Introduction

The delicate balance between excitation and inhibition is a crucial factor in normal brain function. A disruption of this balance in favor of excitation may lead to seizures and neuronal injury. γ-Aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the mammalian central nervous system (CNS). GABA is released from GABAergic neurons and acts on target cells to activate the GABA_A, GABA_B, and GABA_C receptor subtypes. During prolonged seizures such as status epilepticus (SE), large shifts in transmembrane gradients and intense activation of receptors for various neurotransmitters may contribute to short- or long-term decreases in inhibition. This chapter describes the various mechanisms that contribute to decreased GABAergic inhibition during SE and considers the possible causes and cellular mechanisms of long-term changes in GABAergic inhibition that occur as a consequence of SE.