Neuroprotective effects of the CTK 01512-2 toxin against neurotoxicity induced by 3-nitropropionic acid in rats

Antunes, Flavia Tasmin Techera; Souza, Alessandra Hübner de; Caminski, Emanuelle Sistherenn; Greggio, Samuel; Venturin, Gianina Teribele; Costa, Jaderson Costa da; Taffarel, Maitê; Rebelo, Isadora Nunes; Gomez, Marcus V.; Corrêa, Dione Silva; Vilanova, Fernanda Nunes; Regner, Andréa; Dallegrave, Eliane

doi:10.1016/j.neuro.2021.08.016

Cited by 12 publications

(4 citation statements)

References 54 publications

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“…By incorporating residues from optimized NaSpTx1 peptides, optimized Tap1a peptides were designed with greater potency and selectivity for Na V subtypes in chronic pain, as well as greater in vivo effects. Preclinical efficacy in treating several neurological disorders is also demonstrated by the ICK peptide Phα1β isolated from P. nigriventer (Antunes et al, 2021;Silva et al, 2021). Diniz et al investigated how the analgesic effects induced by Phα1β and morphine modify the central nervous system (CNS) function.…”

Section: Editorial On the Research Topicmentioning

confidence: 99%

Editorial: Venom Peptides: A Rich Combinatorial Library for Drug Development

Cardoso

Servent

Lima

2022

Front. Mol. Biosci.

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Section: Editorial On the Research Topicmentioning

confidence: 99%

Editorial: Venom Peptides: A Rich Combinatorial Library for Drug Development

Cardoso

Servent

Lima

2022

Front. Mol. Biosci.

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“…Calcium is an important regulator of cell signalling, and its role in neurological diseases has been reviewed extensively (Pchitskaya et al., 2018; Schrank et al., 2020). Owing to the action of CTK 01512‐2 on calcium channels, and considering that VGCCs are key players in calcium entry into neurons (Catterall, 2011), this isoform has been studied as a potential drug for neurodegenerative disorders (Antunes et al., 2021; Silva et al., 2018), including Huntington's disease (HD) (Joviano‐Santos et al., 2021).…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective effect of CTK 01512‐2 recombinant toxin at the spinal cord in a model of Huntington's disease

Joviano‐Santos¹,

Valadão²,

Magalhães-Gomes³

et al. 2022

Experimental Physiology

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Phα1β is a neurotoxin from the venom of the Phoneutria nigriventer spider, available as CTK 01512-2, a recombinant peptide. Owing to its antinociceptive and analgesic properties, CTK 01512-2 has been described to alleviate neuroinflammatory responses. Despite the diverse actions of CTK 01512-2 on the nervous system, little is known regarding its neuroprotective effect, especially in neurodegenerative conditions such as Huntington's disease (HD), a genetic movement disorder without cure. Here, we investigated whether CTK 01512-2 has a neuroprotective effect in a mouse model of HD. We hypothesized that spinal cord neurons might represent a therapeutic target, because the spinal cord seems to be involved in the motor symptoms of HD (BACHD) mice. We treated BACHD mice with CTK 01512-2 by intrathecal injection and performed in vivo motor behavioural and morphological analyses in the CNS (brain and spinal cord) and muscles. Our data showed that intrathecal injection of CTK 01512-2 significantly improved motor performance in the open field task. CTK 01512-2 protected neurons in the spinal cord (but not in the brain) from death, suggesting a local effect. CTK 01512-2 exerted its neuroprotective effect by inhibiting BACHD neuronal apoptosis, as revealed by a reduction in caspase-3 in the spinal cord. CTK 01512-2 was also able to revert BACHD muscle atrophy. In

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“…CTK 01512-2, the recombinant peptide from the Tx3-6 native isoform, the NTCCs blocker, is displayed to improve the BACHD animal’s motor force, and the locomotor performance when delivered intrastriatal ( Joviano-Santos et al, 2021 ), or intrathecal ( Joviano-Santos et al, 2022 ) by inhibiting the neuronal apoptosis with a site-specific effect. In a chemical-induced HD model, CTK 01512-2 intrathecal was neuroprotective and improved the motor and cognitive behavior against the damage that was caused by an inhibitor of the mitochondrial enzyme succinate dehydrogenase (3-nitropropionic acid) ( Antunes et al, 2021 ). These three studies have suggested that the protective effects of the peptide would be, at least in part, by decreasing the Ca 2+ influx, the glutamate release, and consequently, the excitotoxicity.…”

Section: Introduction: Neuronal Aspects Of Calcium Signalingmentioning

confidence: 99%

Targeting N-type calcium channels in young-onset of some neurological diseases

Antunes

Souza

Figueira

et al. 2022

Front. Cell Dev. Biol.

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Graphical AbstractN-type calcium channels dysregulation and neurotransmission impairment Early-onset of neurological conditions, like Huntington’s disease, Multiple Sclerosis, and Migraine demonstrate harmful processes, such as neuroinflammation, neurodegeneration, and conditions like pain. N-type voltage-gated calcium channels are responsible for the exacerbated calcium influx that triggers neurotransmitter release.

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Neuroprotective effects of the CTK 01512-2 toxin against neurotoxicity induced by 3-nitropropionic acid in rats

Cited by 12 publications

References 54 publications

Editorial: Venom Peptides: A Rich Combinatorial Library for Drug Development

Editorial: Venom Peptides: A Rich Combinatorial Library for Drug Development

Neuroprotective effect of CTK 01512‐2 recombinant toxin at the spinal cord in a model of Huntington's disease

Targeting N-type calcium channels in young-onset of some neurological diseases

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