Ketamine-Induced Potentiation of Morphine Analgesia in Rat Tail-Flick Test: Role of Opioid-, .ALPHA.2-Adrenoceptors and ATP-Sensitive Potassium Channels

Campos, Adriana Rolim; Santos, Flávia Almeida; Rao, V. S. N.

doi:10.1248/bpb.29.86

Cited by 26 publications

(18 citation statements)

References 27 publications

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“…Each group consisted of six rats and received injections as follows: Group 1: animals were treated with the vehicle (DMSO/water, 2 : 3) intraperitoneally (i.p. [20]. Group 2: animals were treated with morphine (80 mg/kg, s.c.) [19].…”

Section: Experimental Designmentioning

confidence: 99%

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The involvement of K_ATP channels in morphine‐induced antinociception and hepatic oxidative stress in acute and inflammatory pain in rats

Afify

Khedr

Omar

et al. 2012

Fundamemntal Clinical Pharma

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This study investigated the role of K(ATP) channels in morphine-induced antinociception and hepatic oxidative stress in acute and inflammatory pain. The K(ATP) channel modulators (K(ATP) channel opener, diazoxide 100 mg/kg, p.o, and K(ATP) channel blocker, glibenclamide, 3 mg/kg i.p.) were administered with morphine (80 mg/kg, i.p.). Antinociception was assessed by the tail-flick and formalin tests in rats and measured by the area under the curve values and the maximum percent effect for 3 h. The indices of hepatic oxidative stress: glutathione, glutathione peroxidase, and malondialdehyde were then determined in the liver homogenates obtained from the treated animals. In both tests, glibenclamide antagonized morphine-induced antinociception, whereas diazoxide augmented it in the tail-flick test only. In the formalin test, glibenclamide alone has a significant hyperalgesic effect, whereas diazoxide decreased the number of flinches. Coadministration of glibenclamide with morphine antagonized the hepatotoxic effect of morphine in both animal models. In the tail-flick test, glibenclamide administered alone significantly increased malondialdehyde's level. Coadministration of diazoxide with morphine increased glutathione level in the formalin test. Diazoxide administered alone exacerbated the hepatic oxidative stress in both animal models. These findings suggest a role of K(ATP) channel modulators on morphine-induced antinociception and hepatic oxidative stress. The administration of glibenclamide may prevent morphine-induced hepatotoxicity. The effectiveness of diazoxide in the management of pain is limited due to its deleterious effect on the liver. However, the interaction of the K(ATP) channel modulators with morphine depends on the differential sensitivity to the pain stimulus.

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Section: Experimental Designmentioning

confidence: 99%

“…The adopted schedule used in our study was employed in separate studies [20,21]. The peak of antinocieption for diazoxide (K ATP channel opener) was found to occur when the opener was administered 15 min before morphine.…”

Section: Experimental Designmentioning

confidence: 99%

The involvement of K_ATP channels in morphine‐induced antinociception and hepatic oxidative stress in acute and inflammatory pain in rats

Afify

Khedr

Omar

et al. 2012

Fundamemntal Clinical Pharma

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“…Rat ELISA kits for the determination of IL-1β, IL-6, and tumor necrosis factor (TNF)-α were from Koma Biotech Inc. (Seoul, Korea). Doses which showed no toxicity or motor impairment in previous studies were chosen [Campos et al, 2006;Farghaly, 2014].…”

Section: Chemicals and Drugsmentioning

confidence: 99%

Reactive Astrogliosis in an Experimental Model of Fibromyalgia: Effect of Dexmedetomidine

Abd-ellatief

Mohamed

Kotb

2018

Cells Tissues Organs

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To our knowledge, this is the first study which investigates the induction of neuroinflammation in rats using an acidic-saline model of fibromyalgia. It is well known that the hippocampus has a fundamental role in pain perception, and astrocytes play a crucial role in pain signaling. Our aim is to evaluate the ability of dexmedetomidine to attenuate the inflammatory responses induced in astrocytes. In a group of healthy rats, induction of chronic muscle pain by intramuscular injection of 100 µL of acidic saline on days 0 and 5 resulted in peripheral sensitization (measured using the von Frey test) and significant (p < 0.05) increases in IL-1β (160.2 ± 1.1 to 335.2 ± 1.8), IL-6 (100.1 ± 1.4 to 202.4 ± 1.1), and TNF-α (60.0 ± 0.7 to 115.5 ± 1). Light and electron microscopy revealed degenerative changes in the hippocampus and reactive astrogliosis. Immunohistochemistry showed increased expression of glial fibrillary acid protein and inducible nitric oxide synthase. Surprisingly, treatment with a single dose of an α₂-adrenergic agonist, dexmedetomidine (5 µg/kg i.p.), attenuated these changes. This trial suggests that dexmedetomidine possibly directly acts on astrocytes, and a peripheral action is also suggested.

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“…With respect to the potentiation observed when morphine was infused in combination with ketamine (BK treatment), the coadministration of ketamine likely potentiated the antinoceptive properties of morphine by inhibiting the counter-productive opioid-induced activation of NMDARs, such that morphine was able to exert its analgesic activity more effectively via its receptors at presynaptic afferent terminals Consistent with what has been reported previously [19,39], diabetic neuropathic rats in our study responded poorly to the antinociceptive effects of acute opioid treatment. The maximum nonsedating dose of morphine (5 mg/kg), as determined using the rotarod and OF test, causes significant antinociception in healthy rats ( [40][41][42]; this study-data not shown). In this study, diabetic neuropathic rats that underwent sham treatment showed an antinociceptive response to 10 mg/kg morphine, but not to 5 mg/kg.…”

Section: )mentioning

confidence: 69%

Long-Term Antihyperalgesic and Opioid-Sparing Effects of 5-Day Ketamine and Morphine Infusion (“Burst Ketamine”) in Diabetic Neuropathic Rats

Mak

Broadbear²,

Kolosov³

et al. 2015

Pain Med

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Ketamine-Induced Potentiation of Morphine Analgesia in Rat Tail-Flick Test: Role of Opioid-, .ALPHA.2-Adrenoceptors and ATP-Sensitive Potassium Channels

Cited by 26 publications

References 27 publications

The involvement of K_ATP channels in morphine‐induced antinociception and hepatic oxidative stress in acute and inflammatory pain in rats

The involvement of K_ATP channels in morphine‐induced antinociception and hepatic oxidative stress in acute and inflammatory pain in rats

Reactive Astrogliosis in an Experimental Model of Fibromyalgia: Effect of Dexmedetomidine

Long-Term Antihyperalgesic and Opioid-Sparing Effects of 5-Day Ketamine and Morphine Infusion (“Burst Ketamine”) in Diabetic Neuropathic Rats

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Ketamine-Induced Potentiation of Morphine Analgesia in Rat Tail-Flick Test: Role of Opioid-, .ALPHA.2-Adrenoceptors and ATP-Sensitive Potassium Channels

Cited by 26 publications

References 27 publications

The involvement of KATP channels in morphine‐induced antinociception and hepatic oxidative stress in acute and inflammatory pain in rats

The involvement of KATP channels in morphine‐induced antinociception and hepatic oxidative stress in acute and inflammatory pain in rats

Reactive Astrogliosis in an Experimental Model of Fibromyalgia: Effect of Dexmedetomidine

Long-Term Antihyperalgesic and Opioid-Sparing Effects of 5-Day Ketamine and Morphine Infusion (“Burst Ketamine”) in Diabetic Neuropathic Rats

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The involvement of K_ATP channels in morphine‐induced antinociception and hepatic oxidative stress in acute and inflammatory pain in rats

The involvement of K_ATP channels in morphine‐induced antinociception and hepatic oxidative stress in acute and inflammatory pain in rats