Biomedical subjects

Wen-Qiao Jin

Publications and source records attributed to Wen-Qiao Jin.

6 recordsLinked to original sources

PubMed2004

Decrease of ventral tegmental area dopamine neuronal activity in nicotine withdrawal rats.

The present study was designed to examine the ventral tegmental area (VTA) dopamine neuronal activity in nicotine withdrawal rats by means of in vivo single-unit extracellular recordings. Animals were treated with nicotine base (6 mg/kg/day, s.c.) four times daily for 12 days. One day after the last nicotine administration, the firing rates of the VTA dopamine neurons were found to be significantly decreased. Following 2, 3, 5 and 10 days of nicotine withdrawal, however, the firing rates returned to the control levels. The number of spontaneously active dopamine cells was not altered at any time points. The results indicate that the VTA dopamine neuronal activity is reduced during the first day of nicotine withdrawal.

Animals↗

PubMed2004

Effect of chronic treatment of ohmefentanyl stereoisomers on cyclic AMP formation in Sf9 insect cells expressing human mu-opioid receptors.

The binding affinity of ohmefentanyl stereoisomers for mu-opioid receptors and the effect of chronic ohmefentanyl stereoisomers pretreatments on intracellular cAMP formation were investigated in Sf9 insect cells expressing human mu-opioid receptors (Sf9-mu cells). Competitive assay of [3H]ohmefentanyl binding revealed that these isomers had high affinity for micro-opioid receptors in Sf9-mu cells. Isomer F9204 had the highest affinity for mu-opioid receptors with the Ki value of 1.66 +/- 0.28 nM. After pretreated Sf9-mu cells with increasing concentrations of these isomers for 6 h, addition of naloxone (1 microM) precipitated an overshoot of foskolin-stimulated cAMP accumulation. The ability of these isomers to induce cAMP overshoot differed greatly with the order of F9202>F9205>F9208>F9206>F9204>F9207. Of these isomers, F9202 was 2.7-fold less potent than F9204 in receptor binding affinity, but 71.5-fold more potent in ability to induce cAMP overshoot. These results suggested that there was a significant stereo-structural difference among ohmefentanyl stereoisomers in ability to induce naloxone-precipitated cAMP overshoot in Sf9-mu cells.

Analgesics↗

PubMed2003

Opioid activity of C8813, a novel and potent opioid analgesic.

Compound trans-4-(p-bromophenyl)-4-(dimethylamino)-1-(2-thiophen-2-yl-ethyl)-cyclohexanol (C8813), structurally unrelated to morphine, is a novel analgesic. The present study examined the antinociception, opioid receptor selectivity and in vitro activity of C8813. The antinociceptive activity was evaluated using mouse hot plate and acetic acid writhing tests. In mouse hot plate test, the antinociceptive ED(50) of C8813 was 11.5 microg/kg, being 591 times and 3.4 times more potent than morphine and fentanyl respectively. In mouse writhing test, the antinociceptive ED(50) of C8813 was 16.9 microg/kg, being 55 times and 2.3 times more active than morphine and fentanyl respectively. In the opioid receptor binding assay, C8813 showed high affinity for mu-opioid receptor (K(i) = 1.37 nM) and delta-opioid receptor (K(i) = 3.24 nM) but almost no affinity for kappa-opioid receptor (at 1 microM). In the bioassay, the inhibitory effect of C8813 in the guinea-pig ileum (GPI) was 16.5 times more potent than in the mouse vas deferens (MVD). The inhibitory effects of C8813 in the GPI and MVD could be antagonized by mu-opioid receptor antagonist naloxone and delta-opioid receptor antagonist ICI174,864 respectively. However, the inhibitory effect of C8813 in the rabbit vas deferens was very weak. These results indicated that C8813 was a potent analgesic and a high affinity agonist for the mu- and delta-opioid receptors.

Analgesics, Opioid↗

PubMed2003

Suppression of morphine-induced conditioned place preference by l-12-chloroscoulerine, a novel dopamine receptor ligand.

The effect of l-12-chloroscoulerine (l-CSL), a novel ligand with dual dopamine D1 receptor agonistic and D2 receptor antagonistic actions, on the development of morphine-induced conditioned place preference (CPP) was investigated in mice. Morphine (10 mg/kg)-induced place preference was dose dependently suppressed by coadministration of l-CSL (5, 10 and 20 mg/kg), which induced neither place preference nor place aversion when administered alone at a dose of 20 mg/kg. The D1 receptor antagonist SCH23390 (0.1 mg/kg) suppressed, whereas the D2 receptor agonist (+/-)-2-(N-phenylethyl-N-propyl)-amino-5-hydroxytetralin (PPHT) (0.5 mg/kg) had no influence on the development of morphine-induced place preference. However, SCH23390 (0.1 mg/kg) did not affect, whereas PPHT (0.5 mg/kg) reversed the suppressive effect of l-CSL on the development of morphine-induced place preference. These results indicate that l-CSL suppresses the development of place preference of morphine by blocking D2 receptors.

Animals↗

PubMed2003

Expression of dopamine D1 receptor in Sf9 insect cells and agonism of l-12-chloroscoulerine on recombinant D1 receptor.

AIM: To express dopamine D1 receptor in baculovirus-Sf9 cell system, and to investigate the effects of l-12-chloroscoulerine (l-CSL) on the recombinant D1 receptor (D1R). METHODS: The recombinant baculovirus, Autographa californica nuclear polyhedrosis virus bearing D1R (AcNPV- D1R) was generated, and then was used to produce recombinant D1R in Sf9 insect cells. Expression of D1R in Sf9 cells was monitored by [3H]SCH23390 binding assay. The effects of l-CSL on recombinant D1R were investigated by [3H]SCH23390 binding assay and cAMP assay. RESULTS: The recombinant baculovirus AcNPV bearing D1R cDNA was generated, and was successfully expressed in Sf9 insect cells. The expression level of (Bmax) was (0.94+/-0.06) nmol/g protein. The Kd value of [3H]SCH23390 was (1.9+/-0.3) nmol/L, which was consistent with the previous results from calf striatum tissues. l-CSL had a high affinity to recombinant D1R with Ki value of (6.3+/-1.4) nmol/L, and increased the intracellular cAMP level in a concentration-dependent manner with EC50 value of 0.72 micromol/L and 95 % confidence limit was 0.67-0.77 micromol/L. Thus l-CSL has the D1 receptor agonism. CONCLUSION: An efficient baculovirus-Sf9 insect cell system for dopamine D1 receptor was constructed and l-CSL presented the D1 receptor agonism on cellular-molecular level directly.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed2003

Binding affinity to and dependence on some opioids in Sf9 insect cells expressing human mu-opioid receptor.

AIM: To investigate the receptor binding affinity and naloxone-precipitated cAMP overshoot of dihydroetorphine, fentanyl, heroin, and pethidine in Sf9 insect cells expressing human mu-opioid receptor (Sf9-mu cells). METHODS: Competitive binding assay of [3H]ohmefentanyl was used to reveal the affinity for mu-opioid receptor in Sf9-mu cells. [3H]cAMP RIA was used to determine cAMP level. Antinociceptive activity was evaluated using degree 55 mouse hot plate test. Naloxone-precipitated withdrawal jumping was used to reflect physical dependence in mice. RESULTS: All drugs displayed antinociceptive activity and produced physical dependence in mice. The K(i) values of dihydroetorphine, fentanyl, heroin, and pethidine in competitive binding assay were (0.85+/-0.20) nmol, (59.1+/-11.7) nmol, (0.36+/-0.13) micromol, and (12.2+/-3.8) micromol respectively. The binding affinities of these drugs for mu-opioid receptor in Sf9-mu cells were paralleled to their antinociceptive activities in mice. After chronic pretreatment with these drugs, naloxone induced cAMP withdrawal overshoot in Sf9-mu cells. The dependence index in Sf9-mu cells was calculated as K(i) value in competitive binding assay over EC(50) value in naloxone-precipitated cAMP assay. The physical dependence index in mice was calculated as antinociceptive ED(50)/withdrawal jumping cumulative ED(50). There was a good linear correlation between dependence index in Sf9-mu cells and physical dependence index in mice. CONCLUSION: The Sf9-mu cells could be used as a cell model to evaluate the receptor binding affinity and physical dependent liability of analgesic agents.

Analgesics, Opioid↗