One evening, when my husband and I were first dating, my husband faked a seizure. We were in mid-conversation, shoulder to shoulder on the couch, his arm wrapped around me when he stopped talking and went into a fit of shaking.
By the time I extracted myself and began to realize that he was having an attack, his mouth went from drawn and open to smiling and laughing. Afterward, he said that he couldn’t continue the joke when he saw the look on my face. As you can imagine, I was less than amused. My horror quickly turned into acidic anger.
Acidity… A new study published in this month’s issue of Nature Neuroscience investigates just how acidity (in the brain) can stop a seizure. Researchers from the University of Iowa and the Iowa City VA Medical Center used mice to show that an acid sensing ion channel (ASIC1a) is key to regulating seizure activity. Through a series of elegant experiments, the scientists develop a model in which brain acidity activates ASIC1a, increasing the firing of specialized cells involved in curbing activity, in turn squelching the seizure.
When ASIC1a levels are decreased (by genetic manipulation or … tarantula toxin — you read that right), seizure sensitivity increases. Alternatively, when ASIC1a is overabundant (in the mouse genetically altered brain), there’s protection. The scientists were able to tease out which cells (inhibitory neurons) might be using these acid detecting proteins and determine that ASIC1a is important for antiepileptic effects.
The brain increases acidity during a seizure by producing lactic acid and accumulating carbon dioxide. Some anticonvulsant medications (used for humans) alter acidity, too. Regulating pH or proteins (ASIC1a) that respond to acidity may be a new strategy in the treatment of epilepsy.
In the 10 years that have followed my reaction to my husband’s episode, no such event has recurred. Acidity.