Effect of the antidepressant nefazodone on the density of cells expressing mu-opioid receptors in discrete brain areas processing sensory and affective dimensions of pain

Ortega-Álvaro, A.; I, Acebes; Saracibar, Gonzalo; Echevarrı́a, Enrique; Casis, Luı́s; Micó, Juan Antonio

doi:10.1007/s00213-004-1894-7

Cited by 13 publications

(10 citation statements)

References 46 publications

(49 reference statements)

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“…Some studies on the acute or sub-chronic action of antidepressant drugs showed that opioid antagonists can block the antidepressant-induced analgesia (Reichenberg et al, 1985;Valverde et al, 1994;Gray et al, 1998;Su and Gebhart, 1998;Schreiber et al, 1999Schreiber et al, , 2002Marchand et al, 2003c;Ortega-Alvaro et al, 2004;Mico et al, 2006;Benbouzid et al, 2008a,b), suggesting the involvement of the opioid system. On the contrary, other studies showed no effect of opioid antagonists on antidepressant drug action (Pick et al, 1992;Fuchs et al, 1996;Ghelardini et al, 2000;Marchand et al, 2003a,b).…”

Section: Introductionmentioning

confidence: 99%

Mu‐opioid receptors are not necessary for nortriptyline treatment of neuropathic allodynia

Bohren¹,

Karavelic²,

Yalçın³

et al. 2010

European Journal of Pain

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Tricyclic antidepressants (TCAs) are among the first line treatments clinically recommended against neuropathic pain. However, the mechanism by which they alleviate pain is still unclear. Pharmacological and genetic approaches evidenced a critical role of delta-opioid receptors (DORs) in the therapeutic action of chronic TCA treatment. It is however unclear whether mu-opioid receptors (MORs) are also necessary to the pain-relieving action of TCAs. The lack of highly selective MOR antagonists makes difficult to conclude based on pharmacological studies. In the present work, we thus used a genetic approach and compared mutant mice lacking MORs and their wild-type littermates. The neuropathy was induced by unilateral sciatic nerve cuffing. The threshold for mechanical response was evaluated using von Frey filaments. MOR-deficient mice displayed the same baseline for mechanical sensitivity as their wild-type littermates. After sciatic nerve cuffing, both wild-type and MOR-deficient mice displayed an ipsilateral mechanical allodynia. After about 10 days of treatment, nortriptyline suppressed this allodynia in both wild-type and MOR-deficient mice. MORs are thus not critical for nortriptyline action against neuropathic pain. An acute injection of the DOR antagonist naltrindole induced a relapse of neuropathic allodynia in both wild-type and MOR-deficient mice, thus confirming the critical role of DORs in nortriptyline action. Moreover, morphine induced an acute analgesia in control and in neuropathic wild-type mice, but was without effect in MOR-deficient mice. While MORs are crucial for morphine action, they are not critical for nortriptyline action. Our results highlight the functional difference between DORs and MORs in mechanisms of pain relief.

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Section: Introductionmentioning

confidence: 99%

Mu‐opioid receptors are not necessary for nortriptyline treatment of neuropathic allodynia

Bohren¹,

Karavelic²,

Yalçın³

et al. 2010

European Journal of Pain

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“…Antidepressants can interact with the opioid system, thus affecting pain-related processes [1] . Results of the present investigations allow to conclude that adrenergic stimulation at least prolonged the fentanyl analgesia since this effect was observed after amitriptyline, moclobemide and reboxetine ( fig.…”

Section: Discussionmentioning

confidence: 99%

Modification of Fentanyl Analgesia by Antidepressants

2009

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Clinical practice often requires simultaneous administration of antidepressants with opioids (oncology, rheumatology). Coadministration may either attenuate or potentiate opioid analgesia. The purpose of this paper was to verify how the analgesic action of fentanyl (0.05 mg/kg) is affected by single administration as well as 4- or 21-day premedication with antidepressants characterized by various mechanisms of action. The effects of amitriptyline 3 mg/kg, moclobemide 5 mg/kg, fluoxetine 5 mg/kg and reboxetine 0.08 mg/kg were investigated. Experiments were conducted on normotensive Wistar Kyoto rats. The pain threshold was measured using an analgesimeter. It was concluded that the single administration of an antidepressant increases the analgesic action of fentanyl. Four-day premedication with fluoxetine and reboxetine significantly attenuated the antinociceptive action of fentanyl, whereas 21-day premedication with all antidepressants investigated (fluoxetine, amitriptyline, moclobemide, reboxetine) markedly decreased it. The potential clinical importance of this observation is discussed.

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“…Indeed, the administration of antidepressants increases opioid receptor density in brain areas implicated in pain and depression (Ortega-Alvaro et al, 2004;Reisine & Soubrie, 1982). For example, chronic citalopram administration increases naloxone binding in cortical membranes (Antkiewicz-Michaluk et al, 1984), while imipramine and fluoxetine increase neuronal μ-opioid receptor expression in the prefrontal cortex, hippocampus and caudate putamen (de Gandarias et al, 1999;.…”

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%