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Biomedical subjects

Z H Song

Publications and source records attributed to Z H Song.

29 records · Page 2Linked to original sources
PubMed1996

A lysine residue of the cannabinoid receptor is critical for receptor recognition by several agonists but not WIN55212-2.

Lys192 in the third transmembrane domain of the human CB1 cannabinoid receptor was converted to an alanine to study its role in receptor recognition and activation by agonists. HU-210, CP-55940, WIN55212-2, and anandamide, four cannabinoid agonists with distinct chemical structures, were used to characterize the wild-type and the mutant receptors. In human embryonal kidney 293 cells stably expressing the wild-type receptor, specific binding to [3H]WIN55212-2 and inhibition of cAMP accumulation by cannabinoid agonists were demonstrated, with different ligands exhibiting the expected rank orders of potency and stereoselectivity in competition binding and functional assays. In cells expressing the mutant receptor, the binding affinity of the receptor for [3H]WIN55212-2 was only slightly affected (the Kd for the mutant receptor was twice that of the wild-type), and the ability of WIN55212-2 to inhibit cAMP accumulation was unchanged. However, HU-210, CP-55940, and anandamide were unable to compete for [3H]WIN55212-2 binding to the mutant receptor. In addition, the potencies of HU-210, CP-55940, and anandamide in inhibiting cAMP accumulation were reduced by > 100-fold. These results demonstrate that Lys192 is critical for receptor binding by HU-210, CP-55940, and anandamide. Because Lys192 is not important for receptor binding and activation by WIN55212-2, WIN55212-2 must interact with the cannabinoid receptor through at least one point of interaction that is distinct from those of the three other agonists.

Base Sequence↗
PubMed1995

Molecular cloning and chromosomal localization of human genes encoding three closely related G protein-coupled receptors.

Cosmids containing human genes for three orphan G protein-coupled receptors, GPR12, GPR6, and GPR3, were isolated using their rat homologs as probes. Previous studies of the mouse and rat cDNAs have shown the receptors to be expressed primarily in brain but have failed to identify their ligands. The three receptor proteins of 334, 363, and 330 amino acids, respectively, are encoded by a single exon in each gene. Excluding the divergent sequences preceding the first transmembrane domain, they have approximately 60% amino acid identity with each other. Fluorescence in situ hybridization of GPR12, GPR6, and GPR3 localized these three genes to human chromosomal regions 13q12, 6q21, and 1p34.3-p36.1, respectively.

Amino Acid Sequence↗
PubMed1994

Molecular cloning of a novel candidate G protein-coupled receptor from rat brain.

A PCR cloning strategy using primers designed from sequences selectively conserved among a cannabinoid receptor and two orphan receptors, was used to isolate novel G protein-coupled receptors. rCNL3, a 1.75 kb cDNA encoding a 363 amino acid protein, was isolated from a rat cerebral cortex library. Sequence analysis showed that rCNL3 possesses a number of structural characteristics of G protein-coupled receptors and has 61% amino acid identity (from transmembrane region one through the carboxyl-terminus) with two other candidate G protein-coupled receptors. Therefore, these three receptors may comprise a receptor subfamily with identical or closely related endogenous ligands. Northern and in situ hybridization experiments demonstrated that rCNL3 mRNA is expressed in the rat brain, with a prominent distribution in striatum.

Amino Acid Sequence↗
PubMed1994

[Study of treatment on acquired infantile mental retardation with traditional Chinese and Western medicine].

80 cases with acquired infantile mental retardation caused by perinatal brain injury was treated with large doses of hyoscyamus, self made Retarded Recovery Pill and acupuncture. At the same time, 50 cases were taken as control group treated with Nao An Tai, Nao Fu Kang, etc. After 3 month treatment, the Intelligence Quotient (IQ) increased by 15 points in 29 cases of treatment group, while 3 cases in control group, chi 2 = 15.2, P < 0.01. After treatment for 6 month the IQ increased in 41 and 5 cases respectively, t = 5.53, P < 0.01. In 58.75% of the faculty of speech and motion greatly improved. It revealed that to treat the acquired infantile mental retardation, the combined therapy of traditional Chinese and Western medicine is effective.

Acupuncture Therapy↗
PubMed1992

Stimulation by corticotropin-releasing factor of the release of immunoreactive dynorphin A from mouse spinal cords in vitro.

Corticotropin-releasing factor (CRF) has been shown to release endogenous opioid peptides from several rat brain regions. Since we have demonstrated previously that the actions produced by intrathecally administered CRF in mice involve spinal kappa opioid receptors, experiments were conducted in this study to test the possibility that CRF may release dynorphin A, a putative endogenous kappa opioid agonist, from the mouse spinal cord. Using a superfusion system in vitro, mouse spinal cords were superfused with aerated (95% O2, 5% CO2) Krebs-Ringer buffer. Fractions of superfusion were collected and dynorphin A levels in each fraction were monitored by radioimmunoassay. The presence of CRF in the perfusion buffer stimulated significantly the release of immunoreactive dynorphin A. The releasing rate of immunoreactive dynorphin A returned to the basal level after withdrawing CRF from the superfusion buffer. The stimulatory effect of CRF on the release of immunoreactive dynorphin A was abolished by alpha-helical CRF-(9-41), a CRF receptor antagonist, indicating that the dynorphin-releasing effect of CRF was mediated by CRF receptors in the spinal cord. Also the dynorphin-releasing effect of CRF was a concentration-related phenomenon, with an estimated EC50 value of 5.3 nM. The results from this study support the hypothesis that intrathecally administered CRF may produce its effects by releasing endogenous dynorphin from the terminals of dynorphin-containing neurons in the spinal cord. This study also provides evidence to support the notion that there is a close communication between CRF- and opioid peptide-containing neuronal pathways in the central nervous system.

Animals↗
PubMed1991

Involvement of spinal kappa opioid receptors in the antagonistic effect of dynorphins on morphine antinociception.

The modulatory effects of intrathecally (i.t.) administered dynorphin A(1-17) and dynorphin A(1-13) on morphine antinociception have been studied previously in rats by other investigators. However, both potentiating and attenuating effects have been reported. In this study, the modulatory effects of i.t. administered dynorphin A(1-17) as well as the smaller fragment, dynorphin A(1-8), were studied in mice. In addition, nor-binaltorphimine (nor-BNI), a highly selective kappa opioid receptor antagonist, and naltrindole (NTI), a highly selective delta opioid receptor antagonist, were used to characterize the possible involvement of spinal kappa and delta opioid receptors in the modulatory effects of the dynorphins. Dynorphin A(1-17) and dynorphin A(1-8) administered i.t. at doses that did not alter tail-flick latencies, were both able to antagonize in a dose-dependent manner, the antinociceptive action of s.c. administered morphine sulfate. The antinociceptive ED50 of morphine sulfate was increased 3.9- and 5.3-fold by 0.4 nmol/mouse of dynorphin A(1-17) and dynorphin A(1-8), respectively. Injections of 0.4 and 0.8 nmol/mouse of nor-BNI i.t., but not its inactive enantiomer (+)-1-nor-BNI, inhibited dose-dependently the antagonistic effects of the dynorphins. These doses of nor-BNI alone did not affect the antinociceptive action of morphine sulfate. Intrathecal administration of 5 nmol/mouse of NTI also did not affect the modulatory effects of dynorphins. These observations that dynorphins exert their antagonistic effects on morphine-induced antinociception stereoselectively through spinal kappa opioid receptors may suggest a coupling between spinal kappa and mu opioid receptors.

Animals↗
PubMed1991

Antagonism of morphine antinociception by intrathecally administered corticotropin-releasing factor in mice.

Intrathecally (i.t.) administered corticotropin-releasing factor (CRF) has been shown to produce antinociception in the mouse abdominal stretching (writhing) assay. It also has been demonstrated that spinal kappa opioid receptors as well as CRF receptors are involved in the antinociception induced by CRF. In the present study, the role of CRF i.t. in modulating nociception was assessed further using the mouse tail-flick test. In addition, the modulatory effect of i.t. administered CRF on the antinociceptive activity of morphine was studied. Despite its potent and long-lasting antinociceptive effect in the writhing assay, CRF injected i.t. produced no consistent antinociception in the tail-flick test at doses up to 20 times the antinociceptive ED50 of CRF in the writhing test. In contrast, i.t. injection of CRF significantly attenuated the antinociceptive action of s.c. administered morphine. CRF at doses of 0.1 and 0.2 nmol/mouse i.t. increased the antinociceptive ED50 of s.c. morphine by 2- and 4-fold, respectively. The antagonistic action of CRF peaked between 15 min and 1 hr after i.t. injection and was still observable 4 hr after injection, demonstrating a time course similar to that of the antinociceptive effect of CRF in the writhing test. Intrathecal injection of alpha-helical CRF(9-41), a competitive CRF receptor antagonist, was able to inhibit, in a dose-dependent manner, the antagonistic activity of CRF. The antagonistic action of CRF also was attenuated dose-dependently by i.t. injection of nor-binaltorphimine (nor-BNI), a highly selective kappa opioid receptor antagonist. However, intrathecal injection of (+)-1-nor-BNI, an inactive enantiomer of nor-BNI, did not affect the antagonistic action of CRF. These data suggest that spinal kappa opioid receptors as well as CRF receptors are involved in the antagonistic effect of CRF against morphine antinociception.

Analgesia↗
PubMed1990

Involvement of spinal kappa opioid receptors in the antinociception produced by intrathecally administered corticotropin-releasing factor in mice.

Corticotropin-releasing factor (CRF), a putative stress transmitter, in previous studies failed to show any antinociceptive effect after central intracerebroventricular administration. In this study, a possible role of intrathecally (i.t.) administered CRF in modulating nociception and the involvement of opioid receptors were examined. CRF (i.t.) produced a dose-dependent antinociceptive effect in the mouse abdominal stretching (writhing) assay, with an ED50 of 22.1 (18.9-25.8) pmol/mouse. This antinociceptive effect of CRF peaked from 10 min to 1 hr after i.t. administration, although a significant antinociceptive effect was still observable 4 hr after injection. The dose-response curve of CRF antinociception was shifted to the right by i.t. administered alpha-helical CRF (9-41), a CRF antagonist, and the ED50 was raised by 3.7-fold. Naloxone, an opioid antagonist, also dose-dependently shifted the antinociceptive dose-response curve of CRF to the right. Naloxone at 1 and 10 mg/kg s.c. increased the ED50 value of CRF by 2- and 4-fold, respectively. In contrast, s.c. injection of 10 mg/kg of (+)-naltrexone, an inactive enantiomer of naltrexone, did not affect significantly the antinociception of i.t. administered CRF. Intrathecal injection of nor-binaltorphimine, a highly selective kappa opioid antagonist, increased the antinociceptive ED50 of CRF by 5.6-fold. However, the antinociceptive activity of CRF (i.t.) was not significantly affected by either beta-funaltrexamine, an irreversible mu selective opioid antagonist, or naltrindole, a highly selective delta opioid antagonist. Furthermore, the antinociceptive ED50 of CRF was not altered by (+)-1-nor-binaltorphimine, an inactive enantiomer of nor-binaltorphimine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Supersensitivity to electrical stimulation for assessing physical dependence on opioids in isolated tissues.

The use of the guinea pig ileum (GPI) and mouse vas deferens (MVD) to quantify opiate tolerance and physical dependence in the same preparation was examined. In the GPI, tolerance to and physical dependence on various opiates were induced by direct incubation with an agonist and tolerance and abstinence were assessed after its rapid removal by extensive washing. Dependence, as evidenced by an increase in twitch height and after removal of the agonist as compared to that before incubation, provided an index of the degree of physical dependence. The extent of the supersensitive response after agonist removal was noted to be related directly to the agonist concentration and the degree of tolerance development. Furthermore, the supersensitive response was found to be stereospecific, naloxone reversible and preferentially mu receptor-mediated. Likewise, tolerance to opiates could be demonstrated in the MVD by direct incubation with an agonist. Unlike the GPI, rapid removal of the agonist by washing did not produce a supersensitive response to electrical stimulation. However, a supersensitive response was demonstrable in the presence of naloxone. Thus, after a tolerant/dependent state was induced by incubation of the vas with a predetermined dose of [D-Ala2, D-Leu5]enkephalin that completely abolished the twitch response, the subsequent addition of naloxone resulted in a supersensitive response to electrical stimulation that was concentration-dependent. The maximum twitch response in the presence of naloxone, compared to that obtained before incubation with the agonist, provided an index of the extent of dependence.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Determination of thermograms of bacterial growth].

The fundamental growth thermograms of bacteria have been determined by using the microcalorimetric method. These perfect thermogram curves reflect the changes of bacterial growth patterns (including the lag phase of growth, log growth, stationary phase and the decline phase of growth). In our experiments, highly characteristic and reproducible growth patterns are observed under the same condition, therefore one can use these thermograms as "finger print" to discriminate bacteria. On the other hand, there thermogram curves contain ample information, which are very significant for the studies on microorganism metabolism, bio-thermokinetic and clinical fields.

Bacteria↗