Methylhistamine levels, as well as plasma histamine concentration were assayed. Binding properties and regional distribution of the autoregulatory histamine H 3 receptors in brain were studied with [ 3 H]-R-α-Methylhistamine receptor binding and autoradiography. In l -histidine loaded rats, tissue histamine levels in cortex, hypothalamus, and rest of the brain were significantly increased by 40%–70%. Histamine concentrations in cerebellum and plasma, and Tele -Methylhistamine concentrations in cortex and hypothalamus did not change. The binding properties of H 3 receptors in cortex were not altered. However, there were changes in the regional distribution of [ 3 H]-R-α-Methylhistamine binding sites, suggestive of a region-selective up-/down-regulation of histamine H 3 receptors or their receptor sub-types. These results imply that following repeated l -histidine administration in the rat (1) there is enhanced synthesis of brain histamine not reflected in its functional release; (2) the excess of histamine is sequestered and stored rather than being metabolized; (3) histamine H 3 receptor binding properties are not altered, whereas receptor density is changed in selected regions. In conclusion, these results demonstrate that the neuronal mechanisms controlling histamine synthesis, storage, and release are adaptable and allow the sequestration of the excess of histamine in order to prevent excessively high neuronal activity.
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Increased brain histamine levels in Parkinson's disease but not in multiple system atrophy.
Journal of neurochemistry, 2002Co-Authors: Juha O. Rinne, Leena Tuomisto, Oleg Anichtchik, Krister Eriksson, Jan Kaslin, Hannu Kalimo, Matias Röyttä, Pertti PanulaAbstract:We investigated histamine concentration in post-mortem brain samples of patients with Parkinson's disease (PD, n = 24), multiple system atrophy (MSA, n = 8) and age-matched controls (n = 27). Histamine concentrations were significantly increased in the putamen (to 159% of the control mean), substantia nigra pars compacta (to 201%), internal globus pallidus (to 234%) and external globus pallidus (to 200%), i.e. in areas which play a crucial role in the motor behaviour and which show typical functional alterations in PD. In MSA no significant differences were seen. Tele-Methylhistamine (histamine metabolite) concentrations were unchanged in PD. These results indicate that histamine concentration, but not its metabolism is increased in PD, but not in MSA. This finding may have implications in developing new drug therapies for PD and in differential diagnosis between PD and MSA.
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Hypothalamic histamine, growth rate, plasma prolactin and growth hormone levels in rats with long-term portacaval anastomosis.
Inflammation research : official journal of the European Histamine Research Society ... [et al.], 1999Co-Authors: V. Lozeva, Pekka T Mannisto, E. Anttila, Raimo K. Tuominen, Mikko Hippeläinen, Leena TuomistoAbstract:Objective and Design: Histamine can modulate feeding behaviour and hormone release; therefore we examined the hypothalamic histamine system, the growth pattern and the serum levels of prolactin and growth hormone in rats with portacaval anastomosis (PCA).¶Material: The growth rate of 30 PCA- and 30 sham-operated male Han:Wistar rats was monitored for 6 months. Thirteen sham and 9 PCA rats were used for biochemical studies.¶Methods: Histamine was assayed by HPLC, Tele-Methylhistamine by GC-MS, prolactin and growth hormone by RIA. Student's t-test was used to compare the groups.¶Results: Six months after surgery, the PCA rats exhibited marked growth retardation (weight gain of 20 g vs. 140 g for the sham rats; p < 0.001), increased plasma levels of prolactin (9.7 ± 2.4 vs. 3.6 ± 0.6; p < 0.01) and unaltered growth hormone levels (6.2 ± 0.5 vs. 8.1 ± 1.0). A six-fold elevation of histamine concentration (29.5 ± 3.9 vs. 4.8 ± 0.4; p < 0.001) and a two-fold increase of Tele-Methylhistamine levels (1.8 ± 0.1 vs. 0.8 ± 0.02; p < 0.001) were found in hypothalamus.¶Conclusion: We suggest that increased histaminergic activity in the hypothalamus may be involved in the development of growth retardation and in the enhanced basal secretion of prolactin in male rats with long-term PCA.
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Diurnal and age-related changes in cerebrospinal fluid Tele-Methylhistamine levels during infancy and childhood.
Pharmacology biochemistry and behavior, 1994Co-Authors: Tuula Kiviranta, Leena Tuomisto, Eila AiraksinenAbstract:Abstract Histamine is a neurotransmitter participating in many physiological functions and behavior, including control of arousal and modulation of the circadian rhythms. Diurnal variation in cerebrospinal fluid (CSF) levels of Tele-Methylhistamine(t-MH), the main histamine metabolite, has been detected in several animal studies. In humans, such changes have not been described. Little is known on the development of histaminergic neurons in human brain. In children, the levels of CSF t-MH are not known. Therefore, we have measured the concentrations of CSF t-MH in 81 chidren, age ranging from 3 months to 14.6 years. t-MH levels were higher in infants, and near adult values were measured in adolescents, the relation between CSF t-MH and age being; CSF t-MH = −0.217 year + 7.31 (n = 81, r = 0.26, p = 0.021). The mean t-MH concentration was higher during the daytime (7.07 ± 0.46 pmol/ml, mean ± SEM) than in the night (5.35 ± 0.60 pmol/ml, p = 0.0019, ANOVA). The results show a developmental change in the concentration of t-MH during childhood and a difference in t-MH levels between the daytime and night indicating a more active metabolism of brain HA in the waking period.
Yves Dauvilliers - One of the best experts on this subject based on the ideXlab platform.
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Cerebrospinal fluid levels of orexin-A and histamine, and sleep profile within the Alzheimer process
Neurobiology of Aging, 2017Co-Authors: Audrey Gabelle, Philippe Robert, Isabelle Jaussent, Christophe Hirtz, Jérôme Vialaret, Sophie Navucet, Caroline Grasselli, Sylvain Lehmann, Yves DauvilliersAbstract:To better understand how sleep/wake dysregulation affects Alzheimer's disease (AD), we compared the cerebrospinal fluid (CSF) orexin and histamine/Tele-Methylhistamine (HA/t-MHA) levels of 82 patients (41 probable-AD-high level of evidence, 41 mild cognitive impairment MCI-due-to-AD), 24 other neurologic disorders (OND) and 24 controls. We determined the relationships between these biomarkers, the CSF AD biomarkers concentrations, and the clinical sleep profile. CSF orexin-A but not HA/t-MHA levels were higher in MCI and AD than OND and controls. CSF orexin-A is correlated to CSF amyloid-β42in MCI and AD, independently of age, gender, MMSE, total-tau/phosphorylated-tau, HA or sleep parameters. Nighttime sleep duration was longer in MCI and AD patients than controls. In MCI, nighttime sleep duration negatively correlated with CSF amyloid-β42 and MMSE. To conclude, CSF orexin-A but not HA/t-HMA was upregulated in AD and correlated with amyloid-β42 level. Our data suggested a change in the sleep-wake pattern at an early stage of the disease that needs further investigation to deeply explain the mechanistic interplay between sleep and Alzheimer.
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Temporal Changes in the Cerebrospinal Fluid Level of Hypocretin-1 and Histamine in Narcolepsy.
Sleep, 2017Co-Authors: Régis Lopez, Philippe Robert, Isabelle Jaussent, Lucie Barateau, Elisa Evangelista, Sofiene Chenini, Yves DauvilliersAbstract:Study Objectives To follow the temporal changes of cerebrospinal fluid (CSF) biomarker levels in narcoleptic patients with unexpected hypocretin level at referral. Methods From 2007 to 2015, 170 human leukocyte antigen (HLA) DQB1*06:02-positive patients with primary narcolepsy and definite (n = 155, 95 males, 60 females, 36 children) or atypical cataplexy (n = 15, 4 males, 3 children) were referred to our center. Cerebrospinal hypocretin deficiency was found in 95.5% and 20% of patients with definitive and atypical cataplexy, respectively. CSF hypocretin-1 (n = 6) and histamine/Tele-Methylhistamine (n = 5) levels were assessed twice (median interval: 14.4 months) in four patients with definite and in two with atypical cataplexy and hypocretin level greater than 100 pg/mL at baseline. Results CSF hypocretin levels decreased from normal/intermediate to undetectable levels in three of the four patients with definite cataplexy and remained stable in the other (>250 pg/mL). Hypocretin level decreased from 106 to 27 pg/mL in one patient with atypical cataplexy, and remained stable in the other (101 and 106 pg/mL). CSF histamine and Tele-Methylhistamine levels remained stable, but for one patient showing increased frequency of cataplexy and a strong decrease (-72.5%) of Tele-Methylhistamine levels several years after disease onset. No significant association was found between relative or absolute change in hypocretin level and demographic/clinical features. Conclusions These findings show that in few patients with narcolepsy with cataplexy, symptoms and CSF marker levels can change over time. In these rare patients with cataplexy without baseline hypocretin deficiency, CSF markers should be monitored over time with potential for immune therapies in early stages to try limiting hypocretin neuron loss.
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Preliminary results on CSF biomarkers for hypothalamic dysfunction in Kleine–Levin syndrome
Sleep medicine, 2014Co-Authors: Régis Lopez, Lucie Barateau, Sofiene Chenini, Yves DauvilliersAbstract:Abstract Objective To measure CSF biomarkers of hypothalamic dysfunction in patients with typical Kleine–Levin syndrome (KLS) during symptomatic and asymptomatic periods. Patients/methods Two patients with typical KLS were admitted during symptomatic and asymptomatic periods to a research Sleep Disorders Center. Cerebrospinalfluid (CSF) hypocretin-1, histamine (HA), and its major metabolite Tele -Methylhistamine (t-MHA) levels were measured in two KLS patients in and out of episode. Results CSF biomarkers of hypothalamic dysfunction measured in two KLS patients in and out of episode revealed low hypocretin levels (within the narcolepsy–cataplexy range) during a hypersomnia episode in the more severe patient, and a 42% decrease (although within normal range) in the second patient. CSF HA and t-MHA measurements in and out of episode revealed a two-fold in-episode decrease in HA in the more severe patient, with no significant change for the second patient, nor for t-MHA levels. Conclusion We reported reversible changes in CSF hypothalamic biomarkers in a typical patient with KLS that reinforces the hypothesis that in some patients KLS episodes may be caused by recurrent functional alterations of the hypothalamus.
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Normal cerebrospinal fluid histamine and Tele-Methylhistamine levels in hypersomnia conditions.
Sleep, 2012Co-Authors: Yves Dauvilliers, Jean-charles Schwartz, Nathalie Delallée, Isabelle Jaussent, Sabine Scholz, Sophie Bayard, Mickael Croyal, Philippe RobertAbstract:STUDY OBJECTIVES To determine the activity of cerebral histaminergic system evaluated by CSF levels of histamine (HA) and Tele-Methylhistamine (t-MHA), its major metabolite, and their relationships with hypocretin-1 levels in a large population of patients with hypersomnia and neurological conditions. DESIGN sensitive liquid chromatographic-electrospray/tandem mass spectrometric assay was developed for the simultaneous quantification of CSF HA and t-MHA. SETTING ata were collected and CSF hypocretin-1 levels were measured using radioimmunoassay at the Sleep Disorders Center, Montpellier, France. CSF HA and t-MHA were measured in Bioprojet-Biotech, France PARTICIPANTS One hundred fourteen unrelated patients with a suspicion of central hypersomnia underwent one night of polysomnography followed by the multiple sleep latency test. Sleep disorders were diagnosed clinically and using sleep studies: narcolepsy-cataplexy NC (n = 56), narcolepsy without cataplexy NwC (n = 27), idiopathic hypersomnia IH (n = 11), secondary narcolepsy (n = 3), and unspecified hypersomnia Uns EDS (n = 17). Fifty neurological patients without daytime sleepiness were included as controls. MEASUREMENTS AND RESULTS No between-hypersomnia group differences were found for CSF HA levels (median 708.62 pM extreme range [55.92-3335.50] in NC; 781.34 [174.08-4391.50] in NwC; 489.42 [177.45-906.70] in IH, and 1155.40 [134.80-2736.59] in Uns EDS) or for t-MHA levels. No association was found between CSF HA, t-MHA, or HA + t-MHA, sleepiness, treatment intake, and frequency of cataplexy. A slight negative correlation was found between age and HA levels. Further adjustment for the age revealed no significant HA levels difference between hypersomnia patients and controls. CONCLUSION CSF histamine and Tele-Methylhistamine did not significantly differ between patients with narcolepsy-cataplexy and other etiologies of non-hypocretin-1 deficient central hypersomnias; these measurements, therefore, are not useful in assessing the etiology or severity of centrally mediated hypersomnia.
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Histamine and Tele-Methylhistamine quantification in cerebrospinal fluid from narcoleptic subjects by liquid chromatography tandem mass spectrometry with precolumn derivatization.
Analytical biochemistry, 2010Co-Authors: Mikaël Croyal, Yves Dauvilliers, Olivier Labeeuw, Marc Capet, Jean-charles Schwartz, Philippe RobertAbstract:An ultra-performance liquid chromatography tandem mass spectrometry (UPLC™-MS/MS) assay was developed for the simultaneous analysis of histamine, its major metabolite Tele-Methylhistamine, and an internal standard (N-Tele-(R)-α-diMethylhistamine) from human cerebrospinal fluid (CSF) samples. The method involves derivatization of primary amines with 4-bromobenzenesulfonyl chloride and subsequent analysis by reversed phase liquid chromatography with mass spectrometry detection and positive electrospray ionization. The separation of derivatized biogenic amines was achieved within 3.5 min on an Acquity® BEH C(18) column by elution with a linear gradient of acetonitrile/water/formic acid (0.1%). The assay was linear in the concentration range of 50-5000 pM for each amine (5.5-555 pg/ml for histamine and 6.25-625 pg/ml for Tele-Methylhistamine). For repeatability and precision determination, coefficients of variation (CVs) were less than 11.0% over the tested concentration ranges, within acceptance criteria. Thus, the developed method provides the rapid, easy, highly sensitive, and selective requirement to quantify these amines in human CSF. No significant difference was found in the mean ± standard error levels of these amines between a group of narcoleptic patients (histamine=392 ± 64 pM, Tele-Methylhistamine=2431 ± 461 pM, n=7) and of neurological control subjects (histamine=402 ± 72 pM, Tele-Methylhistamine=2209 ± 463 pM, n=32).
Hironobu Yoshimatsu - One of the best experts on this subject based on the ideXlab platform.
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Neuronal glucoprivation enhances hypothalamic histamine turnover in rats.
Journal of neurochemistry, 2002Co-Authors: Akihiko Oohara, Mamoru Kurokawa, Hironobu Yoshimatsu, Ryozo Oishi, Kiyomi Saeki, Toshiie SakataAbstract:: Histamine (HA) turnover in the rat hypothalamus following insufficient energy supply due to glucoprivation was examined after administration of insulin or 2-deoxy-d-glucose (2-DG). HA turnover was assessed by accumulation of Tele-Methylhistamine (t-MH), a major metabolite of brain HA, following administration of pargyline. Intraperitoneal injection of 1, 2, and 4 U/kg of insulin, which had no influence on steady-state levels of HA and t-MH, increased pargyline-induced accumulation of t-MH. Accumulation of t-MH due to pargyline was inversely related to the concomitant plasma glucose concentration after different doses of insulin. The level of t-MH accumulated by pargyline did not change compared with that of controls, when a euglycemic condition was maintained or insulin at a dose of 6 mU per rat was infused into the third cerebroventricle. Intracerebroventricular infusion of 24 µmol per rat of 2-DG, which had no influence on steady-state levels of HA and t-MH, increased the level of t-MH enhanced by pargyline. The results indicate that an increase in hypothalamic HA turnover in response to glucoprivation may be involved in homeostatic regulation of energy metabolism in the brain.
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Prostaglandin E2 mediates activation of hypothalamic histamine by interleukin-1beta in rats.
Experimental Biology and Medicine, 1999Co-Authors: Masahiro Kang, Mamoru Kurokawa, Ryuichi Ogawa, Hironobu Yoshimatsu, Toshiie SakataAbstract:The present study was designed to investigate the effects of peripheral interleukin-1beta (IL-1beta) on hypothalamic histamine (HA) systems. Intraperitoneal injection of IL-1beta increased the turnover rate of hypothalamic HA, which was assessed by accumulation of Tele-Methylhistamine after pargyline treatment. IL-1beta increased the activities of both histidine decarboxylase (HDC), an HA synthesizing enzyme, and HA-N-methyltransferase (HMT), an HA catabolizing enzyme. Pretreatment with indomethacin completely blocked the effects induced by IL-1beta on hypothalamic HA. Infusion of prostaglandin E2 (PGE2) into the third cerebroventricle increased the hypothalamic HA turnover rate, and simultaneously activated both HDC and HMT dose-dependently, but intravenous infusion of PGE2 had no effect on the dynamics of hypothalamic HA turnover. These results indicate that hypothalamic PGE2 activated by peripheral administration of IL-1beta, but not by peripheral PGE2, may enhance synthesis and release of hypothalamic HA by activation of HDC, and may facilitate degradation of extracellular histamine by activation of HMT.
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Prostaglandin E2 Mediates Activation of Hypothalamic Histamine by Interleukin‐1β in Rats
Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York N.Y.), 1999Co-Authors: Masahiro Kang, Mamoru Kurokawa, Ryuichi Ogawa, Hironobu Yoshimatsu, Toshiie SakataAbstract:The present study was designed to investigate the effects of peripheral interleukin-1β (IL-1β) on hypothalamic histamine (HA) systems. Intraperitoneal injection of IL-1β increased the turnover rate of hypothalamic HA, which was assessed by accumulation of Tele-Methylhistamine after pargyline treatment. IL-1β increased the activities of both histidine decarboxylase (HDC), an HA synthesizing enzyme, and HA-N-methyltransferase (HMT), an HA catabolizing enzyme. Pretreatment with indomethacin completely blocked the effects induced by IL-1β on hypothalamic HA. Infusion of prostaglandin E2 (PGE2) into the third cerebroventricle increased the hypothalamic HA turnover rate, and simultaneously activated both HDC and HMT dose-dependently, but intravenous infusion of PGE2 had no effect on the dynamics of hypothalamic HA turnover. These results indicate that hypothalamic PGE2 activated by peripheral administration of IL-1β, but not by peripheral PGE2, may enhance synthesis and release of hypothalamic HA by activation of HDC, and may facilitate degradation of extracellular histamine by activation of HMT.
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A physiological role of brain histamine during energy deficiency
Brain research bulletin, 1994Co-Authors: Toshiie Sakata, Mamoru Kurokawa, Akihiko Oohara, Hironobu YoshimatsuAbstract:Abstract Histaminergic activation in the rat hypothalamus was investigated under a deficit in energy supply. Fasting of rats for 24 h increased hypothalamic histamine (HA) content. Intraperitoneal (IP) injection of insulin (2 U/kg) increased pargyline-induced accumulation of Tele-Methylhistamine (t-MH) leaving steady-state HA and t-MH levels unaffected, which implies enhancement of HA turnover rate. The insulin infusion induced hypoglycemia both in rats with and without pargyline pretreatment. Infusion of 2-deoxy- D -glucose (2-DG) into the third cerebroventricle also produced an increase in pargyline-induced accumulation of t-MH and no change in steady-state HA and t-MH levels. The 2-DG infusion induced hyperglycemia. Hypothalamic glycogen content decreased after 24 h starvation, but this decrease was prevented by depletion of HA by α-fluoromethylhistidine. Absolute glycogen contents in the cortex were lower than those in the hypothalamus, and were not affected by fasting or depletion of HA. The results indicate that activation of hypothalamic HA in response to glucoprivation may modulate homeostatic control of energy supply in the brain.
