Inhibition of the NMDA receptor/Nitric Oxide pathway in the dorsolateral periaqueductal gray causes anxiolytic-like effects in rats submitted to the Vogel conflict test
Contribuinte(s) |
UNIVERSIDADE DE SÃO PAULO |
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Data(s) |
26/08/2013
26/08/2013
2009
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Resumo |
Abstract Background Several studies had demonstrated the involvement of the dorsolateral portion of periaqueductal grey matter (dlPAG) in defensive responses. This region contains a significant number of neurons containing the enzyme nitric oxide synthase (NOS) and previous studies showed that non-selective NOS inhibition or glutamate NMDA-receptor antagonism in the dlPAG caused anxiolytic-like effects in the elevated plus maze. Methods In the present study we verified if the NMDA/NO pathway in the dlPAG would also involve in the behavioral suppression observed in rats submitted to the Vogel conflict test. In addition, the involvement of this pathway was investigated by using a selective nNOS inhibitor, Nω-propyl-L-arginine (N-Propyl, 0.08 nmol/200 nL), a NO scavenger, carboxy-PTIO (c-PTIO, 2 nmol/200 nL) and a specific NMDA receptor antagonist, LY235959 (4 nmol/200 nL). Results Intra-dlPAG microinjection of these drugs increased the number of punished licks without changing the number of unpunished licks or nociceptive threshold, as measure by the tail flick test. Conclusion The results indicate that activation of NMDA receptors and increased production of NO in the dlPAG are involved in the anxiety behavior displayed by rats in the VCT. This research was supported by grants from FAEPA, CNPq (305996/20088 and 470042/20095) and FAPESP. We thank to I.A.C. Fortunato and J.C. de Aguiar for the excellent technical support. |
Identificador |
Behavioral and Brain Functions. 2009 Sep 23;5(1):40 1744-9081 http://www.producao.usp.br/handle/BDPI/33094 10.1186/1744-9081-5-40 |
Idioma(s) |
eng |
Relação |
Behavioral and Brain Functions |
Direitos |
openAccess Tonetto et al; licensee BioMed Central Ltd. - This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
Tipo |
article original article publishedVersion |