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Comment published on 30 August 2016, see Toxins 2016, 8(9), 252.

Open AccessArticle
Toxins 2016, 8(3), 70; doi:10.3390/toxins8030070

PhTx3-4, a Spider Toxin Calcium Channel Blocker, Reduces NMDA-Induced Injury of the Retina

1
Institute of Education and Research Santa Casa Belo Horizonte-Laboratory of Toxins, Rua Domingos Vieira 590, Belo Horizonte, Minas Gerais 30150-240, Brazil
2
Ezequiel Dias Foundation (FUNED), Laboratory of Biochemistry, Rua Conde Pereira Carneiro 80, Belo Horizonte, Minas Gerais 30510-010, Brazil
3
Faculty of Medicine, Minas Gerais Federal University, Neuroscience Laboratory, Av. Alfredo Balena 190, Belo Horizonte, Minas Gerais 30130-100, Brazil
4
Department of Dentistry, Montes Claros State University, University Hospital, Health Laboratory Research, Montes Claros, Montes Claros, Minas Gerais 39401-001, Brazil
*
Author to whom correspondence should be addressed.
Academic Editor: Jean-Marc Sabatier
Received: 1 November 2015 / Revised: 26 January 2016 / Accepted: 1 March 2016 / Published: 11 March 2016
(This article belongs to the Special Issue Arthropod Venoms)
View Full-Text   |   Download PDF [2262 KB, uploaded 11 March 2016]   |  

Abstract

The in vivo neuroprotective effect of PhTx3-4, a spider toxin N-P/Q calcium channel blocker, was studied in a rat model of NMDA-induced injury of the retina. NMDA (N-Methyl-d-Aspartate)-induced retinal injury in rats reduced the b-wave amplitude by 62% ± 3.6%, indicating the severity of the insult. PhTx3-4 treatment increased the amplitude of the b-wave, which was almost equivalent to the control retinas that were not submitted to injury. The PhTx3-4 functional protection of the retinas recorded on the ERG also was observed in the neuroprotection of retinal cells. NMDA-induced injury reduced live cells in the retina layers and the highest reduction, 84%, was in the ganglion cell layer. Notably, PhTx3-4 treatment caused a remarkable reduction of dead cells in the retina layers, and the highest neuroprotective effect was in the ganglion cells layer. NMDA-induced cytotoxicity of the retina increased the release of glutamate, reactive oxygen species (ROS) production and oxidative stress. PhTx3-4 treatment reduced glutamate release, ROS production and oxidative stress measured by malondialdehyde. Thus, we presented for the first time evidence of in vivo neuroprotection from NMDA-induced retinal injury by PhTx3-4 (-ctenitoxin-Pn3a), a spider toxin that blocks N-P/Q calcium channels. View Full-Text
Keywords: Neuroprotection; retina; phoneutria nigriventer; spider toxins; PhTx3-4 Neuroprotection; retina; phoneutria nigriventer; spider toxins; PhTx3-4
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Binda, N.S.; Porto Petruceli Carayon, C.; Agostini, R.M.; do Nascimento Pinheiro, A.C.; Nascimento Cordeiro, M.; Romano Silva, M.A.; Figueira Silva, J.; Rita Pereira, E.M.; da Silva Junior, C.A.; de Castro Junior, C.J.; Sena Guimarães, A.L.; Gomez, M.V. PhTx3-4, a Spider Toxin Calcium Channel Blocker, Reduces NMDA-Induced Injury of the Retina. Toxins 2016, 8, 70.

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