Depression-like behavior and mechanical allodynia are reduced by bis selenide treatment in mice with chronic constriction injury: a comparison with fluoxetine, amitriptyline, and bupropion

Jessé, Cristiano Ricardo; Wilhelm, Ethel A.; Nogueira, Cristina W.

doi:10.1007/s00213-010-1977-6

Cited by 49 publications

(25 citation statements)

References 54 publications

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“…The observation that escitalopram produced more robust antinociceptive effects than citalopram [225], is in agreement with previous study showing that the R-enantiomer may antagonize and thus attenuate the effects of the active enantiomer [116,321,322]. All six SSRIs share this analgesic property in chronic models of pain in rodents since fluoxetine, paroxetine and sertraline also produced anti-hyperalgesic and/or anti-allodynic effects in streptozotocin (STZ)-induced diabetic neuropathy, sciatic nerve ligation (SNL) [241,251,254,255,257,266,268,323] or in inflammatory conditions such as formalin or acetic-acid injection [222,233,260,261,265,324] (Table 3). Surprisingly, the antinociceptive effects in chronic models of pain have been revealed after single administration of SSRIs.…”

Section: Monoamines Reuptake Inhibitors and Pain Preclinical Outcomessupporting

confidence: 85%

Monoaminergic Antidepressants in the Relief of Pain: Potential Therapeutic Utility of Triple Reuptake Inhibitors (TRIs)

et al. 2011

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Over 75% of depressed patients suffer from painful symptoms predicting a greater severity and a less favorable outcome of depression. Imaging, anatomical and functional studies have demonstrated the existence of common brain structures, neuronal pathways and neurotransmitters in depression and pain. In particular, the ascending serotonergic and noradrenergic pathways originating from the raphe nuclei and the locus coeruleus; respectively, send projections to the limbic system. Such pathways control many of the psychological functions that are disturbed in depression and in the perception of pain. On the other hand, the descending pathways, from monoaminergic nuclei to the spinal cord, are specifically implicated in the inhibition of nociception providing rationale for the use of serotonin (5-HT) and/or norepinephrine (NE) reuptake inhibitors (SSRIs, NRIs, SNRIs), in the relief of pain. Compelling evidence suggests that dopamine (DA) is also involved in the pathophysiology and treatment of depression. Indeed, recent insights have demonstrated a central role for DA in analgesia through an action at both the spinal and suprasinal levels including brain regions such as the periaqueductal grey (PAG), the thalamus, the basal ganglia and the limbic system. In this context, dopaminergic antidepressants (i.e., containing dopaminergic activity), such as bupropion, nomifensine and more recently triple reuptake inhibitors (TRIs), might represent new promising therapeutic tools in the treatment of painful symptoms with depression. Nevertheless, whether the addition of the dopaminergic component produces more robust effects than single- or dual-acting agents, has yet to be demonstrated. This article reviews the main pathways regulating pain transmission in relation with the monoaminergic systems. It then focuses on the current knowledge regarding the in vivo pharmacological properties and mechanism of action of monoaminergic antidepressants including SSRIs, NRIs, SNRIs and TRIs. Finally, a synthesis of the preclinical studies supporting the efficacy of these antidepressants in analgesia is also addressed in order to highlight the relative contribution of 5-HT, NE and DA to nociception.

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Section: Monoamines Reuptake Inhibitors and Pain Preclinical Outcomessupporting

confidence: 85%

Monoaminergic Antidepressants in the Relief of Pain: Potential Therapeutic Utility of Triple Reuptake Inhibitors (TRIs)

et al. 2011

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“…Consistently, depressive-and anxiety-like behaviors have been observed in animal models of peripheral nerve injury, as indexed by the increase in total immobility time in the forced swimming or tail suspension tests (Gai et al, 2014;Jesse et al, 2010;Wang et al, 2011;Yalcin et al, 2011). Chronic pain-related affective impairments develop already 2 weeks after the SNI surgery (Norman et al, 2010;Palazzo et al, 2015;Suzuki et al, 2007), decreased motivation and anhedonia develop in mice at 7 days following nerve injury e remain stable up to 21 days (Schwartz et al, 2014).…”

Section: Discussionmentioning

confidence: 87%

Enhanced serotonin and mesolimbic dopamine transmissions in a rat model of neuropathic pain

et al. 2015

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“…Interestingly, the antidepressant desipramine decreased the depression-like behavior (decreased the duration of immobility in FST) without altering the pain sensitivity and a cannabinoid CB2 receptor agonist, GW405833, reversed both the increased immobility and pain sensitivity [44]. In a mouse CCI model, the antidepressant amitriptyline and a plant-derived phenolic compound curcumin both reversed the nociceptive hypersensitivity and depression-like behaviors [45, 46]. Moreover, behavioral manipulations such as social interaction also seems to affect the pain-depression comorbidity.…”

Section: Animal Studies Of the Pain-depression Relationshipmentioning

confidence: 99%

Pain and depression comorbidity: A preclinical perspective

2015

Behavioural Brain Research

140

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Pain and depression are two highly prevalent and deleterious disorders with significant socioeconomic impact to society. Clinical observations have long recognized the co-existence and interactions of pain and depression. However, the underlying mechanisms of pain-depression comorbidity and their dynamic interactions remain largely unknown. Preclinical animal studies may provide critical information for the understanding of this important comorbidity. This review analyzed the current preclinical evidence of interactions between pain and depression, which generally supports the causative relationship of the two conditions. In addition, the analysis proposed to apply domain interplay concept in future model development of pain-depression comorbidity and mechanism studies. The application of spectrum-centered animal models will better the understanding of pain-depression dyad and foster the development of more effective therapeutic strategies.

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Depression-like behavior and mechanical allodynia are reduced by bis selenide treatment in mice with chronic constriction injury: a comparison with fluoxetine, amitriptyline, and bupropion

Cited by 49 publications

References 54 publications

Monoaminergic Antidepressants in the Relief of Pain: Potential Therapeutic Utility of Triple Reuptake Inhibitors (TRIs)

Monoaminergic Antidepressants in the Relief of Pain: Potential Therapeutic Utility of Triple Reuptake Inhibitors (TRIs)

Enhanced serotonin and mesolimbic dopamine transmissions in a rat model of neuropathic pain

Pain and depression comorbidity: A preclinical perspective

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