Specifically, the study demonstrated that a group of signaling molecules, known collectively as the mTOR pathway, shows increased activation after a seizure. This increased signaling – above and beyond the surge that normally occurs early in life – disrupted the normal balance of synapse and circuit development to produce epilepsy and altered social behavior. Rapamycin treatment inhibited mTOR signaling, reducing susceptibility to seizures and preventing seizure-induced changes in the synapses.
The study uncovers a new link whereby epilepsy and autism may interact in early development. Last December, Jensen and colleagues published a related study finding that seizures exaggerated excitation and synaptic strengthening too soon in a rat model, causing synapses to lose their plasticity -- their ability to reconfigure in response to input from the outside world. When they gave the rats a drug called NBQX, which blocks receptors associated with excitation, these problems were reversed.