nara lins meira quintão análise dos mecanismos envolvidos na ...

ABSTRACT
Brachial plexus avulsion (BPA) in mice (Swiss, C57/BL6 and J129) produced long-
lasting mechanical and thermal sensitization, which were evaluated in the right hindpaw
and in the tail. These altered sensations were not observed in the operated paw. The
animals also did not show a sickness behaviour characterized by weight loss and
decrease of locomotor activity. Data obtained with knockout TNFα p55 -/- mice, antibody
anti-TNFα or thalidomide demonstrated that TNFα has a fundamental role in the onset
of mechanical and thermal hypernociception. Furthermore, it was verified, by using
antibodies against neurotrophic factors, that NGF, GDNF, BDNF and NT-3 have a role
earlier in the process of mechanical hypernociception induced by BPA, probably in the
sensitization of spinal sensory neurones. On the other hand, only BDNF seemed to
have importance for the maintenance of hypernociceptive responses in this model. B1
kinin receptor, but not B2 kinin receptor, appeared to play a significant role in the
genesis of hypernociceptive responses, confirmed by the use of knockout mice for each
receptor (B1 or B2). Moreover, B1 receptor has an important participation on the
maintenance of these sensory alterations using selective antagonists. We suggested
here that the mediators cited above, and the B1 receptor seem to initiate a cascade of
events responsible for the hypernociceptive state in this neuropathic pain model. On the
other hand, the neurotrophic factor BDNF and B1 kinin receptor seem to be
fundamentally related to the maintenance of mechanical hypernociception induced by
BPA in mice. These results together, collaborate for better understand the mechanisms
involved on the onset and on the maintenance of neuropathic pain.