Effect of periapical inflammation on calcium binding proteins and ERK in the trigeminal nucleus

CANZOBRE, M.C.; PAGANELLI, ALEJANDRA R.; RIOS, HUGO

ACTA ODONTOLOGICA LATINOAMERICANA : AOL.

Argentina

Año: 2019 vol. 32 p. 103 - 110

0326-4815

Peripheral inflammation induces plastic changes in neuronsand glia which are regulated by free calcium and calciumbinding proteins (CaBP). One of the mechanisms associatedwith the regulation of intracellular calcium is linked to ERK(Extracellular Signal­Regulated Kinase) and its phosphorylatedcondition (pERK). ERK phosphorylation is important forintracellular signal transduction and participates in regulatingneuroplasticity and inflammatory responses. The aim of thisstudy is to analyse the expression of two CaBPs and pERK inastrocytes and neurons in rat trigeminal subnucleus caudalis(Vc) after experimental periapical inflammation on the leftmandibular first molar. At seven days post­treatment, theperiapical inflammatory stimulus induces an increase in pERKexpression both in S100b positive astrocytes and CalbindinD28k positive neurons, in the ipsilateral Vc with respect to thecontralateral side and control group. pERK was observed co­expressing with S100b in astrocytes and in fusiform CalbindinD28k neurons in lamina I. These results could indicate thatneural plasticity and pain sensitization could be maintained by ERK activation in projection neurons at 7 days after theperiapical inflammation.