Journal of the Korea Academia-Industrial cooperation Society
/
v.15
no.1
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pp.316-322
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2014
The present study investigated the inflammatory hypersensitivity following activation of the transient receptor potential vanilloid receptor-1(TRPV1) in rats. Experiments were carried out on male Sprague-Dawley rats weighing 220-260g. Following an subcutaneous injection of 5% formalin in the orofacial area, nociceptive scratching behavior was recorded for 9 successive 5-min intervals in rats. The subcutaneous injection of $25{\mu}L$ of 5% formalin produced noxious scratching behavior. Injection of capsaicin, TRPV1 agonist, alone into the vibrissa pad did not produced nociceptive behavior. After subcutaneous injection of capsaicin(0$0.1{\mu}g$, $1{\mu}g/10{\mu}L$) in the formalin-treated rats, nociceptive scratching behavior was recorded for 9 successive 5-min internals. Injection of capsaicin into the vibrissa pad significantly increased the number of scratches at 1 hours after injection. Noxious behavioral responses induced by subcutaneous capsaicin injection were significantly potentiated in formalin-treated rats. Pre or post-treatment with iodo-resinaferatoxin(IRTX), TRPV1 antagonist, significantly attenuated increased nociceptive behavior. These findings suggest that activation of the TRPV1 enhanced formalin-induced inflammatory pain in the orofacial area of rats.
Askari-Zahabi, Khadijeh;Abbasnejad, Mehdi;Kooshki, Razieh;Raoof, Maryam;Esmaeili-Mahani, Saeed;Pourrahimi, Ali Mohammad;Zamyad, Mahnaz
The Korean Journal of Pain
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v.35
no.1
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pp.22-32
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2022
Background: Migraine headaches have been associated with sensory hyperactivity and anomalies in social/emotional responses. The main objective of this study was to evaluate the potential involvement of orexin 1 receptors (Orx1R) within the basolateral amygdala (BLA) in the modulation of pain and psychosocial dysfunction in a nitroglycerin (NTG)-induced rat model of migraine. Methods: Adult male Wistar rats were injected with NTG (5 mg/kg, intraperitoneal) every second day over nine days to induce migraine. The experiments were done in the following six groups (6 rats per group): untreated control, NTG, NTG plus vehicle, and NTG groups that were post-treated with intra-BLA microinjection of Orx1R antagonist SB-334867 (10, 20, and 40 nM). Thermal hyperalgesia was assessed using the hot plate and tail-flick tests. Moreover, the elevated plus maze (EPM) and open field (OF) tests were used to assess anxiety-like behaviors. The animals' sociability was evaluated using the three-chamber social task. The NTG-induced photophobia was assessed using a light-dark box. Results: We observed no change in NTG-induced thermal hyperalgesia following administration of SB-334867 (10, 20, and 40 nM). However, SB-334867 (20 and 40 nM) aggravated the NTG-induced anxiogenic responses in both the EPM and OF tasks. The NTG-induced social impairment was overpowered by SB-334867 at all doses. Time spent in the dark chamber of light-dark box was significantly increased in rats treated with SB-334867 (20 and 40 nM/rat). Conclusions: The findings suggest a role for Orx1R within the BLA in control comorbid affective complaints with migraine in rats.
Jung, Jai Yun;Bang, Kyung Ho;Kim, Sang Hyon;Kim, Yong Ik
The Korean Journal of Pain
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v.18
no.2
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pp.138-141
/
2005
Background: There have been many attempts to alleviate pain after surgery, but there is no common approach to the control of postoperative pain. The use of epidural opioids, with local anesthetics, has been a widely employed formula to date. Ketamine, an N-methyl-d-aspartate receptor antagonist, has an excellent analgesic effect. Although there have been many reports on the dose and route of administrating analgesics, there have been few concerning the continuous epidural infusion of ketamine with fentanyl. We designed this study to find the effects of ketamine compared to those of epidurally injected bupivacaine and fentanyl, and used this trial to study any potential side effects. Methods: In a double blind trial, 55 patients received either fentanyl, $0.3{\mu}g/kg/h$ (Group F), or fentanyl, $0.3{\mu}g/kg/h$, and ketamine, 0.1 mg/kg/h (Group FK), added to 0.125% bupivacaine, at rates as high as 2 ml/h, for patient controlled epidural analgesia (PCEA) following a transabdominal hysterectomy. Ten minutes before the operation, patients received 10 ml of 0.125% bupivacaine, with either 0.5 mg/kg ketamine or the same amount of normal saline with $50{\mu}g$ fentanyl added. The pain scores and the side effects were recorded at 1, 3, 6 and 24 hour post operation. Results: There were no differences in the pain scores or side effects between the two groups. Conclusions: We failed to find any effect of the addition of epidural ketamine compared to the that of the bupivacaine and fentanyl formula. However, it is suggested that further investigations will be required on the dose and route of administration.
Purpose: Radiotracers that bind to the central benzodiazepine receptor are useful for the investigation of various neurological and psychiatric diseases. [C-11]Flumazenil, a benzodiazepine antagonist, is the most widely used radioligand for central benzodiazepine receptor imaging by PET. We synthesized 3-(2-[F-18]fluoro)flumazenil, a new fluorine-18 ($t_{1/2}$= 110 min) labeled analogue of benzodiazepine receptor imaging agent, and evaluated in vivo for biodistribution in mice. Materials and Methods: Flumazenil (Ro 15-1788) was synthesized by a modification of the reported method. Precursor of 3-(2-[F-18]fluoro)flumazenil, the tosylated flumazenil derivative was prepared by the tosylation of the ethyl ester by ditosylethane. [F-18] labeling of tosyl substitued flumazenil precursor was performed by adding F-18 ion at $85^{\circ}C$ in the hot ceil for 20 min. The reaction mixture was trapped by C18 cartridge, washed with 10% ethanol, and eluted by 40% ethanol. Bidistribution in mice was determined after intravenous injection. Results: The total chemical yield of tosylated flumazenil derivative was ${\sim}40%$. The efficiency of labeling 3-(2-[F-18]fluoro)flumazenil was 66% with a total synthesis time of 50 min. Brain uptakes of 3-(2-[F-18]fluoro)flumazenil at 10, 30, 60 min after injection, were $2.5{\pm}0.37,\;2.2{\pm}0.26,\;2.1{\pm}0.11$ and blood activities were $3.7{\pm}0.43,\;3.3{\pm}0.07,\;3.3{\pm}0.09%ID/g$, respectively. Conclusion: We synthesized a tosylated flumazenil derivative which was successfully labeled with no-carrier-added F-18 by nucleophilic substitution.
The Journal of the Korean Society for Microbiology
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v.16
no.1
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pp.49-55
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1981
Recent studies have demonstrated that histamine could have a modulatory influence on the immune response in vitro and in vivo. However, the effect of histamine on immune response in mice has not been extensivley analyzed. In the present study the regulatory effects of cimetidine, a histamine-2-receptor antagonist(H2 blocker) and histamine on the immune response to sheep red blood cells(SRBC) were evaluated in mice. Mice pretreated with daily intraperitoneal injection of varying concentrations of cimetidine for 14 days were immunized intraperitoneally with various concentrations of SRBC($10^6,\;10^7,\;and\;10^8$ cells) and challenged 4 days post immunization. The cellular immune response was determined by measuring the footpad swelling reaction. Footpad swelling reaction of each mouse was measured at 3hr(Arthus) reaction) and 24 or 48 hr(delayed reactions) after challenge. The humoral immune response was determined by measuring hemagglutinins to SRBC. Histamine in varying concentrations($10^{-1},\;10^{-3}\;and\;10^{-5}M$(was added in SRBC suspension at the time of antigen challenge into footpad, and 24-hr delayed type hypersensitivity(DTH) was measured. Cimetidine in varying concentrations(10, 50, 250, 1250 and 6250${\mu}g$) enhanced 24-hr DTH and this enhancement of DTH was more pronounced at 250${\mu}g$ of cimetidine. However, there were no significant differences between the cimetidine-pretreated groups and controls in Arthus reaction and hemagglutinin titers. Histamine suppressed the DTH in the dose-dependent fashion. This suppression was more pronounced at lower concentration of immunizing antigen($10^7\;and\;10^6$ SRBC). However, histamine did not diminish the DTH at higher concentration of antigen($10^8$ SRBC). These results present the evidences which strongly suggest that cimetidine enhances the cell-mediated immune response but not significantlly influences the humoral immune response and that exogenous and endogenous histamine is involved in the modulation of cellular immune response as well as immediate hypersensitivity.
In the electrically stimulated guinea-pig ileum, which was incubated in the modified Krebs-Henseleit bicarbonate buffer solution containing various concentrations of electrolytes at $4^{\circ}C$ for 24 hours, the effect of naloxone on the inhibitory action of morphine was investigated. Incubation potentiated the inhibitory action of morphine. In the incubated preperation, the inhibitory action of morphine was potentiated in the $Na^+\;75mM$, and $K^+\;2.9mM$ groups, while that action of morphine was reduced in the $Ca^{++}\;3.6mM,\;Mg^{++}$ free and $Mn{++}\;0.2mM$ groups. Naloxone in incubation media potentiated in the inhibitory action of morphine. In the preparations which were incubated in various concentrations of electrolytes plus naloxone, the action of morphine was reduced in $Na^+\;75mM,\;K^+\;2.9mM$, and $Ca^{++}\;3.6mM$ groups, while that action of morphine was potentiated in $Mg^{++}$free and $Mn{++}\;0.2mM$ groups. Naloxone antagonised those actions of morphine. However, $pA_2$ values for naloxone (index for affinity for antagonist) was not changed. Thus changes in the inhitory action of morphine caused by incubation are probably not the result of changes in the affinity of receptor, but due to the alterations in the events which precede or follow the receptor binding by incubations.
It has been known that calcium antagonists also inhibit the radioligand binding to muscarinic and $\alpha$-adrenergic receptors and, in case of verapamil, these inhibitions may play a role in the effects of verapamil on the heart. In this study, the effects of nicardipine, nifedipine, nimodipine, diltiazem and verapamil on the binding of [$^3H$]dihydroalprenolol (DHA) to dog cardiac ${\beta}$-adrenergic receptors were examined. A single uniform [$^3H$]DHA binding site ($K_D/= 5nM\;and\;B_{max}=2600$ fmol/mg protein) was identified in dog cardiac sarcolemma. [$^3H$]DHA binding was not affected by the usual therapeutic concentrations of these calcium antagonists (nanomolar range) but in the "nonspecific"concentration ranges ($28-180{\mu}m$) these drugs inhibited [$^3H$]DHA binding to $\beta$-adrenergic receptors. Nicardipine, nifedipine, nimodipine and diltiazem competed for [$^3H$]DHA binding to ${\beta}$-adrenergic receptors with dissociation constants ($K_i$) of $28{\mu}m,\' 74{\mu}m, 39{\mu}m \;and \;35{\mu}m,$ respectively. Verapamil ($K_i=176.5 {\mu}m$) was less potent inhibitor than other drugs and this inhibition was noncompetitive; the maximal binding capacity ($B_{max}$) $300 {\mu}m$ verapamil without change in the apparent dissociation constant (4K_D$) for DHA. These results indicate that the inhibitory action of calcium antagonists at high concentrations on ${\beta}$-adrenergic receptors is not involved in the therapeutic effects of these drugs by the calcium channel blocking action.
Kim, Yeon-Hwa;Lee, Yun-Kyoung;Lee, Han-Sol;Jung, Min-Whan;Lee, Chang-Joong
Animal cells and systems
/
v.13
no.3
/
pp.275-281
/
2009
The effects of pentylenetetrazol (PTZ), a GABA receptor antagonist, were studied on passive avoidance learning and expression of heat shock protein 70 (hsp70), neuroglobin, and fatty acid binding protein-7 (fabp-7) genes. Zebrafish were trained to stay in a dark compartment to avoid a weight dropping in an acryl shuttle box with a central sliding door. In two training sessions of 2 h interval, each consisting of 3 trials, the crossing time was significantly increased from $43.2{\pm}14.4s$ to $149.3{\pm}38.5s$ in the first training session and remained $116.1{\pm}36.0s$ s in the first trial of the second training session in the control. In zebrafish treated with PTZ before the first training session, the crossing time was significantly increased neither in the first nor in the second training session. However, the increased crossing time was maintained in the second training session when 10 mM PTZ was treated three times for 10 min at 30 min intervals between the first and second training session. Quantitative real-time PCR showed that expression level of hsp70 mRNA increased two to eight fold over that of control in the brain at 0-24 h after termination of PTZ treatment. No change in expression of neuroglobin and fabp-7 mRNA was shown in PTZ-treated zebrafish. Our studies suggest that PTZ impairs learning ability in avoidance response and also modifies expression of genes related to the neuroprotection.
Capsaicin is known to be an analgesic agent, affecting the synthesis, storage, , transport and release of substance p, the principal neurotransmitter of pain from periphery to the central nervous system(CNS). DA-5018, a newly synthesized capsaicin derivative has shown potent analgesic effect comparable to that of morphine in various rat models of experimentally inducted acute pairs. In this study the mechanism of analgesic actlvity of DA-5018 was examined. First, the electrically-evoked contraction of guinea pig trachea was inhibited by DA-5018 and these inhibition was recovered by incubation with capsafepine(3$\muM$), capsaicin receptor antagonist and this result suggested that DA-5018 has affinity on capsaicin receptor. The correlation between the norciceptive threshold and the release of substance P was evaluated. In vivo perfusion of slices of the rat spinal cord with DA-5018(10, 100$\muM$) produced a significant increase of the release of substance P and this increase was less than that of capsaicin(10$\muM$). The norciceptive threshold of rat treated with DA-5018(1 mg/kg, p.o) in tall pinch test increased from 2.9$\pm$0.3 to 23.5 $\pm$6.61. Tail pinch latency increased to a maximun at 15 min after DA-5018 treatment and then declined to control values by 120 min. The capsaicin-evoked release ot substance P from the spinal cord slices of rat treated with DA-5018 reduced from 2.38$\pm$ 0.79 to 0.69$\pm$ 0.26 pg/mg wet weight. This reduction reached to a minium at 15 min after DA-5018 treatment and then recovered to control value by 120 min. These results mean that analgesic activity of DA-5018 is due to release of substance P The effect of DA-5018 cream on electrically-evoked neurogenic inflammation of rat saphenous nerve was compared with capsaicin (zostrix-HP). DA-5018 showed 34% inhibition of the neurogenic extravasation while capsaicin showed significant 67% inhibition. This result indicates that the potency of DA-5018 in the release of substance P is less than that of capsaicin. These results suggest that the release of substance P is partially involved in the mechanism of analgesic action of DA-50l8.
Objective: The present study was done to clarify the effects of nicotine and nicotine tartrate on the mouse oocyte maturation in vitro. Methods: GV (germinal vesicle) oocytes were isolated from Graafian follicle of ovaries with sharp needles under a stereomicroscope from female mouse of ICR strain (4 weeks old). Collected oocytes were cultured for 17 hours at $37^{\circ}C$, 5% $CO_2$ in air and 100% humidified condition in incubator. New MHBS was the basic medium used in which nicotine, nicotine tartrate, and mecamylamine (antagonist of nicotinic acetylcholine receptor) were added depending on the experimental group. GV oocytes were cultured in one of these media. Results: Nicotine ($300{\mu}M{\sim}5mM$) had no effects on GVBD (germinal vesicle breakdown) compared to the control, but increasing concentration of nicotine led to an decrease in the first polar body formation. However, nicotine ($10{\sim}500{\mu}M$) induced GVBD in a dose-dependent manner of GV oocytes in a medium containing dbcAMP. Nicotine tartrate ($50{\mu}M{\sim}5mM$) had no effects on GVBD compared to the control but, increasing concentration of nicotine tartrate led to an decrease in the first polar body formation. Mecamylamine $10{\mu}M$ added to the medium containing nicotine ($300{\mu}M{\sim}5mM$) showed higher percentage of the first polar body formation compared to the nicotine ($300{\mu}M{\sim}5mM$) treatment group. Mecamylamine $10{\mu}M$ added to the medium containing nicotine tartrate ($50{\mu}M{\sim}5mM$) showed higher percentage of the first polar body formation compared to the nicotine tartrate ($50{\mu}M{\sim}5mM$) treatment group. Conclusion: The present study suggest that nicotine and nicotine tartrate have the harmful effects on the meiotic maturation of the mouse oocytes in vitro. However, mecamylamine block harmful effects of nicotine and nictine tartrate.
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