Development of the calcium plateau following status epilepticus: role of calcium in epileptogenesis

Abstract

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 (Ca²⁺ plateau). As an important second messenger, Ca²⁺ elevations can lead to changes in gene expression, neurotransmitter release and plasticity. Thus, characterization of the post-injury Ca²⁺ plateau may be important in eventually understanding the pathophysiology of epileptogenesis and preventing the progression to chronic epilepsy after brain injury.

Keywords::

• acquired epilepsy
• calcium homeostasis
• epileptogenesis
• hippocampal neuronal culture
• intracellular calcium
• Sprague-Dawley rat
• status epilepticus

Financial & competing interests disclosure

This research was funded by support from the National Institute of Neurological Disorders and Stroke grants RO1NS051505, RO1NS052529 and UO1NS058213. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.