Participation of opioid and monoaminergic mechanisms on the antinociceptive effect induced by tricyclic antidepressants in two behavioural pain tests in mice

Valverderk, Olga; Micó, J.A.; Maldonado, Rafaël; Mellado, Manuel; Gibert-Rahola, J.

doi:10.1016/0278-5846(94)90132-5

Cited by 82 publications

(47 citation statements)

References 44 publications

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“…They also apparently block calcium ion channels (Choi et al, 1992;Chaplan et al, 1994). However, it has also been considered that antidepressants modulate pain perception by blocking the reuptake of monoaminergic neurotransmitters in noradrenergic and serotonergic systems, which originate from the brain stem and project to the spinal cord dorsal horn (Valverde et al, 1994). Moreover, the antihistaminergic action of TCAs may have a general analgesic effect (Rumore and Schlichting, 1986).…”

Section: Introductionmentioning

confidence: 99%

Usefulness of Antidepressants for Improving the Neuropathic Pain-Like State and Pain-Induced Anxiety through Actions at Different Brain Sites

Matsuzawa-Yanagida

Narita

Nakajima

et al. 2007

Neuropsychopharmacol

121

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Clinically, it is well known that chronic pain induces depression, anxiety, and a reduced quality of life. There have been many reports on the relationship between pain and emotion. We previously reported that chronic pain induced anxiety with changes in opioidergic function in the central nervous system. In this study, we evaluated the anxiolytic-like effects of several types of antidepressants under a chronic neuropathic pain-like state and searched for the brain site of action where antidepressants show anxiolytic or antinociceptive effects. Sciatic nerve-ligated mice exhibited thermal hyperalgesia and tactile allodynia from days 7 to 28 after nerve ligation. At 4 weeks after ligation, these mice showed a significant anxiety-related behavior in the light-dark test and the elevated plus-maze test. Under these conditions, repeated administration of antidepressants, including the tricyclic antidepressant (TCA) imipramine, the serotonin noradrenaline reuptake inhibitor (SNRI) milnacipran, and the selective serotonin reuptake inhibitor (SSRI) paroxetine, significantly prevented the anxiety-related behaviors induced by chronic neuropathic pain. These antidepressants also produced a significant reduction in thermal hyperalgesia and tactile allodynia. Moreover, the microinjection of paroxetine into the basolateral amygdala or cingulate cortex reduced anxiety-related behavior, and microinjection into the primary somatosensory cortex significantly attenuated thermal hyperalgesia. These findings suggest that serotonergic antidepressants are effective for treating anxiety associated with chronic neuropathic pain and may be useful for treating neuropathic pain with emotional dysfunction such as anxiety. Furthermore, SSRIs show anxiolytic and antinociceptive effects by acting on different brain regions.

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Section: Introductionmentioning

confidence: 99%

Usefulness of Antidepressants for Improving the Neuropathic Pain-Like State and Pain-Induced Anxiety through Actions at Different Brain Sites

Matsuzawa-Yanagida

Narita

Nakajima

et al. 2007

Neuropsychopharmacol

121

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“…In contrast, coadministration of either doxepin or venlafaxine with morphine made it less effective in attenuation of neuropathic pain symptoms. The analgesic action of antidepressants after local administration deserves further study due to the first and only experimental and clinical data that focused on the analgesic efficacy of antidepressants after different methods of administration (oral, subcutaneous, intraperitoneal, intrathecal, topical) in different models of pain [9,15,[35][36][37][38]. The analgesic effect of antidepressants is different from their action as a mood elevator.…”

Section: Discussionmentioning

confidence: 99%

Analgesic effects of antidepressants alone and after their local co-administration with morphine in a rat model of neuropathic pain

Jagła

Mika

Makuch

et al. 2014

Pharmacological Reports

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(2014) 'Analgesic eects of antidepressants alone and after their local co-administration with morphine in a rat model of neuropathic pain.', Pharmacological reports., 66 (3). pp. 459-465. Further information on publisher's website: Additional information: Use policyThe full-text may be used and/or reproduced, and given to third parties in any format or medium, without prior permission or charge, for personal research or study, educational, or not-for-prot purposes provided that:• a full bibliographic reference is made to the original source • a link is made to the metadata record in DRO • the full-text is not changed in any way The full-text must not be sold in any format or medium without the formal permission of the copyright holders.Please consult the full DRO policy for further details. IntroductionNeuropathic pain is defined as pain arising as a direct consequence of a lesion or disease affecting the somatosensory system [1]. The most frequent etiologic factors of neuropathic pain are trauma (including post-surgery scars), metabolic disturbances (e.g., diabetes mellitus) and ischemia. The pathological mechanism of neuropathic pain differs significantly from that of inflammatory pain; studies have shown that the changes in spinal gene expression under neuropathy and inflammations are different [2]. Thus, the response to antinociceptive drugs, especially opioids, is not the same. It has generally been accepted that neuropathic pain is somewhat resistant to morphine administration in clinical studies [3,4], and the reduced ability of morphine to attenuate allodynia and hyperalgesia in experimental models of neuropathic pain has been demonstrated [5][6][7][8]. For these reasons, it is a common clinical practice to use analgesic drug combinations. The primary approach to treat neuropathic pain is the use of coanalgesics such as tricyclic antidepressants (TCA); however, their systemic application is associated with significant side effects, which can hinder the desired analgesic effect. An alternative approach to this is the topical administration of analgesics. Currently, the possibility of the topical Background:The therapy of neuropathic pain may include the use of co-analgesics, such as antidepressants, however, their desired analgesic effect is associated with significant side effects. An alternative approach to this is their local administration which has been proposed, but there is little data regarding their local co-administration with morphine and the nature of the interaction between morphine and either doxepin or venlafaxine, two antidepressant drugs that have been recently used in neuropathic pain therapies. Methods: This study was performed on rats after chronic constriction injury (CCI) to the sciatic nerve. The von Frey and Hargreaves' tests were used to assess mechanical allodynia and thermal hyperalgesia, respectively, after intraplantar (ipl) or subcutaneous (sc) administration of amitriptyline, doxepin, or venlafaxine, or their ipl co-administration with morphine on day 12-16 after inj...

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“…Inhibition of noradrenergic, serotonergic or dopaminergic tone significantly attenuates the analgesic effect of antidepressants. For example, the inhibition of tyrosine hydroxylase (an essential enzyme for noradrenaline synthesis) or tryptophan hydroxylase (an essential enzyme for serotonin synthesis) antagonizes the analgesic effect of antidepressants in a wide range of experimental models (Valverde et al, 1994). Monoamines act on multiple receptor subtypes in the nervous system, some of which mediate the analgesic effect of antidepressants, such as -adrenoceptors (Ghelardini et al, 2000;Yokogawa et al, 2002) and -adrenoceptors (Mico et al, 2006b), 5-HT 1A , 5-HT 2 and 5-HT 3 serotonin receptors (Bonnefont et al, 2005;Yokogawa et al, 2002), and D2 dopamine receptors (Gilbert & Franklin, 2001).…”

Section: Animal Studiesmentioning

confidence: 99%

“…For example, the opioid antagonist naloxone or nor-binaltorphimine antagonize the analgesic effect of several TCAs and monoamine reuptake inhibitors in models of acute and chronic pain (Ardid & Guilbaud, 1992;Valverde et al, 1994). As opioid and monoaminergic systems appear to share common molecular mechanisms mediating nociception, opioid compounds are frequently coadministrated with antidepressants for pain relief.…”

Section: The Opioid Systemmentioning

confidence: 99%

“…Most evidences indicate the involvement of ionic channels (such as calcium, potassium and sodium) and neurotransmitter receptors (gamma-aminobutyric acid or GABA, N-methyl-D-aspartate, or NMDA and substance P) in the analgesic mechanism of action of antidepressants. It is interesting to note that among antidepressants, TCAs are those that act on multiple nociceptive targets both at central and Venlafaxine Nomifensine Nefazodone Mirtazapine Mianserin (Gray et al, 1998;Hamon et al, 1987;Marchand et al, 2003;Ortega-Alvaro et al, 2004;Schreiber et al, 1999;Schreiber et al, 2002;Valverde et al, 1994) − (Cai & McCaslin, 1992;Eisenach & Gebhart, 1995;Mjellem et al, 1993;Skolnick et al, 1996;Su & Gebhart, 1998) ↓ Substance P peripheral levels (Table 3) and this may be the reason why TCAs seem to be more effective than other antidepressants with a more selective monoaminergic mechanism of action. For example, many actions have been described for amitriptyline: blocking NMDA receptors and sodium channels (Sudoh et al, 2003).…”

Section: Other Mechanisms Involvedmentioning

confidence: 99%

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Antidepressant Drugs and Pain

Cobo-Realpe¹,

Alba-Delgado²,

Bravo³

et al. 2012

Effects of Antidepressants

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Participation of opioid and monoaminergic mechanisms on the antinociceptive effect induced by tricyclic antidepressants in two behavioural pain tests in mice

Cited by 82 publications

References 44 publications

Usefulness of Antidepressants for Improving the Neuropathic Pain-Like State and Pain-Induced Anxiety through Actions at Different Brain Sites

Usefulness of Antidepressants for Improving the Neuropathic Pain-Like State and Pain-Induced Anxiety through Actions at Different Brain Sites

Analgesic effects of antidepressants alone and after their local co-administration with morphine in a rat model of neuropathic pain

Antidepressant Drugs and Pain

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