Antinociceptive effect of intrathecally administered P2-purinoceptor antagonists in rats

Driessen, Bernd; Reimann, Wolfgang; Selve, Norma; Friderichs, Elmar; Bültmann, Ralph

doi:10.1016/0006-8993(94)90770-6

Cited by 91 publications

(64 citation statements)

References 27 publications

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“…Peripheral administration of ATP and a,b-methylene-ATP have been shown to cause nociceptive responses (12,13). Furthermore, intrathecal administration of a,b-methylene-ATP produced thermal hyperalgesia, which was blocked by P2 purinoceptor antagonists (14,15). These findings show that ATP facilitates pain transmission at peripheral and spinal sites, probably via the P2X purinoceptor.…”

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confidence: 72%

Involvement of β2-Adrenergic and μ-Opioid Receptors in Antinociception Produced by Intracerebroventricular Administration of α,β-Methylene-ATP

Fukui

Nakagawa

Minami

et al. 2001

Japanese Journal of Pharmacology

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ABSTRACT-The present study examined what kind of receptors are involved in the antinociception produced by intracerebroventricular (i.c.v.) administration of a,b-methylene-ATP using antagonists at adrenergic, serotonin or opioid receptors. Antinociceptive effect of a,b -methylene-ATP (10 nmol / rat) was significantly attenuated by subcutaneous pretreatment with propranolol and naloxone, but not phentolamine or methysergide, at a dose of 10 mg / kg. I.c.v. pretreatment with propranolol (100 nmol/ rat), butoxamine (100 nmol /rat), ICI-118,551 (100 nmol/ rat) and naloxone (30 nmol/ rat) significantly attenuated the antinociceptive effect of a,b -methylene-ATP. However, i.c.v. pretreatment with atenolol (100 nmol /rat), naltrindole (30 nmol /rat) or nor-binaltorphimine (30 nmol / rat) did not show any significant effects. These results suggest that supraspinal b 2-adrenergic and m-opioid receptors are involved in the antinociceptive effect of i.c.v. administered a ,b -methylene-ATP.

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mentioning

confidence: 72%

Involvement of β2-Adrenergic and μ-Opioid Receptors in Antinociception Produced by Intracerebroventricular Administration of α,β-Methylene-ATP

Fukui

Nakagawa

Minami

et al. 2001

Japanese Journal of Pharmacology

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“…Intrathecal injection of strychnine has been reported to induce tactile allodynia in rats (Loomis et al, 2001). However, intrathecal injection of suramin was found to inhibit nociceptive responses in formalin- (Driessen et al, 1994) and carrageenaninflamed rats but not in neuropathic rats (Stanfa et al, 2000). Interestingly, Fukuhara et al (2000) reported that intrathecal injection of suramin at low doses inhibited prostaglandin-induced allodynia but at higher doses induced allodynia in mice.…”

Section: Discussionmentioning

confidence: 99%

Antiallodynic Effects of Intrathecal Orexins in a Rat Model of Postoperative Pain

Cheng¹,

Chou²,

Hwang³

et al. 2003

J Pharmacol Exp Ther

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Orexin A and B (hypocretin 1 and 2) are the endogenous ligands of orexin receptors, a G-protein-coupled orphan receptor family containing orexin 1 (OX 1 ) and orexin 2 (OX 2 ) types. Orexin A induces analgesia in acute and inflammatory pain models. We further elucidated the possible antiallodynic effect of intrathecal orexins in a rat model of postoperative pain. Mechanical allodynia was induced by incising the rat hind paw and evaluated with the withdrawal threshold to von Frey filament stimulation. Intrathecal orexin A (0.03-1 nmol) and orexin B (0.1-3 nmol) dose dependently attenuated the incision-induced allodynia. Orexin A (ED 50 ϭ 0.06 nmol) is more potent than orexin B. The effects of orexin A and B were abolished by their respective antibodies, but not by naloxone, and were attenuated by suramin and strychnine, the P 2X purinergic and glycine receptor antagonists, respectively. SB-334867, an OX 1 receptor antagonist, at 30 nmol completely blocked the effect of orexin A but, even at 100 nmol, only partially antagonized the effect of orexin B. Orexin A antibody, SB-334867, suramin, strychnine, or naloxone enhanced the incision-induced allodynic response. It is concluded that intrathecal orexins reduce incision-induced allodynia through OX 1 receptors. Glycine and P 2X purinergic receptors, but not opioid receptors, might be involved in the antiallodynic effects of orexins. Endogenous orexin might be released after incision injury to activate the spinal OX 1 receptors as an endogenous analgesic protector.

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“…Upon peripheral nerve injury, ATP released from primary afferent central terminals in the dorsal horn of the spinal cord modulates neurotransmission in the glutamatergic and GABAergic systems in dorsal horn neurons [12,24,28]. Thus, activation of the P2X4 receptor in the spinal cord causes pain behavior [6,44]. Recent studies indicate that paroxetine inhibits P2X4 receptors expressed in microglia [27,45].…”

Section: Discussionmentioning

confidence: 99%

The effect of selective serotonin reuptake inhibitor (SSRI) on pain-related behavior in a rat model of neuropathic pain

et al. 2014

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Introduction Some antidepressants are effective for treating neuropathic pain independent of any effect on depression. Selective serotonin reuptake inhibitors (SSRIs) are one of the potential agents to treat neuropathic pain. The aims of this study were to compare the effects of SSRI and non-steroidal anti-inflammatory drugs (NSAIDs) on pain-related behavior and expression of cytokines in a rat model of neuropathic pain. Materials and methods Spinal surgery was performed to apply nucleus pulposus (NP) to the dorsal root ganglion (DRG). NP animals were treated with saline (NP ? S

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Antinociceptive effect of intrathecally administered P2-purinoceptor antagonists in rats

Cited by 91 publications

References 27 publications

Involvement of β2-Adrenergic and μ-Opioid Receptors in Antinociception Produced by Intracerebroventricular Administration of α,β-Methylene-ATP

Involvement of β2-Adrenergic and μ-Opioid Receptors in Antinociception Produced by Intracerebroventricular Administration of α,β-Methylene-ATP

Antiallodynic Effects of Intrathecal Orexins in a Rat Model of Postoperative Pain

The effect of selective serotonin reuptake inhibitor (SSRI) on pain-related behavior in a rat model of neuropathic pain

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