Antinociceptive effects and synergistic interaction with morphine of intrathecal metabotropic glutamate receptor 2/3 antagonist in the formalin test of rats

Yoon, Myung Ha; Choi, Jeong Il; Bae, Hong-Beom; Kim, Seok Jai; Chung, Sung Tae; Jeong, Seong‐Jun; Chung, Seung Min; Yoo, Kyung Yeon; Jeong, Chang Yeong

doi:10.1016/j.neulet.2005.10.030

Cited by 20 publications

(19 citation statements)

References 32 publications

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“…Opioid-induced antinociceptive effects were enhanced by antagonists (15,16,45) and agonists (29) of group II mGluR in different types of somatic nociception. Currently, it is unknown whether this interaction between group II mGluR and opioid receptors occurs in visceral nociceptive mechanisms.…”

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confidence: 99%

“…antinociception (15,16,29,45). Opioid-induced antinociceptive effects were enhanced by antagonists (15,16,45) and agonists (29) of group II mGluR in different types of somatic nociception.…”

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confidence: 99%

“…Recently, the interaction between mGluR and opioid receptors has also been identified in studies of opioid-induced antinociception (15,16,29,45). Opioid-induced antinociceptive effects were enhanced by antagonists (15,16,45) and agonists (29) of group II mGluR in different types of somatic nociception. Currently, it is unknown whether this interaction between group II mGluR and opioid receptors occurs in visceral nociceptive mechanisms.…”

mentioning

confidence: 99%

“…An interaction between iGluR and opioid receptor mechanisms is believed to be important in pain pathways, because block of ionotropic Nmethyl-D-aspartate (NMDA) receptors enhances the antinociceptive effect of morphine (an opioid receptor agonist) (14,28,36,37). Recently, the interaction between mGluR and opioid receptors has also been identified in studies of opioid-induced antinociception (15,16,29,45). Opioid-induced antinociceptive effects were enhanced by antagonists (15,16,45) and agonists (29) of group II mGluR in different types of somatic nociception.…”

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Contribution of opioid and metabotropic glutamate receptor mechanisms to inhibition of bladder overactivity by tibial nerve stimulation

Matsuta

Mally

Zhang

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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(mGluR) and opioid receptors to inhibition of bladder overactivity by tibial nerve stimulation (TNS) was investigated in cats under ␣-chloralose anesthesia using LY341495 (a group II mGluR antagonist) and naloxone (an opioid receptor antagonist). Slow infusion cystometry was used to measure the volume threshold (i.e., bladder capacity) for inducing a large bladder contraction. After measuring the bladder capacity during saline infusion, 0.25% acetic acid (AA) was infused to irritate the bladder, activate the nociceptive C-fiber bladder afferents, and induce bladder overactivity. AA significantly (P Ͻ 0.0001) reduced bladder capacity to 26.6 Ϯ 4.7% of saline control capacity. TNS (5 Hz, 0.2 ms) at 2 and 4 times the threshold (T) intensity for inducing an observable toe movement significantly increased bladder capacity to 62.2 Ϯ 8.3% at 2T (P Ͻ 0.01) and 80.8 Ϯ 9.2% at 4T (P ϭ 0.0001) of saline control capacity. LY341495 (0.1-5 mg/kg iv) did not change bladder overactivity, but completely suppressed the inhibition induced by TNS at a low stimulus intensity (2T) and partially suppressed the inhibition at high intensity (4T). Following administration of LY341495, naloxone (0.01 mg/kg iv) completely eliminated the high-intensity TNS-induced inhibition. However, without LY341495 treatment a 10 times higher dose (0.1 mg/kg) of naloxone was required to completely block TNS inhibition. These results indicate that interactions between group II mGluR and opioid receptor mechanisms contribute to TNS inhibition of AA-induced bladder overactivity. Understanding neurotransmitter mechanisms underlying TNS inhibition of bladder overactivity is important for the development of new treatments for bladder disorders.neurotransmitter; neuromodulation; bladder; cat GLUTAMATERGIC NEUROTRANSMISSION involves activation of both ionotropic glutamate receptors (iGluR) and metabotropic glutamate receptors (mGluR) that consist of eight subtypes classified into group I (mGluR 1 and 5), group II (mGluR 2 and 3), and group III (mGluR 4,6,7,and 8). An interaction between iGluR and opioid receptor mechanisms is believed to be important in pain pathways, because block of ionotropic Nmethyl-D-aspartate (NMDA) receptors enhances the antinociceptive effect of morphine (an opioid receptor agonist) (14,28,36,37). Recently, the interaction between mGluR and opioid receptors has also been identified in studies of opioid-induced antinociception (15,16,29,45). Opioid-induced antinociceptive effects were enhanced by antagonists (15,16,45) and agonists (29) of group II mGluR in different types of somatic nociception. Currently, it is unknown whether this interaction between group II mGluR and opioid receptors occurs in visceral nociceptive mechanisms.Recent results from this laboratory (38) revealed that tibial nerve stimulation (TNS) inhibits bladder overactivity elicited by intravesical infusion of acetic acid (AA), which stimulates nociceptive bladder afferent nerves. This TNS-induced antinociceptive effect is completely eliminated by naloxone (an opioid...

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Contribution of opioid and metabotropic glutamate receptor mechanisms to inhibition of bladder overactivity by tibial nerve stimulation

Matsuta

Mally

Zhang

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

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“…In accordance, metabotropic glutamate receptors and morphine demonstrated to possess synergistic drug interaction for antinociception during phase 2 in the formalin test in rats 15 . The application of T ketamine alone (KetG) was analgesic by itself, in accordance to others 16 , and result in greater plasma noradrenaline levels, but apparently blunted the decrease in the Fen-KetG at 6-h.…”

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confidence: 53%

418 the Clinical and Laboratorial Evaluation of Transdermal Ketamine, Fentanyl, Clonidine or Their Combination in Chronic Low Back Pain

Lauretti

Mattos

Lima

et al. 2009

European Journal of Pain

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Antagonism of metabotropic glutamate group II receptors in the potential treatment of neurological and neuropsychiatric disorders

Witkin

Eiler

2006

Drug Dev. Res.

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The metabotropic glutamate Group II receptors (mGlu2 and mGlu3 receptors) regulate the synaptic availability of glutamate and thus control the broad-ranging neural transmission of glutamate as well as glutamate-modulated transmission. The present review focuses on the potential role of Group II mGlu receptor antagonism in neurological and neuropsychiatric disorders. Recent findings have determined that agonists of metabotropic glutamate type 2/3 receptors (mGlu2/3) have antianxiety efficacy. Although it could be assumed that blockade of these receptors might engender anxiogenic responses, new data have indicted that these compounds produce antidepressant-like, wake-promoting, and pro-cognitive effects in rodents. However, there are almost no data available to define the relative importance of mGlu2 versus mGlu3 receptors in these activities. Although there are some hints that antagonism of mGlu2/3 receptors could have additional therapeutic impact, the preponderance of data suggests that agonists of the mGlu2/3 receptors would be more likely to have efficacy in anxiety disorders, positive symptoms of schizophrenia, neurodegenerative disorders, and stroke, pain, and epilepsy. The pharmacology of antagonists of mGlu2/3 receptors suggests that such compounds could have a unique place in the medicinal arsenal for mood disorders as well as disorders of cognition and arousal. Given the activity surrounding the discovery of orally available antagonists for these receptors, there may be an opportunity for clinical investigation of these possibilities in the future. Drug Dev. Res. 67:757-769, 2006.

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Antinociceptive effects and synergistic interaction with morphine of intrathecal metabotropic glutamate receptor 2/3 antagonist in the formalin test of rats

Cited by 20 publications

References 32 publications

Contribution of opioid and metabotropic glutamate receptor mechanisms to inhibition of bladder overactivity by tibial nerve stimulation

Contribution of opioid and metabotropic glutamate receptor mechanisms to inhibition of bladder overactivity by tibial nerve stimulation

418 the Clinical and Laboratorial Evaluation of Transdermal Ketamine, Fentanyl, Clonidine or Their Combination in Chronic Low Back Pain

Antagonism of metabotropic glutamate group II receptors in the potential treatment of neurological and neuropsychiatric disorders

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