Status epilepticus is a clinical emergency defined as continuous seizure activity or rapid, recurrent seizures without regaining consciousness and can lead to the development of acquired epilepsy, characterized by spontaneous, recurrent seizures. Understanding epileptogenesis--the transformation of healthy brain tissue into hyperexcitable neuronal networks--is an important challenge and the elucidation of molecular mechanisms can lend insight into new therapeutic targets to halt this progression. It has been demonstrated that intracellular calcium increases during status epilepticus and that these elevations are maintained past the duration of the injury (Ca(2+) plateau). As an important second messenger, Ca(2+) elevations can lead to changes in gene expression, neurotransmitter release and plasticity. Thus, characterization of the post-injury Ca(2+) plateau may be important in eventually understanding the pathophysiology of epileptogenesis and preventing the progression to chronic epilepsy after brain injury.