| Abstract No.: | C-G3201 |
| Country: | Brazil |
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| Title: | BILATERAL LESIONS OF DORSAL PERIAQUEDUCTAL GRAY DO NOT ALTER EITHER PAIN RESPONSE ASSESSED BY THE FORMALIN TEST OR THE OPEN ELEVATED PLUS MAZE-INDUCED ANTINOCICEPTION IN MICE. |
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| Authors/Affiliations: | 1 Joyce Mendes-Gomes*; 2 Ricardo Luiz Nunes-de-Souza;
1 FCFAr - UNESP - Araraquara; 2 FFCLRP - USP - Ribeirão Preto, Brazil
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| Content: | Objectives: The midbrain periaqueductal gray (PAG) has been highlighted as one of the structures that modulate the defensive reaction (Bandler, Trends Neurosci., 17, 379, 1994; Graeff, Braz. J. Med. Biol. Res., 27, 811, 1994) and as a key component of the descendent inhibitory pain system (Fields, Textbook of Pain, 5ed., 125, 2006). Recently we demonstrated that bilateral lesion of the dorsal PAG (dPAG) attenuates anxiety indices in the elevated plus maze (EPM) (Mendes-Gomes, IBNS, 2007). In addition, evidences have demonstrated that this mesencephalic structure plays a role in the fear-induced antinociception (Fanselow, The Midbrain Periaqueductal Gray Matter, 1, 1991; Harris, J. Physiol. Paris, 90, 15, 1996). The present study evaluated the effect of bilateral lesions of dPAG on nociception response assessed by the formalin test in mice and on the open elevated plus maze-induced antinociception.
Materials and Methods: Swiss male mice (n=12-15/group) had the dPAG bilaterally lesioned with NMDA (N-methyl-D-aspartic acid, 2 µg/0.2 µl) injection. Six days later, animals received 50 µl of formalin 2.5% into the dorsal right hind paw and were exposed to a glass box (30 x 20 x 25 cm) for recording the time spent on licking the formalin injected paw during the first phase (5 minutes after injection) and the second phase (from 25 to 35 minutes after formalin injection) of the nociception test. Other groups (n=12-18/group) were submitted to a similar procedure except that the second phase of nociception test was carried out during animals exposure to two types of elevated plus maze: the enclosed (eEPM: four enclosed arms; control situation) or the open elevated plus-maze (oEPM: four open arms; threatening situation).
Results: The dPAG lesion did not alter the time spent on licking the injected paw either on the first phase (Sham-lesioned: 29.8 ± 5.6 ; Lesioned: 30.4 ± 8.0; t = - 0.06 ; p = 0.95) or the second phase (Sham-lesioned: 120.7 ± 19.2; Lesioned: 105.8 ± 16.8; t = 0.59; p = 0.56) of the formalin test. When exposed to the oEPM, Sham-lesioned mice spent less time licking the injected paw as compared to eEPM exposed animals (Sham-lesioned eEPM: 150.4 ± 24.1; Sham-lesioned oEPM: 8.4 ± 4.1). This antinociceptive response profile was not changed by bilateral dPAG lesion (Lesioned eEPM: 138.3 ± 12.4; Lesioned oEPM: 12.9 ± 2.36) [2-WAY ANOVA: type of maze (F1,56 = 214.77; p < 0.001); Lesion (F1,56 = 0.57, p = 0.45); maze x lesion interaction (F1,56 = 1.55, p = 0.22)].
Conclusion: Present results demonstrated that the bilateral lesions of the dPAG do not alter per se the pain response either in the first phase or in the second phase of the formalin test. Furthermore, the results suggest that the oEPM-induced antinociception is not mediated by dPAG. Such results do not exclude the activation of the ventrolateral portion of the PAG when the animals |
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