Spider venom peptide helps protect the brain after a stroke | Chemical & Engineering News
Volume 95 Issue 13 | p. 7 | Concentrates
Issue Date: March 27, 2017

Spider venom peptide helps protect the brain after a stroke

Study finds the cysteine-rich peptide has a protective and restorative effect in mice hours after a stroke.
Department: Science & Technology
Keywords: biochemistry, venom, spider, stroke
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Credit: Toby Hudson/Wikimedia Commons
Photo of a funnel-web spider and a peptide it makes.
 
Credit: Toby Hudson/Wikimedia Commons
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A double-knotted peptide from this funnel-web spider can protect the brains of stroke victims via its interaction with ion channels (disulfide bonds shown in blue).
Credit: PNAS
An image of the peptide that a funnel-web spider makes.
 
A double-knotted peptide from this funnel-web spider can protect the brains of stroke victims via its interaction with ion channels (disulfide bonds shown in blue).
Credit: PNAS

The Australian funnel-web spider’s venom can be deadly to humans. But a small amount of one peptide in the arachnid’s poison arsenal has been found to protect the brain tissue of rodents after they’ve suffered a stroke. If the work holds true in humans, the venomous disulfide-rich peptide, called Hi1a, could complement current treatments for stroke victims (Proc. Natl. Acad. Sci. USA 2017, DOI: 10.1073/pnas.1614728114). In most strokes, blood supply to the brain is blocked, leading to a shortage of oxygen and glucose. Brain cells start to die quickly in regions closest to the blockage, but over the course of hours to days, tissue located farther away begins to perish. It’s this more-distant tissue that stroke drugs aim to salvage. However, these protective therapeutics—also derived from spider venom—must be delivered within four hours. The new peptide, discovered by Lachlan D. Rash and Glenn F. King of the University of Queensland and their colleagues, blocks an acid-sensing ion channel in neurons with beneficial effects even after eight hours. This ion channel is activated during a stroke because restricted blood flow to the brain lowers tissue pH levels. When these ion channels stay open, several biochemical pathways eventually trigger cell death in the brain. In rodent stroke victims, the venom peptide blocked this ion channel, thereby preventing the detrimental effects. The peptide also helped preserve neuronal architecture and restore neurological and motor function to the animals as they recovered.

 
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