Antinociceptive effect of topiramate in models of acute pain and diabetic neuropathy in rodents

Lopes, Luís Carlos; Pereira, S.S.; Silva, L.L.; Figueiredo, Kayo Alves; Moura, Brinell Arcanjo; Almeida, Fernanda Campos Sousa de; Sousa, F.C.F.

doi:10.1016/j.lfs.2008.11.005

Cited by 37 publications

(20 citation statements)

References 33 publications

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“…[12][13][14] In general, the hot-plate test is seldom used in diabetic rat studies, although it has been sensitive enough to demonstrate thermal hyperalgesia in several studies. 15,16 Thermal hyperalgesia has been registered in some patients with mild PDN, whereas advanced-stage disease is typically characterized by elevated thermal perception thresholds (hypoalgesia) that progress to sensory loss, occurring in conjunction with unmyelinated peripheral nerve fiber degeneration. 17,18 Thus, studies of mechanisms underlying both thermal hyperalgesia and thermal hypoalgesia and the development of agents to prevent and treat both disorders are clinically relevant.…”

Section: Pathogenesis and Experimental Treatments Of Diabetes-associamentioning

confidence: 99%

Diabetic Painful and Insensate Neuropathy: Pathogenesis and Potential Treatments

2009

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Summary:Advanced peripheral diabetic neuropathy (PDN) is associated with elevated vibration and thermal perception thresholds that progress to sensory loss and degeneration of all fiber types in peripheral nerve. A considerable proportion of diabetic patients also describe abnormal sensations such as paresthesias, allodynia, hyperalgesia, and spontaneous pain. One or several manifestations of abnormal sensation and pain are described in all the diabetic rat and mouse models studied so far (i.e., streptozotocin-diabetic rats and mice, type 1 insulinopenic BB/Wor and type 2 hyperinsulinemic diabetic BBZDR/Wor rats, Zucker diabetic fatty rats, and nonobese diabetic, Akita, leptin-and leptin-receptor-deficient, and highfat diet-fed mice). Such manifestations are 1) thermal hyperalgesia, an equivalent of a clinical phenomenon described in early PDN; 2) thermal hypoalgesia, typically present in advanced PDN; 3) mechanical hyperalgesia, an equivalent of pain on pressure in early PDN; 4) mechanical hypoalgesia, an equivalent to the loss of sensitivity to mechanical noxious stimuli in advanced PDN; 5) tactile allodynia, a painful perception of a light touch; and 5) formalin-induced hyperalgesia. Rats with short-term diabetes develop painful neuropathy, whereas those with longer-term diabetes and diabetic mice typically display manifestations of both painful and insensate neuropathy, or insensate neuropathy only. Animal studies using pharmacological and genetic approaches revealed important roles of increased aldose reductase, protein kinase C, and poly(ADPribose) polymerase activities, advanced glycation end-products and their receptors, oxidative-nitrosative stress, growth factor imbalances, and C-peptide deficiency in both painful and insensate neuropathy. This review describes recent achievements in studying the pathogenesis of diabetic neuropathic pain and sensory disorders in diabetic animal models and developing potential pathogenetic treatments. Key Words: Animal models, diabetic insensate neuropathy, diabetic painful neuropathy, formalin-induced hyperalgesia, mechanical hyper-and hypoalgesia, pathogenetic treatments of diabetic neuropathic pain and sensory loss, symptomatic treatments of diabetic pain, tactile allodynia, thermal hyper-and hypoalgesia.

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Section: Pathogenesis and Experimental Treatments Of Diabetes-associamentioning

confidence: 99%

Diabetic Painful and Insensate Neuropathy: Pathogenesis and Potential Treatments

2009

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“…The doses of the drugs used were selected on the basis of literature data and of previous results from our laboratory (2,(14)(15)(16). To determine the possible participation of different systems, we used antagonists of various receptors administered sc 20 min before the HF.…”

Section: Analysis Of Possible Antinociceptive Mechanisms Of Hydroalcomentioning

confidence: 99%

Antinociceptive effect on mice of the hydroalcoholic fraction and (-) epicatechin obtained from Combretum leprosum Mart & Eich

Lopes¹,

Marques²,

Pereira³

et al. 2010

Braz J Med Biol Res

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“…It is well known that the nitric oxide-cGMP-PKG pathway activation modulates the peripheral antinociceptive effects induced by certain drugs during inflammatory pain, including opioids (Ferreira et al, 1991;Pol, 2007;Hervera et al, 2009;Leá nez et al, 2009) and cannabinoids (Lopes et al, 2009). Nitric oxide also regulates the transcription of -and -opioid receptor genes under basal and inflammatory conditions (Park et al, 2002;Pol et al, 2005), but the exact role of nitric oxide in the peripheral actions and expression of DOPr and CB2R during neuropathic pain is not known.…”

Section: Introductionmentioning

confidence: 99%

The Role of Nitric Oxide in the Local Antiallodynic and Antihyperalgesic Effects and Expression of δ-Opioid and Cannabinoid-2 Receptors during Neuropathic Pain in Mice

Hervera¹,

Negrete²,

Leánez³

et al. 2010

J Pharmacol Exp Ther

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Both ␦-opioid receptor (DOPr) and cannabinoid-2 receptor (CB2R) agonists attenuate neuropathic pain, but the precise mechanism implicated in these effects is not completely elucidated. We investigated whether nitric oxide synthesized by neuronal (NOS1) or inducible (NOS2) nitric-oxide synthases could modulate DOPr and/or CB2R antiallodynic and antihyperalgesic effects through the peripheral nitric oxide-cGMP-protein kinase G (PKG) pathway activation and affect their expression during neuropathic pain. , and NOS2-KO mice, also was assessed. The subplantar administration of NANT, L-NIL, ODQ, or Rp-8-pCPTcGMPs dose-dependently inhibited neuropathic pain and enhanced the local effects of DPDPE or JWH-015. Moreover, although the basal levels of DOPr and CB2R mRNA were similar between WT and NOS-KO animals, nerve injury only decreased (DOPr) or increased (CB2R) their expression in the dorsal root ganglia of WT and NOS2-KO mice, and not in NOS1-KO mice. Results suggest that inactivation of the nitric oxide-cGMP-PKG peripheral pathway triggered by NOS1 and NOS2 enhanced the peripheral actions of DOPr and CB2R agonists and that nitric oxide synthesized by NOS1 is implicated in the peripheral regulation of DOPr and CB2R gene transcription during neuropathic pain.

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Antinociceptive effect of topiramate in models of acute pain and diabetic neuropathy in rodents

Cited by 37 publications

References 33 publications

Diabetic Painful and Insensate Neuropathy: Pathogenesis and Potential Treatments

Diabetic Painful and Insensate Neuropathy: Pathogenesis and Potential Treatments

Antinociceptive effect on mice of the hydroalcoholic fraction and (-) epicatechin obtained from Combretum leprosum Mart & Eich

The Role of Nitric Oxide in the Local Antiallodynic and Antihyperalgesic Effects and Expression of δ-Opioid and Cannabinoid-2 Receptors during Neuropathic Pain in Mice

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