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ASIC1a May Have Role in Stopping Seizures

Mice overexpressing acid-sensing ion channel have fewer seizures after injection of chemoconvulsant

WEDNESDAY, June 11 (HealthDay News) -- Adding to previous discoveries linking acidosis with seizure inhibition, investigations with mice found that acid-sensing ion channel 1a (ASIC1a) may mediate the seizure-terminating effects when brain pH falls, according to research published online June 8 in Nature Neuroscience.

Adam E. Ziemann, of the University of Iowa in Iowa City, and colleagues write that seizures lower brain pH due to lactic acid production and accumulation of CO2, and some anticonvulsants reduce extracellular brain pH. After injecting wild-type and Asic1a-/- mice with chemoconvulsants, the wild-type mice had decreased seizure severity.

Inhibition of ASIC1a in wild-type mice increased the incidence of generalized tonic-clonic seizures after a chemoconvulsant injection. In mice that overexpressed ASIC1a, chemoconvulsant injections resulted in less seizure activity and incidence of generalized tonic-clonic seizures, compared to wild-type mice, the researchers report. In another experiment, inhalation of CO2 -- long known to inhibit seizures in humans -- prevented lethal seizures in wild-type mice given a chemoconvulsant, but failed to protect Asic1a-/- from seizures progressing to death, the authors write.

"In addition to providing a foothold for understanding seizure termination, the ability of ASIC1a to stop seizures may have implications for human seizure disorders and treatment," the authors conclude. "The findings described here suggest a new, protective function for ASIC1a in brain physiology. Thus, agents that potentiate ASIC1a activity might reduce seizure severity or duration and possibly prevent status epilepticus."

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