Biomedical subjects

Choon-Gon Jang

Publications and source records attributed to Choon-Gon Jang.

24 records · Page 2Linked to original sources

PubMed2003

Differential effects of morphine and cocaine on locomotor activity and sensitization in mu-opioid receptor knockout mice.

The present study was undertaken to investigate the hypothesis that the mu-opioid receptors play a crucial role in locomotor activity and sensitization to cocaine and morphine in wild-type and mu-opioid receptor knockout mice. Our results show that morphine and cocaine increased locomotor activity in wild-type mice, but failed to increase locomotor activity in mu-opioid receptor knockout mice, suggesting a contribution of mu-opioid receptor. Repeated morphine treatment induced sensitization in wild-type mice, but this was not observed in mu-opioid receptor knockout mice. In contrast repeated cocaine treatment produced sensitization in mu-opioid receptor knockout mice, but not in wild-type mice on day 6. However, the sensitization to cocaine was observed in mu-opioid receptor knockout and wild-type mice on day 12. These results suggest that the expression of mu-opioid receptor may contribute to locomotor sensitization induced by morphine, but that mu-opioid receptor does not play an important role in mediating sensitization to cocaine.

Adaptation, Physiological↗

PubMed2003

Tyrosine kinase is involved in hemin-induced pyresis.

To investigate the mechanisms involved in hemin-induced febrile response, the rectal temperature of rats were measured after intracerebroventricular (i.c.v.) injections of hemin, with or without antagonists. Hemin (10 microg) elicited a significant febrile response, which lasted from 30 min, to more than 6 h, after its administration, but this was not the case with biliverdin (i.c.v.) and bilirubin (i.c.v.). The hemin-induced febrile response was significantly inhibited by pretreatment with an inhibitor of tyrosine kinase (genistein), but not by pretreatment with an inhibitor of protein kinase C (chelerythrine) and a scavenger of iron (deferoxamine). These results suggest that tyrosine kinase is involved in the hemin-induced febrile response.

Alkaloids↗

PubMed2003

Effects of Coptis japonica on morphine-induced conditioned place preference in mice.

Morphine, an analgesic with significant abuse potential, is considered addictive because of drug craving and psychological dependence. It is reported that repeated treatment of morphine can produce conditioned place preference (CPP) showing a reinforcing effect in mice. CPP is a useful method for the screening of morphine-induced psychological dependence. In the present study, we investigated the effect of the methanolic extract of Coptis japonica (MCJ) on morphine-induced CPP in mice. Furthermore, we examined c-fos expression in the parietal cortex, piriform cortex, striatum, nucleus accumbens, and hippocampus of the morphine-induced CPP mouse brain. Treatment of MCJ 100 mg/kg inhibited morphine-induced CPP. Expression of c-fos was increased in the cortex, striatum, nucleus accumbens, and hippocampus of the morphine-induced CPP mouse brain. These increases of expression were inhibited by treatment with MCJ 100 mg/kg, compared to the morphine control group. Taken together, these results suggest that MCJ inhibits morphine-induced CPP through the regulation of c-fos expression in the mouse brain.

Animals↗

PubMed2002

Carbon monoxide as a novel central pyrogenic mediator.

Carbon monoxide (CO) are produced by heme oxygenase (HO), and HO was detected in hypothalamus. However, the roles of CO produced in hypothalamus was not fully elucidated. So, we tested the effects of CO on body temperature because preoptic-anterior hypothalamus was known as the presumptive primary fever-producing site. CO-saturated aCSF (4 microl, i.c.v.) and hemin (10 microg, i.c.v.) elicited marked febrile response. Pretreatment with indomethacin completely inhibited CO- and hemin-induced fever. Zinc protoporphyrin-IX (10 microg, i.c.v.) or ODQ (50 microg, i.c.v.) partially reduced hemin-induced febrile response. Dibutyryl-cGMP (100 microg, i.c.v.) produced profound febrile response and this febrile response was attenuated by indomethacin. These results indicate that endogenous CO may have a role as a pyrogenic mediator in CNS and CO-mediated pyresis is dependent on prostaglandin production and partially on activation of soluble guanylate cyclase.

Animals↗

PubMed2002

Time courses of pCREB expression after dopaminergic stimulation by apomorphine in mouse brain.

Administration of dopamine agonist, apomorphine (2 mg/kg, s.c.), produces cage climbing behavior in mice that exhibit typical dopaminergic stimulation. The present study investigated the pCREB expression level in several brain regions following apomorphine treatment in order to determine whether the increased the dopaminergic activation produced by apomorphine accompanies the changes in pCREB immunoreactivity. A mouse brain was removed at 0 min, 10 min, 30 min, 1 h, 2 h, 7 h, and 24 h after apomorphine treatment. The brain tissue was fixed by an intracardiac perfusion with ice-cold 4% paraformaldehyde in PBS. Immunohistochemical study was conducted using the ABC-DAB method. The data showed that the immunoreactivity of pCREB increased in the striatum, nucleus-accumbens, piriform cortex and the dentate gyrus of the hippocampus of a mouse brain 30 min after the apomorphine treatment. Increased immunoreactivity began to diminish 2 h after the apomorphine treatment in all the brain regions measured. The time course for the pCREB immunoreactivity was similar to the behavioral response induced by the apomorphine treatment. These results suggest that activation of the dopamine receptor is accompanied by an increase in pCREB expression in the mouse brain.

Animals↗

PubMedDate not supplied

A lack of mu-opioid receptors modulates the expressions of neuropeptide Y and substance P mRNA.

The present study was undertaken to investigate changes in the expressions of neuropeptide Y (NPY) and substance P (SP) in mice lacking mu-opioid receptors. In an in situ hybridization study, in which we compared wild type and mu-opioid receptor knockout mice, NPY mRNA levels were found to be lower in the caudate-putamen and nucleus accumbens of mu-opioid receptor knockout mice. In addition, SP mRNA levels were lower in the ventromedial hypothalamic nucleus of mu-opioid receptor knockout mice. Our findings suggest that a lack of mu-opioid receptors modulates basal NPY mRNA levels in striatal regions and SP mRNA levels in the ventromedial hypothalamic nucleus of the mouse, and that these changes are due to compensatory modulation in the brain.

Animals↗