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Epilepsy is a disease of the brain characterized by recurring unprovoked epileptic seizures, caused by a transient abnormality of neuronal activity which results in synchronized electrical discharges of neurons within the central nervous system (CNS). This chapter focuses on the most important characteristics of voltage- and ligand-gated ion channels, their role in determining neuronal excitability, and the impact of some reported mutations on epileptogenesis in idiopathic epilepsies. It describes the importance of the thalamocortical loop and thalamic ion channels for the generation of generalized seizures. The binding of transmitters and the coupling to channel opening are complex processes which can consequently be influenced by amino acid changes in many different regions of these channels. Most anticonvulsant drugs that are in clinical use today act by modulating the function of ion channels and the chapter describes how ion channel function can be altered by genetic defects associated with idiopathic epilepsies.
Important factors of neuronal death in various diseases ranging from acute illness such as head trauma or stroke to rapidly or slowly progressive disorders such as amyotrophic lateral sclerosis or idiopathic parkinsonism are energy deficit and membrane depolarization. The communication of nerve cells via action potentials and synaptic transmission needs a highly negative resting membrane potential as well as strong transmembrane ionic gradients, which guarantee a regulated ion flow across the membrane. A large part of the energy demand of neurons is therefore required for active ionic pumps such as the Na/K ATPase. A reduction of membrane excitability preventing membrane depolarization and decreasing the transmembrane ionic flow therefore diminishes the energy demand of neurons considerably. The pharmacological modification of the gating of voltage- or ligand-activated ion channels thus provides potentially powerful strategies for neuroprotection. The block of voltage-gated sodium or calcium channels directly reduces the influx of respective ions and decreases excitability, whereas the activation of potassium channels leads to a membrane hyperpolarization reducing excitability and secondarily influx of sodium and calcium through voltage-gated channels and other mechanisms. These neuroprotective strategies, the targets and compounds used for pharmacotherapy and available studies in animal models and humans are discussed in this chapter. The concept of excitoxicity and neuroprotection by its antagonism by a block of glutamate receptors belonging to the group of ligand-gated ion channels is discussed in Chapter 4 of this book.
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