Kinin B1 and B2 receptors contribute to orofacial heat hyperalgesia induced by infraorbital nerve constriction injury in mice and rats

Ana Paula Luiz; Samilla Driessen Schroeder; Juliana Geremias Chichorro; João Batista Calixto; Aleksander Roberto Zampronio; Giles Alexander Rae

doi:10.1016/j.npep.2009.10.005

Kinin B₁ and B₂ receptors contribute to orofacial heat hyperalgesia induced by infraorbital nerve constriction injury in mice and rats

Ana Paula Luiz, Samilla Driessen Schroeder, Juliana Geremias Chichorro, João Batista Calixto, Aleksander Roberto Zampronio, Giles Alexander Rae

Résultat de recherche: Article › examen par les pairs

28 Citations (Scopus)

Résumé

Mechanisms coupled to kinin B₁ and B₂ receptors have been implicated in sensory changes associated to various models of neuropathy. The current study aimed to investigate if kinins also participate in orofacial thermal hyperalgesia induced by constriction of the infraorbital nerve (CION), a model of trigeminal neuropathic pain which displays persistent hypersensitivity to orofacial sensory stimulation, in rats and mice. Male Swiss mice (30-35 g) or Wistar rats (200-250 g; n = 6-10 per group in both cases) underwent CION or sham surgery and were submitted repeatedly to application of heat (∼50 °C) to the ipsilateral or contralateral snout, delivered by a heat source placed 1 cm from the vibrissal pad. Decreases in latency to display head withdrawal or vigorous snout flicking were considered indicative of heat hyperalgesia. CION caused long-lasting heat hyperalgesia which started on Day 2 after surgery in both species and lasted up to Day 17 in mice and Day 10 in rats. Administration of DALBK or HOE-140 (peptidic B₁ and B₂ receptor antagonists, respectively; each at 3 nmol in 10 μl) onto the exposed infraorbital nerve of mice at the moment of surgery delayed the development of the thermal hyperalgesia. Systemic treatment on Day 5 (mice) or Day 4 (rats) with Des-Arg⁹, Leu⁸-Bradykinin (DALBK, B₁ receptor antagonist, 0.1-1 μmol/kg, i.p.) or HOE-140 (B₂ receptor antagonist, 0.001-1 μmol/kg, i.p.) transiently reduced heat hyperalgesia in both species. Due to the peptidic nature of DALBK and HOE-140, it is likely that their effects reported herein resulted from blockade of peripheral kinin receptors. Thus, mechanisms operated by kinin B₁ and B₂ receptors, contribute to orofacial heat hyperalgesia induced by CION in both mice and rats. Perhaps kinin B₁ and B₂ receptor antagonists might constitute effective preventive and curative treatments for orofacial thermal hyperalgesia induced by nerve injury.

Langue d'origine	English
Pages (de-à)	87-92
Nombre de pages	6
Journal	Neuropeptides
Volume	44
Numéro de publication	2
DOI	https://doi.org/10.1016/j.npep.2009.10.005
Statut de publication	Published - avr. 2010
Publié à l'externe	Oui

Note bibliographique

Funding Information:
The study was supported by grants from the Brazilian National Research Council (CNPq), Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (Capes), Fundação de Apoio à Pesquisa Científica e Tecnológica do Estado de Santa Catarina (Fapesc), Programas Nacionais de Excelência (PRONEX) and Fundação Araucária. A.P.L., S.D.S. and J.G.C. were the recipients of CNPq doctoral, undergraduate and post-doctoral scholarships, respectively.

ASJC Scopus Subject Areas

Endocrinology
Neurology
Endocrine and Autonomic Systems
Cellular and Molecular Neuroscience

Accès au document

10.1016/j.npep.2009.10.005

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Citer

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title = "Kinin B1 and B2 receptors contribute to orofacial heat hyperalgesia induced by infraorbital nerve constriction injury in mice and rats",

abstract = "Mechanisms coupled to kinin B1 and B2 receptors have been implicated in sensory changes associated to various models of neuropathy. The current study aimed to investigate if kinins also participate in orofacial thermal hyperalgesia induced by constriction of the infraorbital nerve (CION), a model of trigeminal neuropathic pain which displays persistent hypersensitivity to orofacial sensory stimulation, in rats and mice. Male Swiss mice (30-35 g) or Wistar rats (200-250 g; n = 6-10 per group in both cases) underwent CION or sham surgery and were submitted repeatedly to application of heat (∼50 °C) to the ipsilateral or contralateral snout, delivered by a heat source placed 1 cm from the vibrissal pad. Decreases in latency to display head withdrawal or vigorous snout flicking were considered indicative of heat hyperalgesia. CION caused long-lasting heat hyperalgesia which started on Day 2 after surgery in both species and lasted up to Day 17 in mice and Day 10 in rats. Administration of DALBK or HOE-140 (peptidic B1 and B2 receptor antagonists, respectively; each at 3 nmol in 10 μl) onto the exposed infraorbital nerve of mice at the moment of surgery delayed the development of the thermal hyperalgesia. Systemic treatment on Day 5 (mice) or Day 4 (rats) with Des-Arg9, Leu8-Bradykinin (DALBK, B1 receptor antagonist, 0.1-1 μmol/kg, i.p.) or HOE-140 (B2 receptor antagonist, 0.001-1 μmol/kg, i.p.) transiently reduced heat hyperalgesia in both species. Due to the peptidic nature of DALBK and HOE-140, it is likely that their effects reported herein resulted from blockade of peripheral kinin receptors. Thus, mechanisms operated by kinin B1 and B2 receptors, contribute to orofacial heat hyperalgesia induced by CION in both mice and rats. Perhaps kinin B1 and B2 receptor antagonists might constitute effective preventive and curative treatments for orofacial thermal hyperalgesia induced by nerve injury.",

author = "Luiz, {Ana Paula} and Schroeder, {Samilla Driessen} and Chichorro, {Juliana Geremias} and Calixto, {Jo{\~a}o Batista} and Zampronio, {Aleksander Roberto} and Rae, {Giles Alexander}",

note = "Funding Information: The study was supported by grants from the Brazilian National Research Council (CNPq), Coordena{\c c}{\~a}o de Aperfei{\c c}oamento de Pessoal de N{\'i}vel Superior (Capes), Funda{\c c}{\~a}o de Apoio {\`a} Pesquisa Cient{\'i}fica e Tecnol{\'o}gica do Estado de Santa Catarina (Fapesc), Programas Nacionais de Excel{\^e}ncia (PRONEX) and Funda{\c c}{\~a}o Arauc{\'a}ria. A.P.L., S.D.S. and J.G.C. were the recipients of CNPq doctoral, undergraduate and post-doctoral scholarships, respectively.",

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AU - Chichorro, Juliana Geremias

AU - Calixto, João Batista

AU - Zampronio, Aleksander Roberto

AU - Rae, Giles Alexander

N1 - Funding Information: The study was supported by grants from the Brazilian National Research Council (CNPq), Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (Capes), Fundação de Apoio à Pesquisa Científica e Tecnológica do Estado de Santa Catarina (Fapesc), Programas Nacionais de Excelência (PRONEX) and Fundação Araucária. A.P.L., S.D.S. and J.G.C. were the recipients of CNPq doctoral, undergraduate and post-doctoral scholarships, respectively.

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N2 - Mechanisms coupled to kinin B1 and B2 receptors have been implicated in sensory changes associated to various models of neuropathy. The current study aimed to investigate if kinins also participate in orofacial thermal hyperalgesia induced by constriction of the infraorbital nerve (CION), a model of trigeminal neuropathic pain which displays persistent hypersensitivity to orofacial sensory stimulation, in rats and mice. Male Swiss mice (30-35 g) or Wistar rats (200-250 g; n = 6-10 per group in both cases) underwent CION or sham surgery and were submitted repeatedly to application of heat (∼50 °C) to the ipsilateral or contralateral snout, delivered by a heat source placed 1 cm from the vibrissal pad. Decreases in latency to display head withdrawal or vigorous snout flicking were considered indicative of heat hyperalgesia. CION caused long-lasting heat hyperalgesia which started on Day 2 after surgery in both species and lasted up to Day 17 in mice and Day 10 in rats. Administration of DALBK or HOE-140 (peptidic B1 and B2 receptor antagonists, respectively; each at 3 nmol in 10 μl) onto the exposed infraorbital nerve of mice at the moment of surgery delayed the development of the thermal hyperalgesia. Systemic treatment on Day 5 (mice) or Day 4 (rats) with Des-Arg9, Leu8-Bradykinin (DALBK, B1 receptor antagonist, 0.1-1 μmol/kg, i.p.) or HOE-140 (B2 receptor antagonist, 0.001-1 μmol/kg, i.p.) transiently reduced heat hyperalgesia in both species. Due to the peptidic nature of DALBK and HOE-140, it is likely that their effects reported herein resulted from blockade of peripheral kinin receptors. Thus, mechanisms operated by kinin B1 and B2 receptors, contribute to orofacial heat hyperalgesia induced by CION in both mice and rats. Perhaps kinin B1 and B2 receptor antagonists might constitute effective preventive and curative treatments for orofacial thermal hyperalgesia induced by nerve injury.

AB - Mechanisms coupled to kinin B1 and B2 receptors have been implicated in sensory changes associated to various models of neuropathy. The current study aimed to investigate if kinins also participate in orofacial thermal hyperalgesia induced by constriction of the infraorbital nerve (CION), a model of trigeminal neuropathic pain which displays persistent hypersensitivity to orofacial sensory stimulation, in rats and mice. Male Swiss mice (30-35 g) or Wistar rats (200-250 g; n = 6-10 per group in both cases) underwent CION or sham surgery and were submitted repeatedly to application of heat (∼50 °C) to the ipsilateral or contralateral snout, delivered by a heat source placed 1 cm from the vibrissal pad. Decreases in latency to display head withdrawal or vigorous snout flicking were considered indicative of heat hyperalgesia. CION caused long-lasting heat hyperalgesia which started on Day 2 after surgery in both species and lasted up to Day 17 in mice and Day 10 in rats. Administration of DALBK or HOE-140 (peptidic B1 and B2 receptor antagonists, respectively; each at 3 nmol in 10 μl) onto the exposed infraorbital nerve of mice at the moment of surgery delayed the development of the thermal hyperalgesia. Systemic treatment on Day 5 (mice) or Day 4 (rats) with Des-Arg9, Leu8-Bradykinin (DALBK, B1 receptor antagonist, 0.1-1 μmol/kg, i.p.) or HOE-140 (B2 receptor antagonist, 0.001-1 μmol/kg, i.p.) transiently reduced heat hyperalgesia in both species. Due to the peptidic nature of DALBK and HOE-140, it is likely that their effects reported herein resulted from blockade of peripheral kinin receptors. Thus, mechanisms operated by kinin B1 and B2 receptors, contribute to orofacial heat hyperalgesia induced by CION in both mice and rats. Perhaps kinin B1 and B2 receptor antagonists might constitute effective preventive and curative treatments for orofacial thermal hyperalgesia induced by nerve injury.

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