• JoomlaWorks Simple Image Rotator
  • JoomlaWorks Simple Image Rotator
  • JoomlaWorks Simple Image Rotator
  • JoomlaWorks Simple Image Rotator
  • JoomlaWorks Simple Image Rotator
  • JoomlaWorks Simple Image Rotator
  • JoomlaWorks Simple Image Rotator
  • JoomlaWorks Simple Image Rotator
  • JoomlaWorks Simple Image Rotator
  • JoomlaWorks Simple Image Rotator
 
  Bookmark and Share
 
 
Doctoral Thesis
DOI
10.11606/T.42.2004.tde-20012006-143532
Document
Author
Full name
Marucia Chacur
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2004
Supervisor
Committee
Cury, Yara (President)
Antunes, Edson
Beirão, Paulo Sérgio Lacerda
Duarte, Igor Dimitri Gama
Teixeira, Catarina de Fatima Pereira
Title in Portuguese
Efeito nociceptivo induzido por fosfolipases A2 (FLA2 variantes Lys49 e Asp49) isoladas do veneno de serpentes Bothrops asper: caracterização dos mecanismos centrais e determinantes moleculares
Keywords in Portuguese
Alodinia
Canais iônicos
Dor
Fosfolipase A2
Medula espinhal
Abstract in Portuguese
Fosfolipases A2 miotóxicas (Lys49, enzimaticamente inativa, e Asp49, com atividade) isoladas do veneno de Bothrops asper, induzem hipernocicepção. Assim, avaliamos os mecanismos estruturais, moleculares e mediadores centrais envolvidos neste efeito. A injeção intraplantar das FLA2s acarretou hiperalgesia, enquanto que apenas a FLA2-Asp49 induziu alodinia. A região C-terminal é a responsável pelo efeito da FLA2-Lys49, enquanto que a atividade catalítica da FLA2-Asp49 parece ser responsável pela indução de hipernocicepção. Canais de Ca2+ e Na+ participam deste efeito. Na medula espinhal, receptores NK1 e para CGRP, receptores ionotrópicos para glutamato, NO, IL-1, prostanóides e adenosina participam da hiperalgesia induzida pelas FLA2s. Adicionalmente, receptores metabotrópicos para glutamato e o TNF?, estão envolvidos na hiperalgesia induzida pela FLA2-Asp49. Receptores NK1 e NK2 e para CGRP, receptores para glutamato, TNF? e prostanóides medeiam a alodinia. A ativação de astrócitos e microglia, na medula espinhal, contribui para a gênese do efeito hipernociceptivo.
Title in English
Nociceptive effect induced by phospholipase A2 (PLA2-Lys49 and PLA2-Asp49) isolated from Bothrops asper venom: characterization of central mechanisms and molecular determinants.
Keywords in English
Allodynia
ion channels
Pain
Phospholipase A2
Spinal cord
Abstract in English
Phospholipase A2 (Lys49, catalytically-inactive and Asp49, catalytically active), isolated from Bothrops asper snake venom, induce pain. The present studies examined the molecular, structural and central mechanisms involved in hypernociception induced by both PLA2s. These PLA2s induced mechanical hyperalgesia, whereas only PLA2-Lys49 evoked allodynia. The C-terminal region of the PLA2-Lys49 seems to be responsible for hyperalgesia, whereas the enzymatic activity of PLA2-Asp49 contributes to such an effect. Calcium and sodium channels are involved in PLA2s-induced hyperalgesia. In the spinal cord, NK1 and CGRP receptors, glutamate ionotropic receptors, NO, IL-1, prostanoids and adenosine contribute to hyperalgesia caused by PLA2s. Additionally, metabotropic glutamate receptors and TNF are involved in hyperalgesia induced by PLA2-Asp49. NK1, NK2 and CGRP receptors, glutamate receptors, TNF and prostanoids mediate allodynia. Activation of spinal astrocytes and microglia contribute to the generation of hyperalgesia and allodynia induced by both toxins.
 
WARNING - Viewing this document is conditioned on your acceptance of the following terms of use:
This document is only for private use for research and teaching activities. Reproduction for commercial use is forbidden. This rights cover the whole data about this document as well as its contents. Any uses or copies of this document in whole or in part must include the author's name.
2006_001.pdf (1.64 Mbytes)
Publishing Date
2007-02-05
 
WARNING: Learn what derived works are clicking here.
All rights of the thesis/dissertation are from the authors
Centro de Informática de São Carlos
Digital Library of Theses and Dissertations of USP. Copyright © 2001-2020. All rights reserved.