It's well known that conditions such as schizophrenia, as well as strokes, seizures and traumatic brain injuries cause increased acidity around neurons in the brain, but scientists have struggled to understand exactly why this occurs. Now, researchers from the University at Buffalo may have pinpointed the reason, finding that an elusive receptor might play a big role.
The discovery was made while the Buffalo team focused in on a group of brain receptors known as N-methyl-D-aspartate or NMDA receptors, which are known to play a role in memory and learning. While most of these are inhibited by increased acidity, one receptor, known as N3A, was found to be reactivated by it.
When the high acidity acts upon the N3A receptors, they have an effect on the subject's neurons, causing them to become sensitive to the neurotransmitter glutamate. Under certain circumstances, this can cause the neurons to die.
In the past, N3A has been somewhat ignored, with its dormant state causing researchers to dismiss it in playing any significant role in brain activity. The fact that the receptor is only activated in the presence of elevated acidity explains why researchers have failed to observe them in the past. It also points to the receptor playing a key role in neuron death after strokes.
"Given that acidity increases after a stroke or an epileptic seizure, reactivation of N3A receptors may be one reason why neurons die after these neurological events," said senior study author Gabriela K. Popescu. "So finding ways to prevent acidification or the reactivation of N3A receptors may prevent brain damage from strokes of seizures, for example."
Carefully studying the receptors, the researchers were able to pinpoint the exact site on the receptor where acidity acts upon it. With this knowledge it might be possible to create highly-targeted drugs that can nullify N3A's effects, potentially helping victims of strokes and other conditions associated with high acidity and neuron death.
Full details of the work are available online in the journal Scientific Reports.
Source: University at Buffalo
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