Spider venom stops stroke damage

23 March 2017
Posted by Chris Smith.

The venom of one of the world's most dangerous spiders can powerfully protect brain cells following a stroke, a new study has shown. 

Stroke, where the blood supply to the brain is interrupted causing the destruction of the affected tissue, is the second-leading cause of death worldwide. Stroke is also a major cause of long-term disability, because there are no drugs currently available that can protect nerve cells imperilled by the process, meaning that those cells, and the cognitive functions that they subserve, are destined to be lost.

When a stroke occurs, 85% of the time it's because a blood vessel supplying a portion of the brain has become blocked. This starves the territory downstream of oxygen and glucose, forcing the dependent nerve cells into a state of oxygen debt which leads to the local accumulation of acid, which, in the absence of blood flow, cannot be washed away.

This activates a family of acid-sensitive pores that sit in the nerve cell membrane. These are called ASICs, short for acid sensing ion channels, and when they are forced open by the acid build-up they flood the cell with sodium. This is normally kept at very low concentrations inside cells, and the sudden influx pulls with it water, causing the cells to swell and burst destructively.

ASICs are therefore regarded as attractive targets for anti-stroke medicines and previously a number of venom components from both snakes and spiders have been found that can block ASICs for a period of time. However, the pharmacological profile of these agents are not ideal, and their potency tends to be quite low, limiting their usefulness.

Now researchers in Australia have found that the venom of the infamous and feared funnel web spider, a native of New South Wales, contains a protein with much more attractive properties.

Writing in PNAS, University of Queensland researcher Glenn King and his colleagues first spotted the venom component, which they have dubbed Hi1a, because it bore a chemical resemblance to another venom protein called PcTx1, which comes from a different spider species and which has shown some promise in stroke situations.

In tests on cultured cells, the Australian team found that Hi1a potently blocked the chief ASIC pore. Next they tried injecting tiny quantities into the brains of rats with acute stroke. Administered even up to 8 hours after the onset of stroke symptoms, the Hi1a venom component resulted in significant rescue of nerve cells in the affected brain regions, which was mirrored by significantly reduced neurological deficits compared to control animals, at least in the immediate aftermath.

Encouraging as this sounds, commentators are taking a cautionary stance, pointing out that rats are not humans and the current results explore only very short time intervals following the stroke. King acknowledges that they now need to look long-term in their animals to see if the beneficial effects they are seeing acutely are maintained and translate into superior recovery and neurological function.

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