Modulación del dolor orofacial: papel del óxido nítrico en el núcleo trigeminal.

CANZOBRE, M.C.; PENNELLA, C.; HUGO RIOS

Pcia Buenos Aires

Congreso; XXXIX Reunión Anual de la Sociedad Argentina de Investigación Odontológica; 2007

International Association for Dental Research

It is known that a peripheral injury of the trigeminal nerve at the pulpar plexus cause plastic changes in the central nervous system.  It has been described plastic changes at the caudal subnucleous of the spinal trigeminal nucleous, mainly at laminae I and II, both glial and in  different subtypes of neurons.  The gas nitric oxide (NO), a retrograde neuromodulator synthesize at the postsynaptic of glutamatergic neurons, is one of the neurotransmitters involved in the trigeminal pathway.  This neuromodulator acts over glutamatergic neurons, in a feedback mode that can lift the system to an uninterrupted functional condition, even in the absence of the original stimulus.  Our aim in this work was analyze the expression pattern and the relative activity of the oxide nitric synthetase, the enzyme which synthesize NO in our model of pain of dental source.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 histochemical technique for NADPH-diaphorase was done in order to detect the relative activity and distribution of the nitric oxide synthetase. Our results reveal that after 4 days post injury the different neuronal subpopulations who express NADPH-diaphorase reflect an increase in the dendritic branches and in the relative activity of the enzyme analyze as integrated optical densitiy (IOD).  However, after 7 days after the nerve injury a tendency to reach basal levels was observed.  This was interpreted as a control of painful afferent stimuli and a stop to the pain.  In parallel our laboratory had demonstrated that the serotoninergic descending system also shows an increment in the area of innervation at the trigeminal subnucleous at post injury day 4.   This former result and those show now in this work indicates that the plastic response observed could be associated with the serotonine levels.  We will discuss the rol of serotonine and NO in the modulation of the painful pathway.  Grants from UBACyT O007 and PID 6050