Expresión de calbindina y calretinina en el núcleo espinal del trigémino ante el daño pulpar

MARIELA CELESTE CANZOBRE; HUGO RÍOS

San Miguel de Tucumán, Pcia de Tucumán

Congreso; XXXIX Reunión Anual de la Sociedad Argentina de Investigación Odontológica, International Association for Dental Research; 2006

The spinal trigeminal nucleous is the first centre in the modulation of orofacial pain.  Both calcium channels opening and increment of intracellular calcium play a role in central nervous system neuroplasticity.  These mechanisms enhance neuronal excitability and modify nerve pulses as part as the mechanisms of long term potentiation and persistent nociception.  Calbindin and calretinin are calcium proteins buffers present in some neurons but not in glia.  These proteins allow controlling calcium intracellular homeostasis.  Recently they were involved in neuroplastic mechanisms. In this work we have studied the expression pattern of this calcium binding proteins in the spinal nucleous of the trigeminal in a neuroplasticity model after peripheral injury.   Wistar female rats of 50 days old were used and the mesial chamber of the left 1st mandibular molar were exposed.  This procedure produces that animals have painful feelings equivalent to painful perceptions in Humans.  In order to analyze neuronal modifications in this model animals were anesthetized perfused with paraformaldehyde and then brainstem were dissected and an immunohistochemical technique was performed using as primary antibodies anti-calbindin D28K and anti-calretinin.  It was analyzed neuronal changes after 4 and 7 days after pulpar trauma at different levels of the trigeminal nucleous.  The analyses were performed both in the injury and control side of the brainstem. Our results show that these neurons are distributed in the most external layers of the spinal trigeminal nucleous.  We can describe at least 2 populations of small neurons that express these proteins and another largest one.  In this work we demonstrate how calbindin and calretinin immunoreactivity change after pulpar teeth injury.  Grants from UBA UBA [UBACyT O007] and CONICET [PEI6069].