Serotonergic modulation in neuropathy induced by oxaliplatin: Effect on the 5HT2C receptor

Baptista-de-Souza, Daniela; Mannelli, Lorenzo Di Cesare; Zanardelli, Matteo; Micheli, Laura; Nunes-de-Souza, Ricardo Luiz; Canto-de-Souza, Azair; Ghelardini, Carla

doi:10.1016/j.ejphar.2014.04.028

Cited by 44 publications

(39 citation statements)

References 57 publications

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“…There also seem to be mitochondrial injuries with increased oxidative stress, which would induce chronic neuropathy 4 . Baptista-de-Souza et al 7 have shown in experimental study that oxaliplatin is also able to decrease mRNA expression of the 5HT2c receptor in the central nervous system, which could contribute to worsen CIPN neuropathic pain. This would indicate the potential for structural and functional changes in the limbic system caused by oxaliplatin 7 .…”

Section: Pathophysiology Of Chemotherapy-indu-ced Peripheral Neuropathymentioning

confidence: 99%

“…Baptista-de-Souza et al 7 have shown in experimental study that oxaliplatin is also able to decrease mRNA expression of the 5HT2c receptor in the central nervous system, which could contribute to worsen CIPN neuropathic pain. This would indicate the potential for structural and functional changes in the limbic system caused by oxaliplatin 7 . Taxanes, especially paclitaxel, are agents promoting the union of microtubules as from tubuline dimers, stabilizing them and preventing their depolymerization.…”

Section: Pathophysiology Of Chemotherapy-indu-ced Peripheral Neuropathymentioning

confidence: 99%

See 1 more Smart Citation

Chemotherapy-induced peripheral neuropathy: review for clinical practice

Simão¹,

Murad²,

Martins³

et al. 2015

Revista Dor

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Section: Pathophysiology Of Chemotherapy-indu-ced Peripheral Neuropathymentioning

confidence: 99%

Section: Pathophysiology Of Chemotherapy-indu-ced Peripheral Neuropathymentioning

confidence: 99%

Chemotherapy-induced peripheral neuropathy: review for clinical practice

Simão¹,

Murad²,

Martins³

et al. 2015

Revista Dor

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“…In this context, several neurotransmitters have been implicated mediating nociception, for instance, opioids (Yaksh and Noueihed, 1985; Jensen and Yaksh, 1989; Cornelio and Nunes-de-Souza, 2009; Morgan et al, 2014), glutamate (Yaksh and Noueihed, 1985; Palazzo et al, 2013; Wilson-Poe et al, 2013), serotonin (Eschalier et al, 1989; Baptista-de-Souza et al, 2014; de Freitas et al, 2014), and endocannabinoids (Meng et al, 1998; Suplita et al, 2005; Olango et al, 2012). More recently, vanilloid compounds, which are known to activate the Transient Receptor Potential Vanilloid – type 1 (TRPV1) channels, emerged as an important neurotransmission system modulating nociception (e.g., McGaraughty et al, 2003; Starowicz et al, 2007; Mascarenhas et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Blockade of Cannabinoid CB1 Receptors in the Dorsal Periaqueductal Gray Unmasks the Antinociceptive Effect of Local Injections of Anandamide in Mice

et al. 2017

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Divergent results in pain management account for the growing number of studies aiming at elucidating the pharmacology of the endocannabinoid/endovanilloid anandamide (AEA) within several pain-related brain structures. For instance, the stimulation of both Transient Receptor Potential Vanilloid type 1 (TRPV1) and Cannabinoid type 1 (CB1) receptors led to paradoxical effects on nociception. Here, we attempted to propose a clear and reproducible methodology to achieve the antinociceptive effect of exogenous AEA within the dorsal periaqueductal gray (dPAG) of mice exposed to the tail-flick test. Accordingly, male Swiss mice received intra-dPAG injection of AEA (CB1/TRPV1 agonist), capsaicin (TRPV1 agonist), WIN (CB1 agonist), AM251 (CB1 antagonist), and 6-iodonordihydrocapsaicin (6-IODO) (TRPV1 selective antagonist) and their nociceptive response was assessed with the tail-flick test. In order to assess AEA effects on nociception specifically at vanilloid or cannabinoid (CB) substrates into the dPAG, mice underwent an intrinsically inactive dose of AM251 or 6-IODO followed by local AEA injections and were subjected to the same test. While intra-dPAG AEA did not change acute pain, local injections of capsaicin or WIN induced a marked TRPV1- and CB1-dependent antinociceptive effect, respectively. Regarding the role of AEA specifically at CB/vanilloid substrates, while the blockade of TRPV1 did not change the lack of effects of intra-dPAG AEA on nociception, local pre-treatment of AM251, a CB1 antagonist, led to a clear AEA-induced antinociception. It seems that the exogenous AEA-induced antinociception is unmasked when it selectively binds to vanilloid substrates, which might be useful to address acute pain in basic and perhaps clinical trials.

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“…We have recently shown that neuropathic pain induced by the antineoplastic agent oxaliplatin, which possesses toxic properties that lead to neuropathic pain syndrome with paresthesia and dysesthesia, increases 5-HT 2C receptor expression in the dPAG [31]. Although several studies support the role of dPAG 5-HT 2C receptors in acute and chronic pain [17,31], it remains unclear whether neuropathic pain-related changes in 5-HT 2C receptor function are responsible for hyperalgesia that develops following chronic constriction injury (CCI) of the sciatic nerve [32][33][34][35]. Therefore, the present study examined changes in defensive behaviors and nociception induced by predator exposure in mice with CCI, as well as the possible involvement of dPAG 5-HT 2C receptors.…”

Section: Introductionmentioning

confidence: 99%

Rat exposure in mice with neuropathic pain induces fear and antinociception that is not reversed by 5-HT2C receptor activation in the dorsal periaqueductal gray

Furuya-da-Cunha

Souza

Canto-de-Souza

2016

Behavioural Brain Research

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Previous studies have demonstrated that serotonin 5-HT2C receptors in the dorsal periaqueductal gray (dPAG) mediate both anxiety and antinociception in mice submitted to the elevated plus maze. The present study examined the effects of intra-dPAG infusion of the serotonin 5-HT2C receptor agonist (MK-212) in the defensive reactions and antinociception in mice with neurophatic pain confronted by a predator. Neuropathic pain was induced by chronic constriction injury (CCI) of the sciatic nerve, and predator confrontation was performed using the rat exposure test (RET). Our results demonstrated that both sham-operated and CCI mice exhibited intense defensive reactions when confronted by rats. However, rat-exposed CCI mice showed reduced pain reactivity in comparison to CCI mice exposed to a toy rat. Intra-dPAG infusion of MK-212 prior to predator exposure did not significantly alter defensive or antinociceptive responses. To our knowledge, our results represent the first evidence of RET-induced antinociception in mice. Moreover, the results of the present study suggest that 5-HT2C receptor activation in the dPAG is not critically involved in the control of predator-evoked fearful or antinociceptive responses.

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Serotonergic modulation in neuropathy induced by oxaliplatin: Effect on the 5HT2C receptor

Cited by 44 publications

References 57 publications

Chemotherapy-induced peripheral neuropathy: review for clinical practice

Chemotherapy-induced peripheral neuropathy: review for clinical practice

Blockade of Cannabinoid CB1 Receptors in the Dorsal Periaqueductal Gray Unmasks the Antinociceptive Effect of Local Injections of Anandamide in Mice

Rat exposure in mice with neuropathic pain induces fear and antinociception that is not reversed by 5-HT2C receptor activation in the dorsal periaqueductal gray

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