The involvement of endogenous opioid mechanisms in the antinociceptive effects induced by antidepressant drugs, desipramine and trimipramine

Öztürk, Yusuf; Aydın, Süleyman; Beis, Rana; Herekman-Demir, T.

doi:10.1016/j.pbb.2006.03.022

Cited by 5 publications

(3 citation statements)

References 40 publications

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“…Moreover, it has also been proposed that chronic antidepressant treatment can change opioid receptor densities and increase the level of opioid peptides in different regions of the nervous system (Antkiewicz‐Michaluk et al ., ; Hamon et al ., ). While some authors provide pharmacological evidence for the involvement of MOP receptors (Schreiber et al ., ; Marchand et al ., ), this is not supported by studies in MOP receptor‐deficient mice (Bohren et al ., ), and the DOP receptor appears to be a major target for the antiallodynic action of antidepressants (Gray et al ., ; Schreiber et al ., ; Ozturk et al ., ; Benbouzid et al ., ; Choucair‐Jaafar et al ., ). The link between the opioid system and antidepressant drugs is not limited to their action in a pain context (Lutz and Kieffer, ).…”

Section: Discussionmentioning

confidence: 98%

κ‐opioid receptors are not necessary for the antidepressant treatment of neuropathic pain

Megat

Bohren

Doridot

et al. 2014

British J Pharmacology

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Background and Purpose Tricyclic antidepressants are used clinically as first‐line treatments for neuropathic pain. Opioid receptors participate in this pain‐relieving action, and preclinical studies in receptor‐deficient mice have highlighted a critical role for δ‐, but not μ‐opioid receptors. In this study, we investigated whether κ‐opioid (KOP) receptors have a role in the antiallodynic action of tricyclic antidepressants. Experimental Approach We used a model of neuropathic pain induced by unilateral sciatic nerve cuffing. In this model, the mechanical allodynia was evaluated using von Frey filaments. Experiments were conducted in C57BL/6J mice, and in KOP receptor‐deficient mice and their wild‐type littermates. The tricyclic antidepressant nortriptyline (5 mg·kg−1) was delivered twice a day for over 2 weeks. Agonists and antagonists of opioid receptors were used to test the selectivity of the KOP receptor antagonist norbinaltorphimine (nor‐BNI) in mice with neuropathic pain. Key Results After 12 days of treatment, nortriptyline relieved neuropathic allodynia in both wild‐type and KOP receptor‐deficient mice. Surprisingly, acute nor‐BNI reversed the effect of nortriptyline in both wild‐type and KOP receptor‐deficient mice. Further experiments showed that nor‐BNI action was selective for KOP receptors at a late time‐point after its administration (8 h), but not at an early time‐point, when it may also interact with δ‐opioid (DOP) receptors. Conclusions and Implications KOP receptors are not necessary for the effect of a tricyclic antidepressant against neuropathic allodynia. These findings together with previous data indicate that the DOP receptor is the only opioid receptor that is necessary for the antiallodynic action of antidepressants.

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Section: Discussionmentioning

confidence: 98%

κ‐opioid receptors are not necessary for the antidepressant treatment of neuropathic pain

Megat

Bohren

Doridot

et al. 2014

British J Pharmacology

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“…Antidepressants, and in particular tricyclic antidepressants (TCAs), have long been known to interact with the opioid system. A number of studies have shown that the administration of opioid receptor antagonists reverses the anti‐nociceptive effects of TCAs (Biegon and Samuel, 1980; Gray et al ., 1998; Marchand et al ., 2003; Ozturk et al ., 2006; Benbouzid et al ., 2008a,b), and that TCAs potentiate morphine‐induced analgesia in both animals and humans (Mico et al ., 2006). Moreover, in animal behavioural tests predictive of antidepressant activity in humans, such as the forced swimming and learned helplessness tests, the antidepressant action of TCAs has been found to be antagonized by blockade of opioid receptors (Devoize et al ., 1982; Tejedor‐Real et al ., 1995; Besson et al ., 1999).…”

Section: Introductionmentioning

confidence: 99%

The atypical antidepressant mianserin exhibits agonist activity at κ‐opioid receptors

Olianas

Dedoni

Onali

2012

British J Pharmacology

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BACKGROUND AND PURPOSEAntidepressants are known to interact with the opioid system through mechanisms not completely understood. We previously reported that tricyclic antidepressants act as agonists at distinct opioid receptors. Here, we investigated the effect of the atypical antidepressant mianserin at cloned and native opioid receptors. EXPERIMENTAL APPROACHEffects of mianserin were examined in CHO cells transfected with human opioid receptors, C6 glioma cells and rat brain membranes by the use of radioligand binding and functional assays including the stimulation of [ KEY RESULTSMianserin displayed 12-and 18-fold higher affinity for k-than m-and d-opioid receptors respectively. In [ 35 S]GTPgS assays, mianserin selectively activated k-opioid receptors. The agonist activity was antagonized by the selective k-opioid blocker nor-binaltorphimine (nor-BNI). The mianserin analogue mirtazapine also displayed k-opioid agonist activity. Mianserin and mirtazapine increased ERK1/2 phosphorylation in CHO cells expressing k-opioid receptors and C6 cells, and these effects were antagonized by nor-BNI. In rat striatum and nucleus accumbens, mianserin stimulated [35S]GTPgS binding in a nor-BNI-sensitive manner with maximal effects lower than those of the full k-opioid agonists (-)-U50,488 and dynorphin A. When combined, mianserin antagonized the effects of the full k-opioid receptor agonists in [ CONCLUSIONS AND IMPLICATIONSIn different cell systems, mianserin directly activates k-opioid receptors, displaying partial agonist activity at brain receptors. Thus, this property appears to be a common feature of different classes of antidepressants.

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“…Inhibition of the jaw opening reflex and single neurons in the trigeminal subnucleus caudalis by activation of striatal D2 dopamine receptors was suppressed by striatal quinpirole and reversed by systemic naloxone (991). Desimiprimine and trimipramine-induced analgesia were blocked by Nti, but only by high doses of naltrexone (875). A chlorinated chimeric peptide of Menk and FMRFa, [p-Cl Phe(4)], produced a naloxone-reversible analgesia (447).…”

Section: D Opioid Mediation Of Other Analgesic Responsesmentioning

confidence: 99%

Endogenous opiates and behavior: 2009

Bodnar

2010

Peptides

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The involvement of endogenous opioid mechanisms in the antinociceptive effects induced by antidepressant drugs, desipramine and trimipramine

Cited by 5 publications

References 40 publications

κ‐opioid receptors are not necessary for the antidepressant treatment of neuropathic pain

κ‐opioid receptors are not necessary for the antidepressant treatment of neuropathic pain

The atypical antidepressant mianserin exhibits agonist activity at κ‐opioid receptors

Endogenous opiates and behavior: 2009

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