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  • Phα1β Spider Toxin Reverses Glial Structural Plasticity Upon Peripheral Inflammation.

Phα1β Spider Toxin Reverses Glial Structural Plasticity Upon Peripheral Inflammation.

Frontiers in cellular neuroscience (2019-07-30)
Helia Tenza-Ferrer, Luiz Alexandre Viana Magno, Marco Aurélio Romano-Silva, Juliana Figueira da Silva, Marcus Vinicius Gomez
ABSTRACT

The incoming signals from injured sensory neurons upon peripheral inflammation are processed in the dorsal horn of spinal cord, where glial cells accumulate and play a critical role in initiating allodynia (increased pain in response to light-touch). However, how painful stimuli in the periphery engage glial reactivity in the spinal cord remains unclear. Here, we found that a hind paw inflammation induced by CFA produces robust morphological changes in spinal astrocytes and microglia compatible with the reactive phenotype. Strikingly, we discovered that a single intrathecal injection with venom peptides that inhibit calcium channels reversed all the glial pathological features of the peripheral inflammation. These effects were more apparent in rats treated with the Phα1β spider toxin (non-specific calcium channel antagonist) than ω-MVIIA cone snail toxin (selective N-type calcium channel antagonist). These data reveal for the first time a venom peptide acting on glial structural remodeling in vivo. We, therefore, suggest that calcium-dependent plasticity is an essential trigger for glial cells to initiate reactivity, which may represent a new target for the antinociceptive effects of Phα1β and ω-MVIIA toxins in inflammatory pain conditions.

MATERIALS
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Product Description

Millipore
MILLIPLEX® Rat Cytokine/Chemokine Magnetic Bead Panel - Immunology Multiplex Assay, Simultaneously analyze multiple cytokine and chemokine biomarkers with Bead-Based Multiplex Assays using the Luminex technology, in rat serum, plasma and cell culture samples.
Sigma-Aldrich
Monoclonal Anti-Glial Fibrillary Acidic Protein (GFAP) antibody produced in mouse, clone G-A-5, ascites fluid
Sigma-Aldrich
β-Nicotinamide adenine dinucleotide 2′-phosphate reduced tetrasodium salt hydrate, ≥95% (HPLC)