Increased insulin receptor expression in anterior temporal neocortex of patients with intractable epilepsy.

The insulin receptor (IR) is a tyrosine kinase receptor that binds to insulin and plays pivotal roles in energy homeostasis, neuronal growth, neuronal survival, synaptic plasticity and cognitive function. The biological mechanisms of intractable epilepsy involve energy metabolism, neuron loss, neurogenesis and abnormal neural networks. Here, we evaluated the expression of the IR in the anterior temporal neocortex of patients with intractable epilepsy (IE) by immunohistochemistry, double-label immunofluorescence and immunoblotting. We compared these tissues against histologically normal anterior temporal lobes from individuals treated for post-trauma intracranial hypertension. We found that the IR was coexpressed with neuron-specific enolase (NSE) and that IR expression increased in the anterior temporal neocortex of epileptic patients. On the basis of the potential physiological effects of IR, our findings suggest that increased expression of the IR is a consequence of epileptic seizures and a cause of IE.