Involvement of calcium in pain and antinociception

Wa, Prado

doi:10.1590/s0100-879x2001000400003

Cited by 51 publications

(44 citation statements)

References 46 publications

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“…[16,25,32,34]. Furthermore, Ca 2+ chelators or antagonists of L-, N-and P-type Ca 2+ channels, potentated -opioid receptor-mediated antinociception [25,27]. Conversely, the antinociception produced by selective ␦-opioid receptor agonists was potentated by agents that increase intracellular Ca 2+ whereas it was reduced by i.c.v.…”

Section: Introductionmentioning

confidence: 99%

Ryanodine receptors are involved in muscarinic antinociception in mice

Galeotti

Bartolini

Ghelardini

2005

Behavioural Brain Research

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The role of ryanodine receptors (RyRs) in the induction of muscarinic antinociception was investigated in a condition of acute thermal pain by means of the mouse hot-plate test. I.c.v. administration of non-hyperalgesic doses of ryanodine (0.001-0.06 nmol per mouse i.c.v.), an antagonist of ryanodine receptors (RyRs), dose-dependently prevented the antinociception induced by both physostigmine (100-150 g kg −1 s.c.) and oxotremorine (40-70 g kg −1 s.c.). A shift to the right of the dose-response curve of both cholinomimetic compounds was observed. Pretreatment with non-analgesic doses of 4-chloro-m-cresol (4-Cmc; 0.003-0.3 nmol per mouse i.c.v.), an agonist of RyRs, reversed in a dosedependent manner the antagonistic effect produced by ryanodine of muscarinic antinociception. The pharmacological treatments employed neither modified the animals' gross behavior nor produced any behavioral impairment of mice as revealed by the rota-rod and hole-board tests. These results indicate that a variation of intracellular calcium contents at the central nervous system level is involved in muscarinic antinociception. In particular, the stimulation of RyRs appears to play an important role in the increase of the pain threshold produced by physostigmine and oxotremorine in mice.

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Section: Introductionmentioning

confidence: 99%

Ryanodine receptors are involved in muscarinic antinociception in mice

Galeotti

Bartolini

Ghelardini

2005

Behavioural Brain Research

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“…These drugs act as antagonists on N- (15,16) and P/ Q-type (17) VOCC. A marked similarity between the effects of aminoglycoside antibiotics and magnesium ions, as well as a prompt antagonism of their effects when the extracellular Ca 2+ concentration is increased, have been demonstrated earlier in neuromuscular transmission (for a review, see 11), and confirmed in models of artificial membranes, in rodent cardiac and smooth muscles, and isolated mast cells (for a review, see 18). Antinociception following gentamicin has been demonstrated in rodent models of phasic or persistent pain (19)(20)(21)(22).…”

Section: Introductionmentioning

confidence: 76%

“…Ca 2+ influx occurs mainly through L-, N-, P/Q-, and T-type voltage-operated calcium channels (VOCC) (for a review, see 1,10). Antagonists of L-type VOCC potentiate opiate analgesia in rodents, but this effect depends on the route of administration and the algesimetric test used (for a review, see 11). Mibefredil (12), a selective T-type VOCC antagonist, does not alter the response of mice in the tail-flick test.…”

Section: Introductionmentioning

confidence: 99%

Antinociceptive potency of aminoglycoside antibiotics and magnesium chloride: a comparative study on models of phasic and incisional pain in rats

Prado

Filho

2002

Braz J Med Biol Res

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A close relationship exists between calcium concentration in the central nervous system and nociceptive processing. Aminoglycoside antibiotics and magnesium interact with N-and P/Q-type voltageoperated calcium channels. In the present study we compare the antinociceptive potency of intrathecal administration of aminoglycoside antibiotics and magnesium chloride in the tail-flick test and on incisional pain in rats, taken as models of phasic and persistent postsurgical pain, respectively. The order of potency in the tail-flick test was gentamicin (ED 50 = 3.34 µg; confidence limits 2.65 and 4.2) > streptomycin (5.68 µg; 3.76 and 8.57) = neomycin (9.22 µg; 6.98 and 12.17) > magnesium (19.49 µg; 11.46 and 33.13). The order of potency to reduce incisional pain was gentamicin (ED 50 = 2.06 µg; confidence limits 1.46 and 2.9) > streptomycin (47.86 µg; 26.3 and 87.1) = neomycin (83.17 µg; 51.6 and 133.9). The dose-response curves for each test did not deviate significantly from parallelism. We conclude that neomycin and streptomycin are more potent against phasic pain than against persistent pain, whereas gentamicin is equipotent against both types of pain. Magnesium was less potent than the antibiotics and effective in the tail-flick test only.

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“…The VGCCs most extensively studied in nociception are the N-, P/Q-and T-type Ca 2+ channels [45][46][47]. It is well established that an increase in intracellular Ca 2+ has an important role in neurotransmitter release, cell membrane excitability, activation of intracellular proteins, and reduction of the pain threshold [48][49][50]. The concentration of intracellular Ca 2+ is regulated by several mechanisms; one such mechanism is the influx of Ca 2+ via VGCCs through the plasma membrane.…”

Section: Discussionmentioning

confidence: 99%

Role of pertussis toxin-sensitive G-protein, K+ channels, and voltage-gated Ca2+ channels in the antinociceptive effect of inosine

Macedo-Júnior

Nascimento

Luiz-Cerutti

et al. 2012

Purinergic Signalling

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Inosine is the first metabolite of adenosine. It exerts an antinociceptive effect by activating the adenosine A 1 and A 2A receptors. We have previously demonstrated that inosine exhibits antinociceptive properties in acute and chronic mice models of nociception. The aim of this study was to investigate the involvement of pertussis toxinsensitive G-protein-coupled receptors, as well as K + and Ca 2+ channels, in the antinociception promoted by inosine in the formalin test. Mice were pretreated with pertussis toxin (2.5 μg/site, i.t., an inactivator of G i/0 protein); after 7 days, they received inosine (10 mg/kg, i.p.) or morphine (2.5 mg/kg, s.c., used as positive control) immediately before the formalin test. Another group of animals received tetraethylammonium (TEA) or 4-aminopyridine (4-AP) (1 μg/site, i.t., a non-specific voltage-gated K + channel blockers), apamin (50 ng/site, i.t., a small conductance Ca 2+ -activated K + channel blocker), charybdotoxin (250 pg/site, i.t., a largeconductance Ca 2+ -activated K + channel blocker), glibenclamide (100 μg/site, i.t., an ATP-sensitive K + channel blocker) or CaCl 2 (200 nmol/site, i.t.). Afterwards, the mice received inosine (10 mg/kg, i.p.), diclofenac (10 mg/kg, i.p., a positive control), or morphine (2.5 mg/kg, s.c., a positive control) immediately before the formalin test. The antinociceptive effect of inosine was reversed by the pre-administration of pertussis toxin (2.5 μg/site, i.t.), TEA, 4-aminopyridine, charybdotoxin, glibenclamide, and CaCl 2 , but not apamin. Further, all K + channel blockers and CaCl 2 reversed the antinociception induced by diclofenac and morphine, respectively. Taken together, these data suggest that the antinociceptive effect of inosine is mediated, in part, by pertussis toxinsensitive G-protein coupled receptors and the subsequent activation of voltage gated K + channel, large conductance Ca 2+ -activated and ATP-sensitive K + channels or inactivation of voltage-gated Ca 2+ channels. Finally, small conductance Ca 2+ -activated K + channels are not involved in the antinociceptive effect of inosine.

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Involvement of calcium in pain and antinociception

Cited by 51 publications

References 46 publications

Ryanodine receptors are involved in muscarinic antinociception in mice

Ryanodine receptors are involved in muscarinic antinociception in mice

Antinociceptive potency of aminoglycoside antibiotics and magnesium chloride: a comparative study on models of phasic and incisional pain in rats

Role of pertussis toxin-sensitive G-protein, K+ channels, and voltage-gated Ca2+ channels in the antinociceptive effect of inosine

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