Trazodone hydrochloride attenuates thermal hyperalgesia in a chronic constriction injury rat model

Okuda, Keiko; Takanishi, Toshio; Yoshimoto, Kanji; Ueda, Seinosuke

doi:10.1097/00003643-200305000-00011

Cited by 14 publications

(5 citation statements)

References 36 publications

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“…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]. The plasma concentrations of duloxetine, fluoxetine, amitriptyline, desipramine, maprotiline, and trazodone prescribed for the treatment of depression and neuropathic pain in clinical practice are 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, respectively [205,228].…”

Section: Antidepressantsmentioning

confidence: 99%

“…Maprotiline activity was concentration-dependent over concentrations ranging from 0.2 to 5 mM, and an IC 50 value for this activity was 0.95 mM [31]. Trazodone, a 5-HT 2 receptor antagonist and reuptake inhibitor (SARI), is a non-SNRI, non-SSRI, nontricyclic, and non-tetracyclic antidepressant ( [222][223][224][225]; refer to review [226]). Trazodone reduced frog sciatic nerve CAP peak amplitudes in a partial but reversible fashion at concentrations ranging from 0.2 to 2 mM which is the maximum soluble concentration.…”

Section: Antidepressantsmentioning

confidence: 99%

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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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Section: Antidepressantsmentioning

confidence: 99%

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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“…Maprotiline activity was concentration-dependent in a range of 0.2-5 mM with an IC 50 value of 0.95 mM [24]. Trazodone, which is known as 5-HT 2 antagonist and reuptake inhibitor (SARI), is a non-SNRI, -SSRI, -tricyclic and -tetracyclic antidepressant ( [205][206][207][208]; see [209] for review). Frog sciatic nerve CAPs were inhibited by trazodone at concentrations ranging from 0.2 to 2 mM, a maximally dissolved one, in a partially reversible manner.…”

Section: Antidepressantsmentioning

confidence: 99%

“…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: Antidepressantsmentioning

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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“…Okuda and co-authors induced neuropathic pain in rats by sciatic nerve ligation [242]. Then three experiments were performed: (1) hot plate test; (2) injection of 5,7-dihydroxytryptamine (neurotoxin, used to reduce serotonin in the brain) into the dorsal raphe nucleus and medial raphe nucleus or raphe nucleus magnus; and (3) in the third experiment, the authors tested the sedative effect of trazodone by placing rats in an activity cage.…”

Section: Psychotropic Drugs For Management Of Pain and Itching Synmentioning

confidence: 99%

Psychotropic Drugs for the Management of Chronic Pain and Itch

Belinskaia

Barygin

et al. 2019

Pharmaceuticals

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Clinical observations have shown that patients with chronic neuropathic pain or itch exhibit symptoms of increased anxiety, depression and cognitive impairment. Such patients need corrective therapy with antidepressants, antipsychotics or anticonvulsants. It is known that some psychotropic drugs are also effective for the treatment of neuropathic pain and pruritus syndromes due to interaction with the secondary molecular targets. Our own clinical studies have identified antipruritic and/or analgesic efficacy of the following compounds: tianeptine (atypical tricyclic antidepressant), citalopram (selective serotonin reuptake inhibitor), mianserin (tetracyclic antidepressant), carbamazepine (anticonvulsant), trazodone (serotonin antagonist and reuptake inhibitor), and chlorprothixene (antipsychotic). Venlafaxine (serotonin-norepinephrine reuptake inhibitor) is known to have an analgesic effect too. The mechanism of such effect of these drugs is not fully understood. Herein we review and correlate the literature data on analgesic/antipruritic activity with pharmacological profile of these compounds.

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Trazodone hydrochloride attenuates thermal hyperalgesia in a chronic constriction injury rat model

Cited by 14 publications

References 36 publications

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

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

Psychotropic Drugs for the Management of Chronic Pain and Itch

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