To send content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about sending content to .
To send content items to your Kindle, first ensure email@example.com
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about sending to your Kindle.
Note you can select to send to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
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.
Email your librarian or administrator to recommend adding this to your organisation's collection.