Early-life seizures may prematurely switch on key synapses in the brain that may further cause neurodevelopmental delay among children with autism and other intellectual disabilities, finds a new study.
According to the researchers, antiepileptic drug may keep those synapses "silent" longer so brain can develop normally.
The results, revealed a mechanism for the relationship between seizures and later-in-life cognitive impairment, as well as a much-needed potential treatment avenue to pursue.
"Understanding the precise synaptic changes following seizures gives an opportunity to find treatments that can prevent this early 'unsilencing'," said Frances E. Jensen from Perelman School of Medicine at the University of Pennsylvania.
"The timing is important: We need to stop it right after the seizures and before a critical period of development in a child's life so the brain can develop without any problems that may lead to future impairments," Jensen added.
In the study, published in the journal Cell Reports, the team induced seizures in mice with pentylenetetrazol, or PTZ, injections and used voltage-sensitive dye (VSD) imaging to monitor, measure, and visualise brain activity in the auditory cortex.
The results showed that following induced seizures "silent" thalamocortical synapses - the main route of sensory information to the cerebral cortex -- in the auditory cortex - part that possess auditory information-- containing only NMDA receptors, switched to "unsilent" synapses with both NMDA and AMPA receptors -- receptors play important roles in learning and forming new memories.
Further investigations showed that treatment using a drug called NBQX, reduced AMPA receptor enhancement and premature "unsilencing" of the thalamocortical synapses, and also restored synaptic plasticity during the critical period, the researchers reported.
"This is proof of principle that synaptic plasticity is a dynamic target for the treatment of autism and intellectual disabilities that accompany early-life seizures," Jensen added.