Biomedical subjects

Choon-Gon Jang

Publications and source records attributed to Choon-Gon Jang.

At least 19 recordsLinked to original sources

PubMed2006

Involvement of 5-HT receptors in the development and expression of methamphetamine-induced behavioral sensitization: 5-HT receptor channel and binding study.

Methamphetamine (MAP) is one of the most commonly abused drugs in Asia, and previous studies suggest that serotonin 3 receptors (5-HT(3)) are involved in MAP-induced locomotion and reward. However, little is known about the role of 5-HT(3) receptors in MAP-induced behavioral sensitization. Here, we measured the effects of MDL 72222, a 5-HT(3) antagonist, and SR 57227 A, a 5-HT(3) agonist, on the development and expression of MAP-induced behavioral sensitization, and alternations of 5-HT(3) receptor binding labeled with the 5-HT(3)-selective antagonist, [(3)H]GR65630, in mice. In addition, we investigated the effects of MAP on 5-HT(3A) receptor channel activity in Xenopus laevis oocytes expressing 5-HT(3A) receptors. We found that MDL 72222 attenuated both the development and expression of behavioral sensitization to MAP (1.0 mg/kg, i.p.), and that this attenuating effect of MDL 72222 was reversed by pre-treatment with SR 57227 A. In oocytes expressing 5-HT(3A) receptor, MAP exhibited a dual modulation of 5-HT(3A) receptor channel activity, i.e. pre-treatment with a low dose of MAP (0.1 microm) enhanced 5-HT-induced inward peak current (I(5-HT)) but a high dose of MAP (100 microm) inhibited I(5-HT). The acute administration of MDL 72222 with MAP decreased [(3)H]GR65630 binding versus MAP alone in the mouse striatum. Our results suggest that MDL 72222 attenuates MAP-induced behavioral sensitization via 5-HT(3) receptors in the caudate putamen, and that 5-HT(3) receptor antagonists like MDL 72222 have potential as novel anti-psychotic agents for the treatment of MAP dependence and psychosis.

Algorithms↗

PubMed2006

Effect of alpha-tocopherol and deferoxamine on methamphetamine-induced neurotoxicity.

Methamphetamine (MA)-induced dopaminergic neurotoxicity is believed to be associated with the increased formation of free radicals. This study examined the effect of alpha-tocopherol (alpha-TC), a scavenger of reactive oxygen species, and deferoxamine (DFO), an iron chelator, on the MA-induced neurotoxicity. Male rats were treated with MA (10 mg/kg, every 2 h for four injections). The rat received either alpha-TC (20 mg/kg) intraperitoneally for 3 days and 30 min prior to MA administration or DFO (50 mg/kg) subcutaneously 30 min before MA administration. The concentrations of dopamine (DA), serotonin and their metabolites decreased significantly after MA administration, which was inhibited by the alpha-TC and DFO pretreatment. alpha-TC and DFO attenuated the MA-induced hyperthermia as well as the alterations in the locomotor activity. The level of lipid peroxidation was higher and the reduced glutathione concentration was lower in the MA-treated rats. These changes were significantly attenuated by alpha-TC and DFO. This suggests that alpha-TC and DFO ameliorate the MA-induced neuronal damage by decreasing the level of oxidative stress.

Analysis of Variance↗

PubMed2006

HPLC determination of tolperisone in human plasma.

A simple high performance liquid chromatographic (HPLC) method was developed for the determination of tolperisone in human plasma. Tolperisone and internal standard (chlorphenesin) were isolated from 1 mL of plasma using 8 mL of dichlormethane. The organic phase was collected and evaporated under nitrogen gas. The residue was then reconstituted with 300 mL aliquot of mobile phase and a 100 mL aliquot was injected onto the C18 reverse-phased column. The mobile phase, 45% methanol containing 1% glacial acetic acid and 0.05% 1-hexanesulfonic acid was run at a flow rate of 1 mL/min. The column effluent was monitored using UV detector at 260 nm. The retention times for tolperisone and the internal standard were approximately 7.1 and 8.4 min, respectively. The standard curve was linear with minimal intra-day and inter-day variability. The quantification limit of tolperisone in human plasma was 10 ng/ mL. The proposed method has been applied to the determination of pharmacokinetic profile of tolperisone in Koreans. The Tmax of tolperisone in Koreans (0.94 +/- 0.42 h) was not significantly differ from that reported in Europeans (0.5-1 h), but the mean half-life in Koreans (1.14 +/- 0.27 h) was shorter than that in Europeans (2.56 +/- 0.2 h). The proposed HPLC method is simple, accurate, reproducible and suitable for pharmacokinetic study of tolperisone.

Adult↗

PubMed2005

Increases in [(3)H]-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor binding and mRNA expression of AMPA-sensitive glutamate receptor A (GluR-A) subunits in rats withdrawn from butorphanol.

An autoradiographic study of [(3)H]-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid(AMPA) receptor binding and an assessment of in situ hybridization of AMPA-sensitive glutamate receptor A (GluR-A) subunits in the rat brain were performed 7 h after withdrawal from butorphanol infusion. Animals were rendered dependent by intracerebroventricular (icv) infusion of butorphanol (26 nmol/microl/h) via osmotic minipumps for 3 d. Brain sections for binding of [(3)H]AMPA were incubated with 15 nM [(3)H]AMPA. The probes for in situ hybridization were labeled at its 3 cent end using terminal deoxynucleotidyl transferase and [(35)S]dATP. The highest degree of [(3)H]AMPA binding was shown in the hippocampus. The extent of [(3)H]AMPA binding was increased significantly in each of the brain areas examined, cortex, septum, caudate putamen, and hippocampus of rats, following withdrawal from butorphanol. The highest level of mRNA for GluR-A receptor for flop and flip subunits, was found in the dentate gyrus and in the CA3 region of the hippocampus. The amounts of mRNA for the flop form of GluR-A receptor were significantly increased in the cortex, caudate putamen, thalamus, and dentate gyrus of hippocampus of rat brain. The amounts of mRNA for the flip form of GluR-A receptor were markedly elevated in the cortex, thalamus, caudate putamen, and hippocampus. These findings suggest that increases in expression of mRNA for the GluR-A receptor and in the binding of AMPA to its receptor may play an important role during withdrawal from butorphanol dependence.

Analgesics, Opioid↗

PubMed2005

Differential effects of morphine- and cocaine-induced nNOS immunoreactivity in the dentate gyrus of hippocampus of mice lacking mu-opioid receptors.

This study investigated the expression of nNOS after repeated morphine or cocaine administration in order to determine if nNOS (neuronal nitric oxide synthase) is involved in the morphine- or cocaine-induced behavioral sensitization in mu-opioid receptor knockout (MOR(-/-)) mice. Higher numbers of nNOS-positive cells were observed in the dentate gyrus of the hippocampus (DG) of the wild-type (MOR(+/+)) mice repeatedly treated with either morphine or cocaine than in the saline treated MOR(+/+) mice (morphine, +122%; cocaine, +82%). Moreover, the MOR(-/-) mice also showed significantly higher morphine- or cocaine-induced nNOS expression levels in the DG than in the saline treated MOR(+/+) mice (morphine, +234%; cocaine, +54%). The MOR(-/-) mice showed a significantly higher morphine-induced nNOS expression level (+103%) or a lower cocaine-induced nNOS expression level (+38%) in the DG than in the morphine- or cocaine-treated MOR(+/+) mice. These results suggest that morphine and cocaine sensitization is differentially regulated by the mu-opioid receptors in MOR(-/-) mice via the nNOS systems in the DG.

Animals↗

PubMed2005

Cloning and expression of Ca2+-activated chloride channel from rat brain.

To clone the gene product responsible for the calcium-activated chloride channel (CLCA) in rat brain cerebrum, we performed a reverse transcription-PCR (RT-PCR) with gene-specific primers of a rat EST clone. We successfully cloned a rat brain CLCA (rbCLCA). The full-length cDNA is 2895 bp long and codes for a 902 amino acid protein. The clone consists of four transmembrane domains and shows a 79.1% of significant homology with previously reported mouse smooth muscle chloride channel sequence. We also performed RT-PCR using single neuron and glia, and various tissues to determine the tissue expression of rbCLCA. We found that rbCLCA was expressed in both neuron and glia. In peripheral organs, rbCLCA showed the predominant expressions in cerebrum, cerebellum, kidney, small intestine, and stomach but not in heart, large intestine, liver, lung, and spleen. Whole-cell patch clamp studies in HEK293 cells transfected with the clone identified a niflumic acid (a CLCA channel blocker)-sensitive and voltage-dependent chloride current but we could not observe this chloride current in mock-transfected cells. The identification of genes belonging to the CLCA family from rat brain and its functional expression will help to evaluate its physiological role in brain as anion channel.

Amino Acid Sequence↗

PubMed2005

Characteristics of ginsenoside Rg3-mediated brain Na+ current inhibition.

We demonstrated previously that ginsenoside Rg(3) (Rg(3)), an active ingredient of Panax ginseng, inhibits brain-type Na(+) channel activity. In this study, we sought to elucidate the molecular mechanisms underlying Rg(3)-induced Na(+) channel inhibition. We used the two-microelectrode voltage-clamp technique to investigate the effect of Rg(3) on Na(+) currents (I(Na)) in Xenopus laevis oocytes expressing wild-type rat brain Na(V)1.2 alpha and beta1 subunits, or mutants in the channel entrance, the pore region, the lidocaine/tetrodotoxin (TTX) binding sites, the S4 voltage sensor segments of domains I to IV, and the Ile-Phe-Met inactivation cluster. In oocytes expressing wild-type Na(+) channels, Rg(3) induced tonic and use-dependent inhibitions of peak I(Na). The Rg(3)-induced tonic inhibition of I(Na) was voltage-dependent, dose-dependent, and reversible, with an IC(50) value of 32 +/- 6 microM. Rg(3) treatment produced a 11.2 +/- 3.5 mV depolarizing shift in the activation voltage but did not alter the steady-state inactivation voltage. Mutations in the channel entrance, pore region, lidocaine/TTX binding sites, or voltage sensor segments did not affect Rg(3)-induced tonic blockade of peak I(Na). However, Rg(3) treatment inhibited the peak and plateau I(Na) in the IFMQ3 mutant, indicating that Rg(3) inhibits both the resting and open states of Na(+) channel. Neutralization of the positive charge at position 859 of voltage sensor segment domain II abolished the Rg(3)-induced activation voltage shift and use-dependent inhibition. These results reveal that Rg(3) is a novel Na(+) channel inhibitor capable of acting on the resting and open states of Na(+) channel via interactions with the S4 voltage-sensor segment of domain II.

Animals↗

PubMed2005

Reduced nNOS expression induced by repeated nicotine treatment in mu-opioid receptor knockout mice.

To determine whether neuronal nitric oxide synthase (nNOS) is involved in nicotine-induced behavioral sensitization in mu-opioid receptor knockout mice we adopted an immunohistochemical approach. Our results confirm that repeated nicotine administration increased locomotor activity in wild-type mice, but failed to increase locomotor activity in mu-opioid receptor knockout mice, thus suggesting that the mu-opioid receptor is involved in behavioral sensitization. Higher numbers of nNOS-positive cells were observed in the striatum of wild-type mice repeatedly treated with nicotine than in saline-treated wild-type mice. However, mu-opioid receptor knockout mice showed significantly lower nicotine-induced nNOS expression in the striatum versus wild-type mice. No differences were found in the hilus of the dentate gyrus between wild-type and mu-opioid receptor knockout mice. These findings demonstrate that the absence of mu-opioid receptors can cause a significant reduction in the expression of nNOS in the striatum, as induced by repeated nicotine treatment.

Analysis of Variance↗

PubMed2005

Pharmacological action of Panax ginseng on the behavioral toxicities induced by psychotropic agents.

Morphine-induced analgesia has been shown to be antagonized by ginseng total saponins (GTS), which also inhibit the development of analgesic tolerance to and physical dependence on morphine. GTS is involved in both of these processes by inhibiting morphine-6-dehydrogenase, which catalyzes the synthesis of morphinone from morphine, and by increasing the level of hepatic glutathione, which participates in the toxicity response. Thus, the dual actions of ginseng are associated with the detoxification of morphine. In addition, the inhibitory or facilitated effects of GTS on electrically evoked contractions in guinea pig ileum (mu-receptors) and mouse vas deferens (delta-receptors) are not mediated through opioid receptors, suggesting the involvement of non-opioid mechanisms. GTS also attenuates hyperactivity, reverse tolerance (behavioral sensitization), and conditioned place preference induced by psychotropic agents, such as methamphetamine, cocaine, and morphine. These effects of GTS may be attributed to complex pharmacological actions between dopamine receptors and a serotonergic/adenosine A2A/ delta-opioid receptor complex. Ginsenosides also attenuate the morphine-induced cAMP signaling pathway. Together, the results suggest that GTS may be useful in the prevention and therapy of the behavioral side effects induced by psychotropic agents.

Animals↗

PubMed2005

Effect of chronic Albizzia julibrissin treatment on 5-hydroxytryptamine1A receptors in rat brain.

Quantitative receptor autoradiography and behavioral studies were employed to investigate whether the aqueous extract of Albizzia julibrissin (AEAJ) specifically targets serotonergic systems in rat brain. AEAJ was orally administered at 50 and 200 mg/kg to adult male SD rats for 7 days. Treatment with AEAJ (200 mg/kg) significantly increased time-spent in open arms and the number of open arm entries in an elevated plus-maze (EPM) versus saline controls (P<0.05). Moreover, those effects of AEAJ were blocked by WAY 100635, a 5-HT1A receptor antagonist. Following behavioral evaluation, the binding of [3H]8-hyroxy-2-(di-n-propylamino) tertalin ([3H]8-OH-DPAT) to 5-HT1A receptors in rat brain was investigated. [3H]8-OH-DPAT binding after AEAJ (200 mg/kg) treatment showed a marked increase in the frontal cortex, hippocampus (CA2 and CA3 regions) and in the lateral septum versus vehicle-treated controls. No changes of [3H]8-OH-DPAT binding were observed in the caudate putamen, dentate gyrus and CA1 areas of the hippocampus or in the hypothalamus. In the dorsal raphe region, [3H]8-OH-DPAT binding was significantly reduced by AEAJ (50 mg/kg) treatment but was unchanged by AEAJ (200 mg/kg). These results suggest that the anxiolytic-like effect of A. julibrissin is mediated by the changes of serotonergic nervous system, especially 5-HT1A receptors.

Albizzia↗

PubMed2005

Allele and genotype frequencies of CYP2C9 in a Korean population.

AIMS: To determine the frequencies of the variant alleles and the genotypes of CYP2C9 in a Korean population. METHODS: Three hundred and fifty-eight healthy Korean subjects were studied. CYP2C9 alleles were detected by polymerase chain reaction-restriction fragment length polymorphism assays and direct sequencing assays. RESULTS: The allele frequencies were 0.934 for CYP2C9*1, 0.060 for CYP2C9*3 and 0.006 for CYP2C9*13. The CYP2C9*2,*4,*5 and *11 alleles were not detected. The frequencies of the CYP2C9*1/*1, *1/*3 and *1/*13 genotypes were 0.869, 0.120 and 0.011, respectively. CONCLUSION: The frequency of the CYP2C9*3 allele in the Korean population studied was significantly higher than reported elsewhere, and a novel allele, CYP2C9*13, was found at a frequency of 0.006 (95% confidence interval 0, 0.012). Only three genotypes of CYP2C9, CYP2C9*1/*1,*1/*3 and *1/*13 were observed in this Korean population.

Adult↗

PubMed2005

Nelumbinis Semen reverses a decrease in hippocampal 5-HT release induced by chronic mild stress in rats.

Depression is associated with a dysfunctional serotonin system. Recently, several lines of evidence have suggested that a very important evoking factor in depression may be a serotonin deficit in the hippocampus. This study assessed the antidepression effects of Nelumbinis Semen (NS) through increasing serotonin concentrations under normal conditions and reversing a decrease in serotonin concentrations in rat hippo-campus with depression-like symptoms induced by chronic mild stress (CMS). Using an in-vivo microdialysis technique, the serotonin-enhancing effect of NS on rat hippocampus was investigated and its effects compared with those of two well-known antidepressants, Hypericum perforatum (St John's wort) and fluoxetine (Prozac). Rats were divided into five groups: saline-treated normal, without CMS; saline-treated stress control; NS-, St John's wort- and fluoxetine-treated rats under CMS for 8 weeks or no stress treatment. NS and fluoxetine significantly increased serotonin in normal conditions and reversed a CMS-induced decrease in serotonin release in the hippocampus (P<0.05 compared with normal group or control group under CMS). These results suggest that NS increases the serotonin levels normally decreased in depression, resulting in an enhancement of central serotonergic transmission and possible therapeutic action in depression. It is suggested that NS may present an antidepressant effect through enhancement of serotonin.

Animals↗

PubMed2004

Loss of nicotine-induced behavioral sensitization in micro-opioid receptor knockout mice.

Repeated administration of nicotine produces behavioral sensitization. However, the possible mechanism of behavioral sensitization to nicotine remains unclear. The present study was undertaken in micro-opioid receptor knockout mice, to examine the hypothesis that micro-opioid receptors play a crucial role in behavioral sensitization to nicotine. All mice received saline or nicotine (0.05 mg/kg, s.c) twice a day for 7 consecutive days. The mice remained drug free for 3 days and on day 11 each group was challenged with saline or nicotine (0.05 mg/kg, s.c.). On day 1, it was observed that the single injection of nicotine (0.05 mg/kg, s.c.) did not influence locomotor activity in either micro-opioid receptor knockout or in wildtype mice. On day 7 (24 h after mice had been treated twice daily for 6 consecutive days with an injection of 0.05 mg/kg of nicotine), the mice were challenged with a single injection of nicotine, which produced behavioral sensitization in the wildtype but not in micro-opioid receptor knockout mice. On day 11, following 3 days of withdrawal after the second injection of nicotine on day 7, nicotine-treated mice were challenged with a single injection of nicotine and showed the behavioral sensitization of wildtype. However, nicotine challenge did not induce behavioral sensitization in micro-opioid receptor knockout mice. Our data indicate that a lack of micro-opioid receptors can inhibit the effects of nicotine-induced behavioral sensitization. This result strongly suggests that the micro-opioid receptor plays an important role in behavioral sensitization to nicotine.

Animals↗

PubMed2004

Altered emotional behaviors and the expression of 5-HT1A and M1 muscarinic receptors in micro-opioid receptor knockout mice.

Anxiety and depression alterations have been reported in micro-opioid receptor knockout mice after exon 2 disruption. However, emotional behaviors, such as novelty and emergence responses have not been reported in micro-opioid receptor knockout mice due to the disruptions of exon 2 and 3. Here, we report that mu-opioid receptor knockout mice, with deletion of exon 2 and 3, display significant emotional behavior changes; they showed less anxiety in the elevated plus maze and emergence tests, reduced response to novel stimuli in the novelty test, and less depressive-like behavior in the forced-swim test. Analysis of the compensatory mechanism in mu-opioid receptor knockout mice revealed that the M1 mRNA levels were reduced in the cortex, caudate putamen, nucleus accumbens, and hippocampus, and that M1 receptor levels were reduced in the nucleus accumbens, CA1, and the dentate gyrus of the hippocampus, versus the wild-type. However, 5-HT1A receptor levels were significantly elevated in the cerebral cortex and in the hypothalamus of mu-opioid receptor knockout mice versus the wild-type. These aberrant emotional behavioral phenotypes are possibly related to M1 and 5-HT1A receptor alterations in the micro-opioid receptor knockout mice. Overall, our study suggests that micro-opioid receptor may play a role in the modification of emotional responses to novelty, anxiety, and depression.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed2004

Transdermal eperisone elicits more potent and longer-lasting muscle relaxation than oral eperisone.

Eperisone hydrochloride is widely used for the treatment of plasticity to relieve muscle stiffness and back pain. However, oral eperisone has a very low bioavailability and short muscle relaxant activity, because of the profound intestinal first-pass metabolism. To improve the efficacy and compliance of eperisone, we designed a new dosage form, a transdermal patch, and evaluated the efficacy of the eperisone patch with the muscle relaxant activity of rats. The muscle relaxant activity was assessed by the measurement of forelimb grip strength and hanging test in rats. The transdermal patch of eperisone showed significantly enhanced muscle relaxant activity at 0.5 1.5 and 3 cm2/200 g rat (1.39, 4.17 and 8.33 mg of eperisone hydrochloride/kg, respectively) in a dose-dependent manner and the effects lasted over 24 h. Even though oral eperisone hydrochloride showed significant muscle relaxant activity at 12.5, 25 and 50 mg/kg in a dose-dependent manner, the activity lasted only 1 or 2 h after administration. These results suggest that eperisone as transdermal patch form showed efficient absorption with more potent and longer-lasting muscle relaxant activity than oral solution. The transdermal patch form of eperisone will increase the efficacy and compliance in the clinical use of eperisone.

Administration, Cutaneous↗

PubMed2004

PAP 9704, a Korean herbal medicine attenuates methamphetamine-induced hyperlocomotion via adenosine A2A receptor stimulation in mice.

The effect of PAP 9704, a traditional prescription in Korea consisting of Polygala tenuifolia, Acorus gramineus, and Poria cocos at a ratio of 1:1:1 (dry weight), on methamphetamine (MA)-induced hyperlocomotion was examined in mice. The increased locomotor activity induced by MA (1 mg/kg/d, i.p. x 7) was significantly attenuated by co-administration with PAP 9704 (100 or 200 mg/kg/d, p.o. x 7) in a dose dependent manner. Consistently, it was found that the hyperlocomotor activity occurred in parallel with the expression of striatal fos-related antigen immunoreactivity. The adenosine A(2A) receptor antagonist, 1,3,7-trimethyl-8-(3-chlorostyryl)xanthine (0.5 or 1.0 mg/kg, i.p.), significantly reversed the pharmacological action of PAP 9704 in a dose related manner, but the adenosine A(1) receptor antagonist 8-cyclopentyl-1,3-dimethylxanthine (0.5 or 1.0 mg/kg, i.p.) and the A(2B) receptor antagonist alloxazine (1.5 or 3.0 mg/kg, i.p.) did not significantly affect this pharmacological action. Our results suggest that PAP 9704 prevents MA-induced hyperlocomotion, at least in part, via the stimulation of the adenosine A(2A) receptor.

Animals↗

PubMed2004

Nelumbinis Semen reverses a decrease in 5-HT1A receptor binding induced by chronic mild stress, a depression-like symptom.

Depression is associated with a dysfunctional serotonin (5-hydroxytryptamine; 5-HT) system. More recently, several lines of evidence suggest that an important factor in the development of depression may be a deficit in the function and expression of 5-HT1A receptors. The present study assessed if Nelumbinis Semen (N.s.) had an anti-depression effect through reversing a decrease in 5-HT1A receptor binding in rats with depression-like symptoms induced by chronic mild stress. Using a 5-HT1A receptor binding assay, with a specific 5-HT1A receptor agonist, 8-OH-DPAT (8-hydroxy-2-(di-n-propylamino) tetralin), the mechanism of the anti-depression effect of N.s. on rats was investigated, and the effects compared with two well-known antidepressants, Hyperium Perforatum (St. Johns Wort) and fluoxetine (Prozac). Animals were divided into five groups: the normal (N) group without chronic mild stress (CMS), the control (C) group under CMS for 8 weeks, the Nelumbinis Semen (N.s.) treatment group under CMS for 8 weeks, the Hyperium Perforatum (H.p.) treatment group under CMS for 8 weeks and finally, the fluoxetine (F) treatment group under CMS for 8 weeks. Each treatment was administered to rats during the last 4 weeks of the 8-week CMS. A sucrose intake test was performed to test the anti-depression effect of N.s. The N.s. treatment significantly reversed the decreased sucrose intake under CMS (P < 0.05 compared to control group under CMS). In the CA2 and CA3 regions of the hippocampus, both N.s. and H.p. reversed the CMS-induced decrease in 5-HT1A receptor binding. In the I to II regions of the frontal cortex, N.s. and H.p. also reversed the CMS-induced decrease in 5-HT1A receptor binding, and even showed a significant increase in 5-HT1A receptor binding compared to the F treatment group (N.s. vs. P, p < 0.05, H.p. vs. P, p < 0.05). However, in the hypothalamus, all treatments reversed the CMS-induced decrease in 5-HT1A receptor binding. This reversal effect of N.s. on the decrease in 5-HT1A receptor binding in the frontal cortex, hippocampus and hypothalamus of rat brains was very similar to that of H.p, but different from that of F. It is concluded that N.s. presents an anti-depression effect through enhancing 5-HT1A receptor binding.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed2003

Impaired water maze learning performance in mu-opioid receptor knockout mice.

Previous study has demonstrated that the lack of mu-opioid receptor decreased LTP in the dentate gyrus of the hippocampus, suggesting the possibility that the lack of mu-opioid receptor may accompany a change in learning and memory. However, no behavioral study has been undertaken to correlate LTP deficits with spatial memory impairment in mu-opioid receptor knockout mice. Therefore, the present study investigated the hypothesis that mu-opioid receptors contribute to learning and memory by using the Morris water maze, and comparing responses in wild type and mu-opioid receptor gene knockout mice. Our results indicated that mu-opioid receptor knockout mice showed a significant spatial memory impairment compared to wild type in the Morris water maze. This result suggests that the expression of mu-opioid receptor plays an important role in spatial learning and memory examined by Morris water maze.

Animals↗