• Title/Summary/Keyword: opiate receptor

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The Mechanism of Immunomodulatory Effect by Electro-acupuncture in 2, 4-Dinitrophenylated Keyhole Limpet Protein Immunized Mice (족삼리(足三里) 전침자극(電鍼刺戟)이 알러지모델 생쥐의 면역능(免疫能)에 미치는 영향(影響) 및 기전(機轉)에 관한 연구(硏究))

  • Kim, Jeung-shin;Kim, Yong-suk;Nam, Sang-soo
    • Journal of Acupuncture Research
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    • v.22 no.3
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    • pp.23-35
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    • 2005
  • Objective : The aim of the study is to investigate the effect of electro-acupuncture (EA) on ST36 to modulate immune reaction in BALB/c mice immunized intraperitoneally with 2,4-dinitrophenylated keyhole limpet protein(DNP-KLH). Methods : Experimental mice were divided into four groups : 1) Normal group was not performed by any operation. 2) IM(Immunized) group was immunized intraperitoneally with DNP-KLH and aluminum hydroxide without electro-acupunture stimulation. 3) IM-EA(immunized-elctro- acupuncture) group was performed by successive electro-acupuncture on the ST36 acupoint after immunization. 4) IM-NA(immunized-naloxone) group was performed by immunization and electro-acupuncture with same method, but naloxone was injected intraperitoneally 30 minutes before eletro-acupuncture to inhibit the opiate receptor in spleen. Serum total immunoglobulin I(IgE) and antigen-specific IgE was measured in each group. The expression of interferon-${\gamma}$ and interleukin-4 mRNA in spleen was researched by real-time RT-PCR Results : Serum total-IgE and antigen-specific IgE were significantly decreased only in IM-EA group. The expression of interleukin-4 in spleen cell was significantly reduced not only in IM-EA group, but also in IM-EA group. Conclusions : Above results indicate that the mechanism of immunomodulatory effect of electro-acupuncture is related to opioid system especially in B-cell immune reaction. Further research on the T-cell immunity is necessary to explain the mechanism of immunomodulatory effect of electro-acupuncture.

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Pharmacological Evaluation of the Mechanism of ${\alpha}-Adrenoceptor-Mediating$ Sleep in Chickens (${\alpha}$-아드레나린 수용체의 매개에 의한 병아리 수면에 대한 약리학적 고찰)

  • Jeong, S.H.;Sohn, U.D.;Song, C.S.;Hong, K.W.
    • The Korean Journal of Pharmacology
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    • v.20 no.2
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    • pp.15-21
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    • 1984
  • It was aimed to study the effects of ${\alpha}_2-adrenoceptor$ agonists on the sleeping time in $one{\sim}two-day-old$ chickens. Furthermore, it was also evaluated whether ${\alpha}_1-adrenoceptor$ agonist and antagonist might affect the sleeping in the chickens and discussed in relation with opiate receptor. 1) Guanabenz, clonidine, guanfacine and B-HT 933 decreased the latency of the loss of righting reflex in a dose-dependent manner, but B-HT 920 and oxymetazoline slightly prolonged it. 2) ${\alpha}_2-Adrenoceptor$ agonists produced dose·related increase in sleeping time. The potency was guanabenz>clonidine>oxymetazoline${\geq}$B-HT 933${\geq}$B-HT 920>guanfacine in this order. 3) ${\alpha}_2-Adrenoceptor$ antagonists decreased guanabenz-induced sleeping time in a dose ·dependent manner. The rank order of ${\alpha}_2-adrenoceptor$ antagonists was yohimbine>rauwolscine>piperoxan${\geq}$RX 781094. 4) Sleeping time caused by both ethanol and hexobarbital was not affected by yohimbine in chickens. 5) Methoxamine and phenylephrine showed little significant effect on the guanabenz-induced sleeping time. However, prazosin increased it. Paradoxically, corynanthine rather caused to decrease it. These results suggest that the stimulation of central ${\alpha}_2-adrenoceptor$ mediates sleeping, however it is remained uncertain in the role of central ${\alpha}_1-adrenoceptor$ in chickens. In addition, the one~two-day-old chickens may be considered as a useful, inexpensive and simple experimental model to evaluate the in vivo pharmacological action of the ${\alpha}_2-adrenoceptor$ agonist and antagonist related to sedation.

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An Analysis of Nerve Block for Cancer Pain Patients (암성통증환자(癌性痛症患者)의 신경차단요법(神經遮斷療法)의 분석(分析))

  • Lee, Jung-Seok;Kim, Hae-Gyu;Kim, Inn-Se;Chung, Kyoo-Sub
    • The Korean Journal of Pain
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    • v.1 no.1
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    • pp.53-58
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    • 1988
  • We have treated patients who have visited pain clinic and those admitted to the other departments of Pusan National University Hospital from Mar. 1987 to Feb. 1988 with complaints of severe cancer pain on both upper and lower abdomen and extremities by continuous administration of a very small amount of morphine in the lumbar subarachnoid(group I) and epidural(group II) space in 10 cases respectively. The results of analgesia obtained are as follows: 1. The average duration in onset of analgesia was 8 mins. in group I and 23 mins. in group II. 2. The average duration In maintaining analgesia was 12.4 hrs. in group I and 18.4 hrs. in group II. 3. The efficiency of analgesia in group I was excellent in 5, good in 4, and null in 1, and group II was excellent in 5, good in 2, and moderate in 3. 4. The degree of tolerance in group I was rather mild comparable ti that of pain score 4 till the 22nd. day of morphine administration. 5. The complications are: 2 of respiratory distress in group I, 2 of voiding difficulties in both group I and II, 1 of itching sensation in both group I and II, 1 of euphoria with hallucination In group I, and 1 of C.S.F leakage in group II. As results, it is thought that epidural administration is safer than subarachnoid administration in achieving analgesia with morphine among patients with malignant pain if the problem of tolerance is solved.

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Regulator of G-Protein Signaling 4 (RGS4) Controls Morphine Reward by Glutamate Receptor Activation in the Nucleus Accumbens of Mouse Brain

  • Kim, Juhwan;Lee, Sueun;Kang, Sohi;Jeon, Tae-Il;Kang, Man-Jong;Lee, Tae-Hoon;Kim, Yong Sik;Kim, Key-Sun;Im, Heh-In;Moon, Changjong
    • Molecules and Cells
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    • v.41 no.5
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    • pp.454-464
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    • 2018
  • Crosstalk between G-protein signaling and glutamatergic transmission within the brain reward circuits is critical for long-term emotional effects (depression and anxiety), cravings, and negative withdrawal symptoms associated with opioid addiction. A previous study showed that Regulator of G-protein signaling 4 (RGS4) may be implicated in opiate action in the nucleus accumbens (NAc). However, the mechanism of the NAc-specific RGS4 actions that induce the behavioral responses to opiates remains largely unknown. The present study used a short hairpin RNA (shRNA)-mediated knock-down of RGS4 in the NAc of the mouse brain to investigate the relationship between the activation of ionotropic glutamate receptors and RGS4 in the NAc during morphine reward. Additionally, the shRNA-mediated RGS4 knock-down was implemented in NAc/striatal primary-cultured neurons to investigate the role that striatal neurons have in the morphine-induced activation of ionotropic glutamate receptors. The results of this study show that the NAc-specific knock-down of RGS4 significantly increased the behaviors associated with morphine and did so by phosphorylation of the GluR1 (Ser831) and NR2A (Tyr1325) glutamate receptors in the NAc. Furthermore, the knock-down of RGS4 enhanced the phosphorylation of the GluR1 and NR2A glutamate receptors in the primary NAc/striatal neurons during spontaneous morphine withdrawal. These findings show a novel molecular mechanism of RGS4 in glutamatergic transmission that underlies the negative symptoms associated with morphine administration.

Imaging Neuroreceptors in the Living Human Brain

  • Wagner Jr Henry N.;Dannals Robert F.;Frost J. James;Wong Dean F.;Ravert Hayden T.;Wilson Alan A.;Links Jonathan M.;Burns H. Donald;Kuhar Michael J.;Snyder Solomon H.
    • The Korean Journal of Nuclear Medicine
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    • v.18 no.2
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    • pp.17-23
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    • 1984
  • For nearly a century it has been known that chemical activity accompanies mental activity, but only recently has it been possible to begin to examine its exact nature. Positron-emitting radioactive tracers have made it possible to study the chemistry of the human mind in health and disease, using chiefly cyclotron-produced radionuclides, carbon-11, fluorine-18 and oxygen-15. It is now well established that measurable increases in regional cerebral blood flow, glucose and oxygen metabolism accompany the mental functions of perception, cognition, emotion and motion. On May 25, 1983 the first imaging of a neuroreceptor in the human brain was accomplished with carbon-11 methyl spiperone, a ligand that binds preferentially to dopamine-2 receptors, 80% of which are located in the caudate nucleus and putamen. Quantitative imaging of serotonin-2, opiate, benzodiazapine and muscarinic cholinergic receptors has subsequently been accomplished. In studies of normal men and women, it has been found that dopamine and serotonin receptor activity decreases dramatically with age, such a decrease being more pronounced in men than in women and greater in the case of dopamine receptors than serotonin-2 receptors. Preliminary studies in patients with neuropsychiatric disorders suggests that dopamine-2 receptor activity is diminished in the caudate nucleus of patients with Huntington's disease. Positron tomography permits quantitative assay of picomolar quantities of neuro-receptors within the living human brain. Studies of patients with Parkinson's disease, Alzheimer's disease, depression, anxiety, schizophrenia, acute and chronic pain states and drug addiction are now in progress. The growth of any scientific field is based on a paradigm or set of ideas that the community of scientists accepts. The unifying principle of nuclear medicine is the tracer principle applied to the study of human disease. Nineteen hundred and sixty-three was a landmark year in which technetium-99m and the Anger camera combined to move the field from its latent stage into a second stage characterized by exponential growth within the framework of the paradigm. The third stage, characterized by gradually declining growth, began in 1973. Faced with competing advances, such as computed tomography and ultrasonography, proponents and participants in the field of nuclear medicine began to search for greener pastures or to pursue narrow sub-specialties. Research became characterized by refinements of existing techniques. In 1983 nuclear medicine experienced what could be a profound change. A new paradigm was born when it was demonstrated that, despite their extremely low chemical concentrations, in the picomolar range, it was possible to image and quantify the distribution of receptors in the human body. Thus, nuclear medicine was able to move beyond physiology into biochemistry and pharmacology. Fundamental to the science of pharmacology is the concept that many drugs and endogenous substances, such as neurotransmitters, react with specific macromolecules that mediate their pharmacologic actions. Such receptors are usually identified in the study of excised tissues, cells or cell membranes, or in autoradiographic studies in animals. The first imaging and quantification of a neuroreceptor in a living human being was performed on May 25, 1983 and reported in the September 23, 1983 issue of SCIENCE. The study involved the development and use of carbon-11 N-methyl spiperone (NMSP), a drug with a high affinity for dopamine receptors. Since then, studies of dopamine and serotonin receptors have been carried out in over 100 normal persons or patients with various neuropsychiatric disorders. Exactly one year later, the first imaging of opitate receptors in a living human being was performed [1].

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Influence of Blockade of Sympathetic Nervous System, Renin-Angiotensin System, and Vasopressin System on Basal Blood Pressure Levels and on Pressor Response to Norepinephrine, Angiotensin II, and Vasopressin (교감신경계, Renin-Angiotensin계, Vasopressin계의 차단이 혈압 및 Norepinephrine, Angiotensin II 및 Vasopressin의 승압효과에 미치는 영향)

  • Chung, Haeng-Nam
    • The Korean Journal of Pharmacology
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    • v.28 no.1
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    • pp.61-74
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    • 1992
  • Influence of the blockade of the three major pressor systems-sympathetic nervous system (SNS), renin-angiotensin system (RAS) and vasopressin system-on the pressor responsiveness to norepinephrine (NE), angiotensin II (AII), and vasopressin (VP) as well as on basal blood pressure (BP) levels was investigated in urethane-anesthetized rabbits. To block the SNS and RAS, chlorisondamine (CS) and pirenzepine (PZ), sympathetic ganglionic blockers, and enalapril (ENAL), an inhibitor of angiotensin converting enzyme, respectively were used. And for suppressing the VP system bremazocine (BREM), a kappa opiate receptor agonist shown to suppress plasma levels of VP, was employed. Each of CS (0.4 mg/kg), ENAL (2 mg/kg), and BREM (0.25 mg/kg) produced almost same levels of steady hypotensive state. The hypotensive effect of BREM was significantly attenuated by desmopressin, a synthetic VP-like analogue, suggesting the hypotension being at least in part due to suppression of plasma levels of VP. CS, ENAL and BREM elicited further fall of the BP which had been lowered by ENAL or BREM, CS or BREM, and CS or ENAL, respectively. The hypotension produced by both CS and PZ together with either of ENAL or BREM was more marked than that produced by the three drugs other than CS. CS potentiated the pressor response not only to NE but to AII and VP. The pressor effect of AII was increased by ENAL and BREM, too. The pressor response to VP was also enhanced by BREM. Blockade of ${\alpha}-adrenergic$ receptors with phentolamine or phenoxybenzamine potentiated the pressor response to AII and that to VP. The results on basal BP levels indicate that the three major pressor systems are all participating in control of BP, but SNS has the greatest potential for supporting BP. The finding that blockade of one of the pressor systems induced enhanced pressor responsiveness to the pressor hormone of that particular system as well as to the pressor hormone(s) of the other systems(s) provides evidence for important interactions among the three major pressor systems.

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