P.1.g.021 Antinociceptive effects of maprotiline in a rat model of peripheral neuropathic pain: Possible involvement of opioid system

Banafshe, Hamid Reza; Abed, Alireza

doi:10.1016/s0924-977x(15)30280-7

Cited by 6 publications

(4 citation statements)

References 31 publications

(36 reference statements)

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“…Rats were located into the Plexiglas apparatus and permitted to acclimatize to the environment ( 16 ). The hind paw is exposed to an infrared beam from a heat source (Plantar Analgesia Meter, Ugo Basile, and Varese, Italy).…”

Section: Methodsmentioning

confidence: 99%

Anti-nociceptive effect of black seed oil on an animal model of chronic constriction injury

Talaei¹,

Banafshe²,

Moravveji³

et al. 2022

Res Pharma Sci

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Background and purpose: Traditionally, Nigella sativa L. has been known as a medical intervention to treat numerous diseases. This study aimed at investigating the antihyperalgesic effect of black seed oil (BSO) in an experimental model of neuropathic pain. Experimental approach: Chronic constriction injury (CCI) was performed under anesthesia. The sciatic nerve was ligated with four loose ties. Two separate protocols were used to administer BSO. In chronic treatment, rats were given daily doses of BSO (250, 500, and 1000 mg/kg p.o.) from the 1 st day until the 21 st post-CCI day. While, in acute treatment, BSO (250, 500, and 1000 mg/kg p.o.) was administered only on the 7 th , 14 th , and 21 st days. CCI and sham groups were given almond oil according to the same schedule. Behavioral scores were determined by evaluation of the paw withdrawal in the plantar, Von Frey, and acetone tests, on the 7 th , 14 th , and 21 st days. Findings/Results: Our results showed that CCI leads to significant allodynia and hyperalgesia in the ipsilateral paw after surgery. Chronic administration of BSO (500 and 1000 mg/kg) obviously attenuated heat hyperalgesia and mechanical allodynia. However, daily administration of BSO did not alter cold allodynia. Nevertheless, when BSO was administered, 30 min before the pain assessment tests, hypersensitivity was not improved in the treated animals. Conclusion and implications: These results demonstrated BSO can inhibit neuropathic pain progression and suggests a potential use of BSO to manage hyperalgesia and allodynia. However, additional research is necessary to approve BSO effectiveness, in neuropathic pain conditions.

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Section: Methodsmentioning

confidence: 99%

Anti-nociceptive effect of black seed oil on an animal model of chronic constriction injury

Talaei¹,

Banafshe²,

Moravveji³

et al. 2022

Res Pharma Sci

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“…Amitriptyline and desipramine effectively attenuated pain in patients suffering from diabetic neuropathy [200]. Maprotiline suppressed neuropathic pain in rats undergoing chronic constriction injury to the sciatic nerve [241]. Trazodone depressed hyperalgesia produced in chronic constriction injury models in rats [222].…”

Section: Antidepressantsmentioning

confidence: 99%

Inhibitory Actions of Clinical Analgesics, Analgesic Adjuvants, and Plant-Derived Analgesics on Nerve Action Potential Conduction

Kumamoto

2022

Encyclopedia

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The action potential (AP) conduction in nerve fibers plays a crucial role in transmitting nociceptive information from the periphery to the cerebral cortex. Nerve AP conduction inhibition possibly results in analgesia. It is well-known that many analgesics suppress nerve AP conduction and voltage-dependent sodium and potassium channels that are involved in producing APs. The compound action potential (CAP) recorded from a bundle of nerve fibers is a guide for knowing if analgesics affect nerve AP conduction. This entry mentions the inhibitory effects of clinically used analgesics, analgesic adjuvants, and plant-derived analgesics on fast-conducting CAPs and voltage-dependent sodium and potassium channels. The efficacies of their effects were compared among the compounds, and it was revealed that some of the compounds have similar efficacies in suppressing CAPs. It is suggested that analgesics-induced nerve AP conduction inhibition may contribute to at least a part of their analgesic effects.

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“…The antidepressants tested are clinically used to treat chronic pain [ 8 , 9 , 198 , 200 , 203 , 222 , 223 ] and inhibit neuropathic pain in animal models. For instance, duloxetine suppressed tactile allodynia and heat hyperalgesia in neuropathic pain rat models [ 197 ]; fluoxetine produced antinociception in streptozotocin-induced diabetic neuropathic pain mouse models [ 185 ]; amitriptyline and desipramine were effective in alleviating pain in patients with diabetic neuropathy [ 184 ]; maprotiline depressed neuropathic pain produced by chronic constriction injury of the sciatic nerve in rats [ 224 ]; trazodone inhibited hyperalgesia in chronic constriction injury rat models [ 206 ]. The plasma concentrations of duloxetine, fluoxetine, amitriptyline, desipramine, maprotiline and trazodone used to clinically treat depression and neuropathic pain are, respectively, 0.09–0.3, 0.3–1.6, 0.36–0.90, 0.47–1.1, 0.72–1.4 and 2.2–4.3 μM [ 189 , 211 ], values much smaller than those of IC 50 for frog sciatic nerve CAP inhibition.…”

Section: Actions Of Analgesic Adjuvants On Nerve Conductionmentioning

confidence: 99%

Inhibition of Fast Nerve Conduction Produced by Analgesics and Analgesic Adjuvants—Possible Involvement in Pain Alleviation

Kumamoto

2020

Pharmaceuticals

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Nociceptive information is transmitted from the periphery to the cerebral cortex mainly by action potential (AP) conduction in nerve fibers and chemical transmission at synapses. Although this nociceptive transmission is largely inhibited at synapses by analgesics and their adjuvants, it is possible that the antinociceptive drugs inhibit nerve AP conduction, contributing to their antinociceptive effects. Many of the drugs are reported to inhibit the nerve conduction of AP and voltage-gated Na+ and K+ channels involved in its production. Compound action potential (CAP) is a useful measure to know whether drugs act on nerve AP conduction. Clinically-used analgesics and analgesic adjuvants (opioids, non-steroidal anti-inflammatory drugs, α2-adrenoceptor agonists, antiepileptics, antidepressants and local anesthetics) were found to inhibit fast-conducting CAPs recorded from the frog sciatic nerve by using the air-gap method. Similar actions were produced by antinociceptive plant-derived chemicals. Their inhibitory actions depended on the concentrations and chemical structures of the drugs. This review article will mention the inhibitory actions of the antinociceptive compounds on CAPs in frog and mammalian peripheral (particularly, sciatic) nerves and on voltage-gated Na+ and K+ channels involved in AP production. Nerve AP conduction inhibition produced by analgesics and analgesic adjuvants is suggested to contribute to at least a part of their antinociceptive effects.

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P.1.g.021 Antinociceptive effects of maprotiline in a rat model of peripheral neuropathic pain: Possible involvement of opioid system

Cited by 6 publications

References 31 publications

Anti-nociceptive effect of black seed oil on an animal model of chronic constriction injury

Anti-nociceptive effect of black seed oil on an animal model of chronic constriction injury

Inhibitory Actions of Clinical Analgesics, Analgesic Adjuvants, and Plant-Derived Analgesics on Nerve Action Potential Conduction

Inhibition of Fast Nerve Conduction Produced by Analgesics and Analgesic Adjuvants—Possible Involvement in Pain Alleviation

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