Trigeminal pain transmission requires reactive oxygen species production

Viggiano, Andrea; Monda, Marcellino; Viggiano, Alessandro; Viggiano, Davide; Viggiano, Emanuela; Chiefari, M; Aurilio, Caterina; Luca, B. De

doi:10.1016/j.brainres.2005.05.021

Cited by 57 publications

(46 citation statements)

References 40 publications

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“…Furthermore, increased production of ROS and enhanced antioxidant activity (Guedes et al, 2006) were observed in the spinal cord after a peripheral nerve injury. Increased levels of extracellular hydrogen peroxide were also observed in the spinal trigeminal nucleus after formalin injection into the lip of the rat, and this increase coincided with pain behaviors (Viggiano et al, 2005). These studies suggest that higher levels of ROS and increased antioxidant activity in the spinal cord and brainstem after peripheral nerve injury or tissue inflammation may be important factors in persistent pain.…”

Section: Introductionmentioning

confidence: 60%

The role of reactive oxygen species in capsaicin-induced mechanical hyperalgesia and in the activities of dorsal horn neurons

Lee

Kim²,

Kim³

et al. 2007

Pain

144

122

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Previous findings that reactive oxygen species (ROS) are involved in neuropathic pain, mainly through spinal mechanisms, suggest that ROS may be involved in central sensitization. To investigate the possible role of ROS in central sensitization, we examined in rats the effects of ROS scavengers on capsaicin-induced secondary hyperalgesia, which is known to be mediated by central sensitization. We used two different ROS scavengers: phenyl N-tert-butylnitrone (PBN) and 4-hydroxy-2,2,6,6-tetramethylpiperidine 1-oxyl (TEMPOL). Intradermal capsaicin injection (20 μg in 20 μl olive oil) into the hind paw produced primary and secondary hyperalgesia. A systemic administration of PBN (100 mg/kg, i.p.) or TEMPOL (200 mg/kg, i.p.) alleviated capsaicin-induced secondary, but not primary, hyperalgesia. Intrathecal injection of PBN (1 mg in 50 μl saline) greatly reduced hyperalgesia, whereas intracerebroventricular or intradermal injection of PBN produced only a minor analgesic effect, suggesting that PBN takes effect mainly through the spinal cord. Electrophysiological recordings from wide dynamic range (WDR) neurons in the dorsal horn showed that intradermal capsaicin enhanced the evoked responses to peripheral stimuli; systemic PBN or TEMPOL restored the responses to normal levels. Removal of ROS thus restored the responsiveness of spinal WDR neurons to normal levels, indicating that ROS may be involved in central sensitization, at least in part by sensitizing WDR neurons.

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Section: Introductionmentioning

confidence: 60%

The role of reactive oxygen species in capsaicin-induced mechanical hyperalgesia and in the activities of dorsal horn neurons

Lee

Kim²,

Kim³

et al. 2007

Pain

144

122

View full text Add to dashboard Cite

show abstract

“…An alternative putative mechanism for the role of DAO in pain may be the generation of high amounts of H 2 O 2 in the spinal cord after its oxidation of neutral and polar D-amino acids such as D-serine (Pollegioni et al, 2007), D-alanine (Moreno et al, 1999), and glycine (De Marchi and Johnston, 1969). Spinal H 2 O 2 has been reported to be involved in central sensitization-mediated pain states including neuropathic pain (Kim et al, 2004(Kim et al, , 2006Viggiano et al, 2005;Hacimuftuoglu et al, 2006;Lee et al, 2007). Further studies are warranted to explore the exact mechanisms for the algesic action of spinal DAO.…”

Section: Discussionmentioning

confidence: 99%

Spinal d-Amino Acid Oxidase Contributes to Neuropathic Pain in Rats

Zhao

Gao²,

Wang³

et al. 2009

J Pharmacol Exp Ther

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D-Amino acid oxidase (DAO) is an enzyme catalyzing oxidative deamination of neutral and polar D-amino acids and is expressed in the kidneys, liver, and central nervous system (CNS) including the spinal cord. We have previously demonstrated that DAO gene deletion/mutation by using mutant ddY/ DAO(Ϫ/Ϫ) mice and systemic administration of the DAO inhibitor sodium benzoate blocked formalin-induced hyperalgesia in mice. In this study, we further investigated the potential role of DAO in neuropathic pain in a rat model of tight L 5 /L 6 spinal nerve ligation. After L 5 /L 6 spinal nerve ligation, the mRNA expression (measured by real-time quantitative polymerase chain reaction) and enzyme activity (measured by a colorimetric method) of DAO in the lumbar spinal cord were markedly increased, in agreement with the development of neuropathic pain (mechanical allodynia). Intraperitoneal injection of sodium benzoate (400 mg/kg) specifically blocked mechanical allodynia in neuropathic rats and formalin-induced hyperalgesia but did not suppress acute pain responses in the tail-flick test or formalin test. Systemic injection of sodium benzoate also inhibited DAO activity in the lumbar spinal cord of rats. Furthermore, direct intrathecal (spinal cord) injection of benzoate (30 g/rat) specifically blocked spinal nerve ligation-induced mechanical allodynia in neuropathic rats and formalin-induced hyperalgesia (but not acute pain) in the formalin test. Based on the above results, we conclude that spinal DAO plays a pronociceptive (rather than an antinociceptive) role and might be a target molecule for the treatment of chronic pain of neuropathic origin.

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“…Furthermore, the number of neurons showing mitochondrial ROS production was significantly increased in the lumbar spinal dorsal horn in spinal nerve ligated neuropathic rats (35). Also, in cre ased levels of extracellular hydrogen peroxide were observed in the spinal trigeminal nucleus after formalin injection into the lip of the rat, and this increase coincided with pain behaviors (36).…”

Section: Discussionmentioning

confidence: 88%

The Effects of Central Angiotensin II and Its Specific Blockers on Nociception. Possible Interactions with Oxidative Stress Status / Efekti Centralnog Angiotenzina II I Njegovih Specifičnih Blokatora Na Nocicepciju. Moguće Interakcije Sa Statusom Oksidativnog Stresa

Arcan¹,

Ciobîcă²,

Bild³

et al. 2013

Journal of Medical Biochemistry

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Summary:It has already been demonstrated that a complete brain renin-angiotensin system (RAS) exists distinctly separate from the peripheral system and is implicated in complex functions such as memory, emotional responses and pain. Regarding the implications of angiotensin II (the main bioactive peptide of RAS) in pain, although there are many studies in this area of research, most of the results are contro versial. Also, it seems that oxidative stress follows angio tensin II infusion, but the role of AT1 vs. AT2 receptors is not well established. In this context, we were interested in studying the effects of central RAS on nociception, through the in tra cerebroventricular administration of losartan and PD-123177 (antagonists for the AT1/AT2 receptors), as well as an ACE inhibitor (captopril) and also angiotensin II in rats, which were subsequently tested using the hot-plate task, a well known behavio ral test for pain perception. We present here the analgesic effect of angiotensin II administration, as shown by in crea sed latency-time in the hot-plate, as well as a nociceptive effect of angiotensin II blockers like AT1 and AT2 specific antagonists (losartan and PD-123177) and an ACE inhibitor (captopril), as their administration resulted in decreased la ten cy-time. Moreover, we demonstrated a significant correlation between the results of the nociceptive Kratak sadr`aj: Do sada je ve} pokazano da kompletan mo`dani renin-angiotenzin sistem (RAS) postoji zasebno od perifernog sistema i da je uklju~en u slo`ene funkcije kao {to su memorija, emocionalni odgovori i bol. [to se ti~e implikacija angiotenzina II (glavnog bioaktivnog peptida RAS) u bolu, mada u ovoj oblasti istra`ivanja postoje mnoge studije, rezultati su ve}inom opre~ni. Tako|e, izgleda da infuziju angiotenzina II prati oksidativni stres, ali uloga receptora AT1 i AT2 jo{ nije razja{njena. U tom kontekstu hteli smo da prou~imo efekte centralnog RAS na nocicepciju preko intracerebroventrikularne administracije lozartana i PD-123177 (antagonista za receptore AT1/AT2) kao i jednog ACE in hibitora (kaptopril) i angiotenzina II kod pacova, koji su potom testirani metodom grejne plo~e, poznatim bihevioralnim testom za percepciju bola. Predstavljamo analgeti~ki efekat administracije angiotenzina II pokazan kroz pove}anu latenciju na grejnoj plo~i, kao i nociceptivni efekat blokatora angiotenzina II kao {to su antagonisti specifi~ni za AT1 i AT2 (lozartan i PD-123177) i ACE inhibitora (kaptopril), po{to je rezultat njihove administracije bila smanjena latencija. [tavi{e, uo~ili smo zna~ajnu korelaciju izme|u rezultata nociceptivnog bihevioralnog testa i nivoa nekih od glavnih markera oksidativnog stresa. Na taj na~in obezbe|eni su novi

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Trigeminal pain transmission requires reactive oxygen species production

Cited by 57 publications

References 40 publications

The role of reactive oxygen species in capsaicin-induced mechanical hyperalgesia and in the activities of dorsal horn neurons

The role of reactive oxygen species in capsaicin-induced mechanical hyperalgesia and in the activities of dorsal horn neurons

Spinal d-Amino Acid Oxidase Contributes to Neuropathic Pain in Rats

The Effects of Central Angiotensin II and Its Specific Blockers on Nociception. Possible Interactions with Oxidative Stress Status / Efekti Centralnog Angiotenzina II I Njegovih Specifičnih Blokatora Na Nocicepciju. Moguće Interakcije Sa Statusom Oksidativnog Stresa

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