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M Kang

Publications and source records attributed to M Kang.

69 records · Page 4Linked to original sources
PubMed1995

Zinc modulation of GABAA receptor-mediated chloride flux in rat hippocampal slices.

We studied the effect of ZnCl2 application on GABAA receptor-mediated 36CI- flux in microsacs prepared from whole rat hippocampus and in region-specific hippocampal slices. Slices were obtained from the dentate gyrus (DG), which contains the zinc-enriched hilar region, and from the CA1 region which contains lower levels of endogenous zinc. Muscimol (10 microM)-evoked 36Cl- flux was significantly reduced by ZnCl2 (100 microM) in hippocampal microsacs. In hippocampal slices, muscimol (50 microM)-evoked 36Cl- efflux was higher in CA1 (112.5 +/- 27.9% above basal efflux rate) than in DG slices (29.7 +/- 5.6%). In the presence of ZnCl2, the muscimol effect on efflux rate in CA1 and DG regions was decreased to 10.6 +/- 5.4% and 6.9 +/- 4.9%, respectively. Preincubation with the zinc chelator, tetrakis(2-pyridylmethyl)ethylenediamine (TPEN, 20 microM), caused a significant increase in muscimol-evoked 36Cl- efflux only in DG slices (57.2 +/- 7.0%), suggesting that GABAA receptors in the DG of rat hippocampus under physiological conditions may function under the inhibitory influence of endogenous chelatable zinc. In intracellular recordings, ZnCl2 (100 microM) application had no effect on the responses to GABA applied perisomatically or in the dendritic region of CA1 neurons. The lack of Zn2+ effect on the postsynaptic GABAA receptor-mediated responses suggests that the decreases of the 36Cl- efflux observed in the biochemical assays may be due to zinc action on neurons other than the principal pyramidal CA1 cells, and possibly the non-neuronal cell populations.

Animals↗
PubMed1995

Hypothalamic neuronal histamine modulates adaptive behavior and thermogenesis in response to endogenous pyrogen.

Homeostatic involvement of hypothalamic neuronal histamine in adaptive behavior and thermogenesis was investigated when interleukin-1 beta (IL-1 beta), one of the endogenous pyrogens, was infused peripherally in rats. IL-1 beta decreased food and water intake and elevated body temperature. Depletion of neuronal histamine in the hypothalamus induced by alpha-fluoromethylhistidine, a suicide inhibitor of the histamine synthesizing enzyme histidine decarboxylase (HDC), attenuated the suppressive effect of IL-1 beta on food intake, facilitated the inhibitory effect on water intake, and enhanced its thermogenic effect. Simultaneously IL-1 beta increased activity of HDC and histamine-N-methyltransferase (HMT), a neuronal histamine catabolizing enzyme. Pretreatment with indomethacin completely blocked those increases in turnover of neuronal histamine induced by IL-1 beta. Hypothalamic prostaglandin E2 (PGE2) activated by peripheral IL-1 beta, but not peripheral PGE2, increased both activities of HDC and HMT. Ginsenoside Rg1, a major component of panax ginseng, modulated the suppressive effects of IL-1 beta on ingestive behavior, resulting in a lowering of body temperature. The findings suggest that the effects of IL-1 beta on ingestive behavior and thermogenesis may be modulated by dynamics of hypothalamic neuronal histamine through activation of hypothalamic PGE2 which is elevated by peripheral IL-1 beta.

Adaptation, Physiological↗
PubMed1995

Ginsenoside Rg1 modulates ingestive behavior and thermal response induced by interleukin-1 beta in rats.

Effects of ginsenoside Rg1 (Rg1), a major component of panax ginseng, on changes in ingestive behavior and rectal temperature induced by interleukin-1 beta (IL-1 beta) were investigated in rats. Intraperitoneal (ip) injection of IL-1 beta suppressed food and water intake and elevated rectal temperature. The suppressive effect of IL-1 beta on water intake was converted to an increase when 4.0 mM Rg1 was continuously infused into the third cerebroventricle (ICV) at a rate of 0.966 microliters/h. The elevation of rectal temperature induced by IL-1 beta was attenuated by ICV infusion of Rg1. The feeding suppression caused by IL-1 beta was unaffected by ICV infusion of Rg1. These results suggest that sustained ICV infusion of Rg1 may modulate the effects of IL-1 beta on ingestive behaviors, i.e., increase in water intake and sustained decrease in food intake, resulting in a lowering of body temperature.

Animals↗
PubMed1995

Hypothalamic neuronal histamine modulates physiological responses induced by interleukin-1 beta.

Dynamic involvement of hypothalamic histamine in ingestive behavior and thermogenesis induced by interleukin-1 beta (IL-1 beta) was examined in rats. Intraperitoneal injection of 0.12 nmol/rat IL-1 beta decreased food and water intake and elevated body temperature. However, depletion of neuronal histamine induced by intraperitoneal injection of 160 mumol/rat alpha-fluoromethylhistidine, a suicide inhibitor of histidine decarboxylase (HDC), attenuated the suppressive effect of IL-1 beta on food intake, facilitated the suppressive effect on drinking, and enhanced the elevating effect on rectal temperature. Intraperitoneal injection of 0.12 nmol/rat IL-1 beta increased hypothalamic histamine turnover rate. The same dose of IL-1 beta also increased activity of HDC and histamine-N-methyltransferase (HMT). These results suggest that IL-1 beta may stimulate synthesis and release of hypothalamic histamine in presynaptic terminals by activation of HDC and facilitate degradation of extracellular histamine by activation of MHT. These changes in the dynamics of hypothalamic histamine modulate IL-1 beta-induced ingestive behavior and body temperature.

Animals↗
PubMed1995

Histamine effect on ornithine decarboxylase of rat intestine in cases of ischemia-reperfusion compared with refeeding.

Our previous study suggested that histamine might enhance the increase of ornithine decarboxylase activity in injured intestinal mucosa. To test this hypothesis, we measured histamine content in mesenteric lymph and ornithine decarboxylase activity in intestinal mucosa after ischemia-reperfusion in the rat. We examined the effect of alpha-fluoromethylhistidine, a suicide inhibitor of histidine decarboxylase, on ornithine decarboxylase activity after ischemia-reperfusion and compared this with its effect on the rat after refeeding. Ischemia-reperfusion was performed by 15-min occlusion of the superior mesenteric artery. After ischemia-reperfusion, histamine content in mesenteric lymph increased, and this increase was completely suppressed by alpha-fluoromethylhistidine pretreatment. In contrast to ischemia-reperfusion, histamine content in mesenteric lymph did not change after refeeding. Ornithine decarboxylase activity increased markedly 3 and 6 hr after ischemia-reperfusion and refeeding, whereas alpha-fluoromethylhistidine attenuated the increase in ornithine decarboxylase activity only in the ischemia-reperfusion group. These results indicate that increase in histamine synthesis in the intestinal mucosa plays an important role in the increase of ornithine decarboxylase activity after ischemia-reperfusion but that histamine is not related to the increase in ornithine decarboxylase activity after refeeding.

Animals↗
PubMed1994

Role of histamine receptors in intestinal repair after ischemia-reperfusion in rats.

BACKGROUND/AIMS: Previously, we showed that an elevated production of histamine promotes the healing of injured intestinal mucosa after ischemia-reperfusion. The aim of the present study was to determine whether histamine-mediated repair of the intestinal mucosa after ischemia-reperfusion involves the engagement of H1 or H2 receptors. METHODS: The superior mesenteric artery was occluded for 15 minutes followed by reperfusion, and H1- or H2-receptor antagonists were infused intraduodenally. After ischemia-reperfusion, ornithine decarboxylase activity in the jejunal mucosa and lipid transport to mesenteric lymph were examined. RESULTS: In jejunal mucosa, ornithine decarboxylase activity markedly increased at 6 hours after reperfusion and remained elevated at 48 hours. The ischemia-reperfusion-induced increase in ornithine decarboxylase activity was attenuated (in a dose-dependent manner) by an H1-receptor antagonist (chlorpheniramine maleate) but not by an H2 antagonist (cimetidine). Intraperitoneal injection of an H3 antagonist (thioperamide) increased histamine output in mesenteric lymph and stimulated intestinal ornithine decarboxylase activity. Transport of dietary lipid into mesenteric lymph was depressed 24 hours after an ischemic insult, yet it returned to the normal level 48 hours after ischemia-reperfusion. The recovery of the lipid transport normally observed at 48 hours after ischemia-reperfusion was attenuated by the H1 antagonist. CONCLUSIONS: The beneficial effects of histamine on the repair of intestinal mucosa after ischemia-reperfusion results from the engagement and activation of the H1 receptor.

Animals↗
PubMed1994

Thermoregulation and hypothalamic histamine turnover modulated by interleukin-1 beta in rats.

To clarify the involvement of hypothalamic histamine in thermogenic response provoked by high ambient temperature, or interleukin-1 beta (IL-1 beta), changes in rectal temperature and histamine turnover were investigated. Rectal temperature was maintained normally after exposure to high ambient temperature, but elevated by IL-1 beta. In spite of these different responses of body temperature, hypothalamic histamine turnover was increased in each treatment. The results suggest that hypothalamic histaminergic neurons are activated not only peripherally by high ambient temperature, but also centrally by IL-1 beta as endogenous pyrogen.

Animals↗
PubMed1994

2-deoxy-D-glucose suppresses food intake through activation of hypothalamic histamine in rats.

The aim of this experiment was to demonstrate whether brain histamine contributes to delayed suppression of food intake after administration of 2-deoxy-D-glucose (2-DG). Food intake decreased significantly for 48 h after infusion of 2-DG into the rat third cerebroventricle. This delayed decrease in food intake was abolished by depletion of neuronal histamine by intraperitoneal pretreatment with alpha-fluoromethylhistidine (160 mumol/rat), a suicide inhibitor of a histamine-synthesizing enzyme. Intracerebroventricular infusion of 24 mumol 2-DG accelerated turnover rate of hypothalamic histamine. These results indicate that the delayed feeding suppression by 2-DG is modulated through histaminergic neurons in the hypothalamus. This histaminergic response may be related, at least in part, to homeostatic control of energy metabolism in the brain.

Animals↗
PubMed1993

Aminoglucose-induced feeding suppression is regulated by hypothalamic neuronal histamine in rats.

Central mechanisms involved in feeding suppression produced by 1-deoxy-D-glucosamine (1-DGlcN) and 1-deoxy-N-acetylglucosamine (1-DGlcNAc) are unclear. To clarify the mechanisms, we investigated the role of hypothalamic neuronal histamine (HA) in feeding suppression induced by 1-DGlcN and 1-DGlcNAc in rats. Food intake was suppressed for 3 days after a single infusion of 24 mumol 1-DGlcN into the third cerebroventricle (i.c.v.). Depletion of presynaptic HA due to intraperitoneal infusion (i.p.) of alpha-fluoromethylhistidine (FMH), a specific inhibitor of the HA synthesizing enzyme histidine decarboxylase (HDC), abolished feeding suppression completely. Blockade of postsynaptic H1-receptors by i.p. injection of 26 mumol chlorpheniramine also abolished the suppression. Oral administration of 2.4 mmol 1-DGlcNAc suppressed food intake. However, depletion of neuronal HA due to FMH did not affect the suppression. I.c.v. infusion of 24 mumol 1-DGlcN increased turnover rate of HA at 1 h after the infusion. Hypothalamic HA concentration, but not that of tele-methylhistamine (t-MH), increased at 24 h after i.c.v. infusion of 1-DGlcN, which suggests a correlation between HA concentration and the behavioral response. These results indicate that 1-DGlcN, but not 1-DGlcNAc, modulates feeding suppression through HA neurons in the hypothalamus. Differences in mechanisms of feeding suppression by these aminoglucoses may depend on the principal sites of action in the brain and/or peripheral organs.

Acetylglucosamine↗
PubMed1993

Abnormalities in obese Zuckers: defective control of histaminergic functions.

Histaminergic functions in the hypothalamus of Zucker obese rats were investigated. Blockade of postsynaptic H1-receptor after infusion of chlorpheniramine into the third cerebroventricle (ICV) failed to affect feeding in obese Zuckers, although feeding was potently elicited in Wistar King A control rats. Presynaptic increase in histamine by an H3-receptor antagonist, thioperamide, suppressed feeding in Wistar controls, but not in obese Zuckers. Under high ambient temperature, Wistar controls decreased food intake and maintained their rectal temperature normally. However, obese Zuckers and histamine depleted rats due to alpha-fluoromethyl-histidine (FMH), a specific "suicide" inhibitor of a histamine synthesizing decarboxylase enzyme (HDC), failed to show this decrease in food intake as adaptive behavior. Their rectal temperature concomitantly elevated in response to heated circumstance. ICV infusion of thioperamide increased the blood glucose level in Wistar controls, but not in obese Zuckers. The defect in all these regulatory functions found in obese Zuckers may be derived from an excessive decrease in hypothalamic histamine content due to inactivity of HDC. The histamine-depleted model sufficiently mimicked the abnormalities in obese Zuckers.

Animals↗
PubMed1984

Circadian rhythms and patterns of running-wheel activity, feeding and drinking behaviors of old male rats.

Running-wheel activity of 7 young adult male rats (3 to 6.5 months of age) and 11 old male rats (22 to 34 months of age), feeding behavior of 10 each of young adult and old male rats and drinking behavior of 6 each of young adult and old male rats were recorded. Circadian rhythms were lost in 2, 6 and 1 old rats respectively in running activity, feeding and drinking behaviors. Loss of circadian rhythm of three behaviors seems not to occur concomitantly. Although the remaining old rats still showed as high a percentage of nocturnal activities in these three behaviors as young rats, the patterns of the behaviors revealed age-related changes. Old rats had decreased daily activity with small numbers and short duration of bursts of activity. Total frequencies of the head of rats interrupting the photobeam of a feeder during 24 hour period increased in old age with patterns of a small number of long meals with a rapid ingestion rate. Total numbers of licking the spout per day increased in old rats with patterns of a small number of short duration draft with a rapid licking rate. Old rats still maintained diurnal difference of drinking-to-feeding ratio. The similarity of the feeding and drinking patterns between old male rats and ventromedial hypothalamus lesioned rats was discussed.

Aging↗
PubMedDate not supplied

Prevalence of human foamy virus-related sequences in the Korean population.

The possible association of human foamy virus (HFV) with human thyroid disorders such as Graves' disease (GD) has been a topic of controversy due to the inconsistent results reported by several groups of investigators. Here we report the investigation of the presence of HFV-related sequences in the Korean population. DNA was obtained from peripheral blood lymphocytes from 24 GD patients and 23 healthy blood donors and subjected to PCR amplification using three sets of nested primers derived from gag, env, and LTR regions of the HFV genome. Contrary to previously reported studies, our analysis identified HFV-related sequences in the genomes of both healthy individuals and the GD patients. However, the nature of the HFV genome present in each group appeared to be different. We detected all 3 regions of HFV-related sequences in 29% of the HFV-positive GD patients, while no samples in the control group amplified all three regions. This suggests that the LTR may be used as a tool for screening for HFV in GD patients. Our data favor the hypothesis of a relationship between GD and the presence of HFV-related sequences, though in a complex way.

Adult↗