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Parawixin2 Protects Hippocampal Cells in Experimental Temporal Lobe Epilepsy
Journal article   Open access   Peer reviewed

Parawixin2 Protects Hippocampal Cells in Experimental Temporal Lobe Epilepsy

José Luiz Liberato, Lívea Dornela Godoy, Alexandra Olimpio Siqueira Cunha, Marcia Renata Mortari, Rene de Oliveira Beleboni, Andréia C K Fontana, Norberto Peporine Lopes and Wagner Ferreira Dos Santos
Toxins, v 10(12), p486
22 Nov 2018
PMID: 30469496
url
https://www.mdpi.com/2072-6651/10/12/486/pdfView
Published, Version of Record (VoR) Open
url
https://doi.org/10.3390/toxins10120486View
Published, Version of Record (VoR) Open

Abstract

Animals Disease Models, Animal Epilepsy, Temporal Lobe - drug therapy Epilepsy, Temporal Lobe - pathology Hippocampus - drug effects Hippocampus - pathology Male Neurons - drug effects Neurons - pathology Neuroprotective Agents - therapeutic use Rats, Wistar Spider Venoms - therapeutic use Urea - analogs & derivatives Urea - therapeutic use
Epilepsy is considered as one of the major disabling neuropathologies. Almost one third of adult patients with temporal lobe epilepsy (TLE) do not respond to current antiepileptic drugs (AEDs). Additionally, most AEDs do not have neuroprotective effects against the inherent neurodegenerative process underlying the hippocampal sclerosis on TLE. Dysfunctions in the GABAergic neurotransmission may contribute not only to the onset of epileptic activity but also constitute an important system for therapeutic approaches. Therefore, molecules that enhance GABA inhibitory effects could open novel avenues for the understanding of epileptic plasticity and for drug development. Parawixin2, a compound isolated from spider venom, inhibits both GABA and glycine uptake and has an anticonvulsant effect against a wide range of chemoconvulsants. The neuroprotective potential of Parawixin2 was analyzed in a model of TLE induced by a long-lasting Status Epilepticus (SE), and its efficiency was compared to well-known neuroprotective drugs, such as riluzole and nipecotic acid. Neuroprotection was assessed through histological markers for cell density (Nissl), astrocytic reactivity (GFAP) and cell death labeling (TUNEL), which were performed 24 h and 72 h after SE. Parawixin2 treatment resulted in neuroprotective effects in a dose dependent manner at 24 h and 72 h after SE, as well as reduced reactive astrocytes and apoptotic cell death. Based on these findings, Parawixin2 has a great potential to be used as a tool for neuroscience research and as a probe to the development of novel GABAergic neuroprotective agents.

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Collaboration types
Domestic collaboration
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Web of Science research areas
Food Science & Technology
Toxicology
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