Antinociceptive actions of different classes of excitatory amino acid receptor antagonists in mice

Näsström, Jacques; Karlsson, Urban; Post, Claes

doi:10.1016/0014-2999(92)90067-e

Cited by 160 publications

(34 citation statements)

References 46 publications

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“…For example, we have shown that most chemosensitive abdominal visceral endings are Cfibers (21), that the responses of visceral afferent C-fibers to ischemia display characteristics of visceral nociceptors (29), and that throughout the ischemic period metabolites associated with nociception are produced (21,34,40). Our finding that NMDA and non-NMDA receptors play a role in the spinal transmission of the afferent arm of the abdominal ischemia reflex arc not only is consistent with other studies showing that glutamatergic receptors are important for the synaptic transmission of nociceptive input to the dorsal horn of the spinal cord (4,27,32) but also provides the first evidence that spinal NMDA and non-NMDA receptors mediate spinal sensory neurotransmission of impulse activity from visceral afferent fibers to the CNS during abdominal ischemia.…”

Section: Discussionsupporting

confidence: 91%

Role of spinal NMDA and non-NMDA receptors in the pressor reflex response to abdominal ischemia

Gee

Tjen‐A‐Looi

Hill

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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Abdominal ischemia induces a pressor reflex caused mainly by C-fiber afferent stimulation. Because excitatory amino acids, such as glutamate, bind to N-methyl-D-aspartate (NMDA) and non-NMDA [dl-␣-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA)] receptors and serve as important spinal neurotransmitters, we hypothesized that both receptors play a role in the abdominal ischemia pressor reflex. In chloralose-anesthetized cats, NMDA receptor blockade with 25.0 mM dl-2-amino-5-phosphonopentanoate did not alter the pressor reflex (33 Ϯ 9 to 33 Ϯ 7 mmHg, P Ͼ 0.05, n ϭ 4), whereas AMPA receptor blockade with 4.0 mM 6-nitro-7-sulfamylbenzo(f)quinoxaline-2,3-dione significantly attenuated the reflex (29 Ϯ 5 to 16 Ϯ 4 mmHg, P Ͻ 0.05, n ϭ 6). Because several studies suggest that anesthesia masks the effects of glutamatergic receptors, this experiment was repeated on decerebrate cats, and in this group, NMDA receptor blockade with 25.0 mM dl-2-amino-5-phosphonopentanoate significantly altered the pressor reflex (36 Ϯ 3 to 25 Ϯ 4 mmHg, P Ͻ 0.05, n ϭ 5). Our combined data suggest that spinal NMDA and AMPA receptors play a role in the abdominal ischemia pressor reflex.6-nitro-7-sulfamylbenzo(f)quinoxaline-2,3-dione; dl-2-amino-5-phosphonopentanoate; ␣-chloralose; decerebrate ACTIVATION OF CHEMOSENSITIVE C-fibers and, to a lesser extent, mechanosensitive A-␦ fibers in the abdominal visceral region causes large cardiovascular reflex responses. The blood pressure response to abdominal ischemia is bimodal. There is a rapid shift in blood volume evoked by occlusion of the celiac and superior mesenteric arteries that accounts for the initial, rapid, and transient increase in blood pressure (13,17,38,39). A reflex evoked by visceral ischemia accounts for the second, and more prolonged, increase in blood pressure (33, 39). Our previous studies have shown that interruption of blood flow to visceral organs during abdominal ischemia causes the production of endogenous metabolites such as bradykinin (5, 21, 30), histamine (12), leukotrienes (22), prostaglandins (6), protons (37), reactive oxygen species (36, 38), serotonin (11, 21), and substance P (21, 28), which, in turn, stimulate abdominal C-fiber afferent nerve endings. The axonal terminals of these afferent fibers synapse in the dorsal horn of the spinal cord onto neurons that project through interneurons to cardiovascular regions of the medulla. From these medullary neurons, projections extend to sympathetic preganglionic cell bodies, the activation of which ultimately stimulates efferent nerves innervating the heart and blood vessels. Thus stimulation of abdominal visceral afferent fibers evokes reflex increases in blood pressure through alterations in cardiac contractility, heart rate, and peripheral vasoconstriction. A number of studies from our laboratory have examined the role of various endogenous metabolites (and the receptors that bind to them) in the activation of visceral afferent nerves during the abdominal ischemia pressor reflex (5,6,11,12,21,22,28,30,(36)(37)(38)...

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Section: Discussionsupporting

confidence: 91%

Role of spinal NMDA and non-NMDA receptors in the pressor reflex response to abdominal ischemia

Gee

Tjen‐A‐Looi

Hill

et al. 2002

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Therefore, activation of NMDA receptors is well known to be essential for central sensitization-mediated chronic pain (see reviews by Basbaum et al, 2009 andHulsebosch et al, 2009). Intrathecal administration of NMDA receptor antagonists has been reported to suppress formalin-induced tonic pain (Nä sström et al, 1992;Yamamoto and Yaksh, 1992;Chaplan et al, 1997). For example, MK-801 attenuated tonic pain in rats by 67 Ϯ 16% (Chaplan et al, 1997), consistent with our MK-801 observation.…”

Section: Downloaded Frommentioning

confidence: 99%

A Series of d-Amino Acid Oxidase Inhibitors Specifically Prevents and Reverses Formalin-Induced Tonic Pain in Rats

Gong

Gao²,

Wang³

et al. 2010

J Pharmacol Exp Ther

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We have found that mutation of D-amino acid oxidase (DAO) diminished formalin-induced tonic pain. The present research further studied the analgesic effects of a series of DAO inhibitors in this model. 5-Chlorobenzo[d]isoxazol-3-ol (CBIO), 4H-thieno[3,2-b]pyrrole-5-carboxylic acid (compound 8), 5-methylpyrazole-3-carboxylic acid (AS057278), sodium benzoate, and 4-nitro-3-pyrazole carboxylic acid (NPCA) inhibited rat spinal cord-derived DAO activity in a concentration-dependent manner, with maximal inhibition of 100% and potency rank of CBIO Ͼ compound 8 Ͼ AS057278 Ͼ sodium benzoate Ͼ NPCA. In rats, intrathecal injections of CBIO, compound 8, AS057278, and sodium benzoate but not NPCA specifically prevented formalin-induced tonic pain but not acute nociception, with the same potency order as in the DAO activity assay. The highly potent analgesia of DAO inhibitors was evidenced by CBIO, which prevented 50% pain at 0.06 g, approximately 5-fold the potency of morphine. CBIO given after formalin challenge also reversed the established pain state to the same degree as prevention. The antihyperalgesic potencies of these DAO inhibitors were highly correlated to their inhibitions of spinal DAO activity. Maximum inhibition of pain by these compounds was approximately 60%, comparable with that of the N-methyl-D-aspartic acid receptor antagonist (ϩ)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801), suggesting that a larger portion of formalin-induced tonic pain is "DAO-sensitive," whereas the remaining 40% of tonic pain and acute nociception is "DAO-insensitive." These findings, combined with our previous DAO gene mutation and induction results, indicate spinal DAO mediates both induction and maintenance of formalin-induced tonic pain and further validate spinal DAO as a novel and efficacious target molecule for the treatment of chronic pain.

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“…13,14,[16][17][18] Ketamine also has antinociceptive effects for acute pain induced by the tailflick test, 19,20 in which NMDA receptor antagonists are not effective. 21 Several behavioural and electrophysiologic studies suggest that ketamine produces antinociceptive effects through activation of monoaminergic descending inhibitory pathways. 19,20,[22][23][24] The mechanism of the antinociceptive effects of ketamine is suggested to depend upon the presence peripheral inflammation.…”

Section: Objectifmentioning

confidence: 99%

Systemic ketamine inhibits hypersensitivity after surgery via descending inhibitory pathways in rats

Koizuka

Obata

Sasaki

et al. 2005

Can J Anesth/J Can Anesth

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P Pu ur rp po os se e: : Systemic ketamine suppresses several types of chronic pain. Although ketamine is used as a general anesthetic agent, the analgesic effect of systemic ketamine for early-stage postoperative pain is not clear. We investigated the efficacy and mechanism of systemic ketamine in a rat model of postoperative pain.M Me et th ho od ds s: : An incision was made in the plantar aspect of the left hind paw in male Wistar rats. Mechanical hypersensitivity was measured using calibrated von Frey filaments. The anti-hypersensitivity effect of systemic or intrathecal administration of ketamine was determined every hour after making the incision. We examined the effects of intrathecal pretreatment with yohimbine, an α 2 -adrenoceptor antagonist, and methysergide, a serotonergic receptor antagonist, on the anti-hypersensitivity effect of ketamine. We also examined the effect of systemic ketamine on the c-fos immunoreactivity in the spinal cord.R Re es su ul lt ts s: : Systemic administration of ketamine at doses from 3 to 30 mg·kg -1 produced anti-hypersensitivity effects in a dose-dependent manner. Intrathecal administration of ketamine had no effect. There was no significant difference between effects of pre-and post-incisional administration. Intrathecal pretreatment with yohimbine (10 µg) or methysergide (15 µg) completely reversed the anti-hypersensitivity effects of systemic ketamine. Systemic ketamine reduced fos expression in laminae I-II in the dorsal horn of the lumbar spinal cord ipsilateral to the paw incision.C Co on nc cl lu us si io on ns s: : The results suggest that systemic administration of ketamine perioperatively suppresses early-stage postoperative pain via monoaminergic descending inhibitory pathways. Objectif Méthode : Une incision a été faite dans la partie plantaire de la patte arrière gauche de rats mâles Wistar. L'hypersensibilité mécanique a été mesurée à l'aide de filaments von Frey calibrés. L'effet d'antihypersensibilité de la kétamine vasculaire ou intrathécale a été déter-miné toutes les heures après l'incision. Nous avons étudié les effets du prétraitement intrathécal avec yohimbine, un antagoniste des récep-teurs α 2 -adrénergiques, et méthysergide, un antagoniste des récep-teurs sérotoninergiques, sur l'effet anti-hypersensibilité de la kétamine. Nous avons aussi vérifié l'effet de la kétamine intravasculaire sur l'immunoréactivité des c-fos dans la moelle épinière. Résultats : L'administration intravasculaire de kétamine en doses de

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Antinociceptive actions of different classes of excitatory amino acid receptor antagonists in mice

Cited by 160 publications

References 46 publications

Role of spinal NMDA and non-NMDA receptors in the pressor reflex response to abdominal ischemia

Role of spinal NMDA and non-NMDA receptors in the pressor reflex response to abdominal ischemia

A Series of d-Amino Acid Oxidase Inhibitors Specifically Prevents and Reverses Formalin-Induced Tonic Pain in Rats

Systemic ketamine inhibits hypersensitivity after surgery via descending inhibitory pathways in rats

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