Activation of the TRKB receptor mediates the panicolytic-like effect of the NOS inhibitor aminoguanidine

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http://hdl.handle.net/10138/313964

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Ribeiro , D E , Casarotto , P C , Júnior , A S , Fernandes , G G , Pinheiro , L C , Tanus- Santos , J E , Zangrossi Jr , H , Silveira Guimarães , F , Lourenço Joca , S R & Biojone , C 2019 , ' Activation of the TRKB receptor mediates the panicolytic-like effect of the NOS inhibitor aminoguanidine ' , Progress in Neuro-Psychopharmacology & Biological Psychiatry , vol. 93 , pp. 232-239 . https://doi.org/10.1016/j.pnpbp.2019.04.007

Title: Activation of the TRKB receptor mediates the panicolytic-like effect of the NOS inhibitor aminoguanidine
Author: Ribeiro, Deidiane Elisa; Casarotto, Plinio Cabrera; Júnior, Ailton Spiacci; Fernandes, Gabriel Gripp; Pinheiro, Lucas César; Tanus- Santos, José Eduardo; Zangrossi Jr, Hélio; Silveira Guimarães, Francisco; Lourenço Joca, Samia Regiane; Biojone, Caroline
Contributor: University of Helsinki, Neuroscience Center
University of Helsinki, Neuroscience Center
Date: 2019-07-13
Language: eng
Number of pages: 8
Belongs to series: Progress in Neuro-Psychopharmacology & Biological Psychiatry
ISSN: 0278-5846
URI: http://hdl.handle.net/10138/313964
Abstract: Nitric oxide (NO) triggers escape reactions in the dorsal periaqueductal gray matter (dPAG), a core structure mediating panic-associated response, and decreases the release of BDNF in vitro. BDNF mediates the panicolytic effect induced by antidepressant drugs and produces these effects per se when injected into the dPAG. Based on these findings, we hypothesize that nitric oxide synthase (NOS) inhibitors would have panicolytic properties associated with increased BDNF signaling in the dPAG. We observed that the repeated (7 days), but not acute (1 day), systemic administration of the NOS inhibitor aminoguanidine (AMG; 15 mg/kg/day) increased the latency to escape from the open arm of the elevated T-maze (ETM) and inhibited the number of jumps in hypoxia-induced escape reaction in rats, suggesting a panicolytic-like effect. Repeated, but not acute, AMG administration (15 mg/kg) also decreased nitrite levels and increased TRKB phosphorylation at residues Y706/7 in the dPAG. Notwithstanding the lack of AMG effect on total BDNF levels in this structure, the microinjection of the TRK antagonist K252a into the dPAG blocked the anti-escape effect of this drug in the ETM. Taken together our data suggest that the inhibition of NO production by AMG increases the levels of pTRKB, which is required for the panicolytic-like effect observed.
Subject: ANTIDEPRESSANT DRUGS
BDNF
BEHAVIOR
DORSOLATERAL PERIAQUEDUCTAL GRAY
MESSENGER-RNA
NEUROTROPHIC FACTOR
NITRIC-OXIDE SYNTHASE
NMDA RECEPTORS
Nitric oxide
Panicolytic-like effect
RAT-BRAIN
SEROTONIN
dPAG
3112 Neurosciences
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