IBCN   20355
INSTITUTO DE BIOLOGIA CELULAR Y NEUROCIENCIA "PROFESOR EDUARDO DE ROBERTIS"
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
ERK expression in astrocytes in trigeminal subnucleus caudalis induced by experimental endodontic treatment
Autor/es:
CANZOBRE, M.C.; RIOS, H.
Lugar:
Boston
Reunión:
Conferencia; Internacional Association for Dental Research. Hatton; 2015
Institución organizadora:
Internacional Association for Dental Research
Resumen:
Incentral nervous system astrocytes interact with neurons andplay an important role in the control of pain and central sensitization.The ERKis one of the mitogen-activated protein kinases (MAPKs)that are rapidly phosphorylated in neurons after a peripheral noxious. Objective: To analyze the expression of p-ERK in astrocytes ofthe caudal subnúcleo trigeminal (Vc), after a periodontal inflammatory stimulusgenerated by unilateral endodontic treatment in rats.  Methods: 16 rats Wistar females of 50 days, were divided into group control andexperimental group which was realized an endodontic treatment in the left lowerfirst molar. To analyze the plastic changes in the trigeminal in response toinflammatory injury, immunohistochemical, immunofluorescence and western blot(WB) for primary antibodies pERK and S100B were used in both sides of thesubnucleus caudalis (Vc). Results: The ipsilateral Vc of the experimental group showed an increase in thenumber of astrocytes S100B (5.45 0.61) per area, respect to the contralateralside (4,20 0.85) p = 0, 02 and thegroup control p = 0, 002. Withimmunofluorescence, we observed a strong p-ERK Immunoreactivity in theipsilateral Vc, and that most of the cells pERK-IRco-expressed theastroglial marker S100B. Thegreatest expression of these proteins after endodontic treatment, also wasconfirmed with WB. Conclusion: Ourresults support the hypothesis that the signaling and activation of ERK in astrocytes at 7 days postendodontic,play an important role in the temporal evolution and modulation oftrigeminalnociceptive pathway.  Therefore, MAPK pathways in inflammatory pain, may be potential targetsfor pharmacological intervention, that their inhibition will alter the function of neurons and gliaduringcentral sensitization This work was supported by grants from UBACyT 2013-2016.