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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Neuropharmacological effects of Phoneutria nigriventer venom on astrocytes

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Raposo, Catarina [1, 2, 3] ; Bjorklund, Ulrika [4] ; Kalapothakis, Evanguedes [5] ; Biber, Bjorn [6] ; da Cruz-Hofling, Maria Alice [1] ; Hansson, Elisabeth [4]
Total Authors: 6
[1] State Univ Campinas UNICAMP, Inst Biol, Dept Biochem & Tissue Biol, BR-13083970 Campinas, SP - Brazil
[2] Paulista State Univ UNESP, Dept Anim Physiol & Morphol, BR-14884900 Jaboticabal, SP - Brazil
[3] UNESP, Dept Morphol, BR-14801903 Araraquara, SP - Brazil
[4] Univ Gothenburg, Sahlgrenska Acad, Inst Neurosci & Physiol, Dept Clin Neurosci, SE-41345 Gothenburg - Sweden
[5] Univ Fed Minas Gerais, Inst Biol Sci, Dept Gen Biol, BR-31270901 Belo Horizonte, MG - Brazil
[6] Univ Gothenburg, Sahlgrenska Acad, Inst Clin Sci, Dept Anaesthesiol & Intens Care Med, SE-41345 Gothenburg - Sweden
Total Affiliations: 6
Document type: Journal article
Source: NEUROCHEMISTRY INTERNATIONAL; v. 96, p. 13-23, JUN 2016.
Web of Science Citations: 4

Bites from genus Phoneutria (Ctenidae, Araneomorpha) are the second most frequent source of spider accidents in Southeast Brazil. Severe envenoming from Phoneutria nigriventer produces vision disturbance, tremor and convulsion, suggesting that the CNS is involved; however, the mechanisms by which P. nigriventer venom (PNV) affects the CNS remain poorly understood. The present study aimed to investigate whether PNV directly impairs astrocytes. Cultured astrocytes were exposed to PNV, and intracellular Ca2+ release and signaling were measured (Fura-2/AM), Na+/K+-ATPase and Toll-like receptor 4 (TLR4) involvement were investigated, actin filaments were stained (Alexa (TM) 488-conjugated phalloidin probe), the G-actin/F-actin ratio was determined, and the expression level of connexin 43 (Cx43) was assessed. Incubation in Ca2+-free buffer did not change the Ca2+ responses. However, pre-incubation in thapsigargin/caffeine completely abolished these responses, suggesting that PNV-evoked Ca2+ transients were from intracellular Ca2+ stores. Pretreatment with a Na+/K+-ATPase antagonist (ouabain) or a TLR4 antagonist (LPS-RS) decreased or increased the Ca2+-evoked transients, respectively. Astrocytes showed altered actin filament structure after PNV exposure. PNV treatment increased the expression levels of Na+/K+-ATPase and Cx43 but decreased those of TLR4. The present results suggest that PNV directly affects astrocytes. Na+/K+-ATPase may thus represent a more specific drug target for controlling the neurotoxicity of PNV. (C) 2016 Elsevier Ltd. All rights reserved. (AU)

FAPESP's process: 12/19245-0 - Analysis of Intracellular Ca2+ fluctuation and of inflammation markers in astrocytes co-cultured with brain endothelial cells, after exposure to Phoneutria nigriventer spider venom
Grantee:Catarina Raposo Dias Carneiro
Support type: Scholarships abroad - Research Internship - Post-doctor
FAPESP's process: 11/08005-6 - Study of Phoneutria nigriventer spider venom mechanism in the blood brain barrier and in the neural tissue and analysis of two purified toxins action as vehicle in the Glioma treatment
Grantee:Catarina Raposo Dias Carneiro
Support type: Scholarships in Brazil - Post-Doctorate