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Issues in Clinical Epileptology: A View from the Bench

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Cover of 'Issues in Clinical Epileptology: A View from the Bench'

Table of Contents

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    Book Overview
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    Chapter 1 How Can We Identify Ictal and Interictal Abnormal Activity?
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    Chapter 2 What Is the Clinical Relevance of In Vitro Epileptiform Activity?
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    Chapter 3 What Is the Importance of Abnormal “Background” Activity in Seizure Generation?
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    Chapter 4 What Is a Seizure Focus?
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    Chapter 5 What Is a Seizure Network? Long-Range Network Consequences of Focal Seizures
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    Chapter 6 What Is a Seizure Network? Very Fast Oscillations at the Interface Between Normal and Epileptic Brain
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    Chapter 7 Is There Such a Thing as “Generalized” Epilepsy?
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    Chapter 8 Are There Really “Epileptogenic” Mechanisms or Only Corruptions of “Normal” Plasticity?
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    Chapter 9 When and How Do Seizures Kill Neurons, and Is Cell Death Relevant to Epileptogenesis?
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    Chapter 10 How Is Homeostatic Plasticity Important in Epilepsy?
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    Chapter 11 Is Plasticity of GABAergic Mechanisms Relevant to Epileptogenesis?
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    Chapter 12 Do Structural Changes in GABA Neurons Give Rise to the Epileptic State?
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    Chapter 13 Does Mossy Fiber Sprouting Give Rise to the Epileptic State?
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    Chapter 14 Does Brain Inflammation Mediate Pathological Outcomes in Epilepsy?
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    Chapter 15 Are Changes in Synaptic Function That Underlie Hyperexcitability Responsible for Seizure Activity?
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    Chapter 16 Does Epilepsy Cause a Reversion to Immature Function?
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    Chapter 17 Are Alterations in Transmitter Receptor and Ion Channel Expression Responsible for Epilepsies?
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    Chapter 18 How Do We Make Models That Are Useful in Understanding Partial Epilepsies?
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    Chapter 19 Aligning Animal Models with Clinical Epilepsy: Where to Begin?
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    Chapter 20 What Non-neuronal Mechanisms Should Be Studied to Understand Epileptic Seizures?
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    Chapter 21 What Epilepsy Comorbidities Are Important to Model in the Laboratory? Clinical Perspectives
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    Chapter 22 Epilepsy Comorbidities: How Can Animal Models Help?
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    Chapter 23 What New Modeling Approaches Will Help Us Identify Promising Drug Treatments?
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    Chapter 24 What are the arguments for and against rational therapy for epilepsy?
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    Chapter 25 How Can Advances in Epilepsy Genetics Lead to Better Treatments and Cures?
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    Chapter 26 How Might Novel Technologies Such as Optogenetics Lead to Better Treatments in Epilepsy?
Attention for Chapter 17: Are Alterations in Transmitter Receptor and Ion Channel Expression Responsible for Epilepsies?
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Chapter title
Are Alterations in Transmitter Receptor and Ion Channel Expression Responsible for Epilepsies?
Chapter number 17
Book title
Issues in Clinical Epileptology: A View from the Bench
Published in
Advances in experimental medicine and biology, January 2014
DOI 10.1007/978-94-017-8914-1_17
Pubmed ID
Book ISBNs
978-9-40-178913-4, 978-9-40-178914-1
Authors

Kim L. Powell, Katarzyna Lukasiuk, Terence J. O’Brien, Asla Pitkänen, Powell, Kim L., Lukasiuk, Katarzyna, O’Brien, Terence J., Pitkänen, Asla

Abstract

Neuronal voltage-gated ion channels and ligand-gated synaptic receptors play a critical role in maintaining the delicate balance between neuronal excitation and inhibition within neuronal networks in the brain. Changes in expression of voltage-gated ion channels, in particular sodium, hyperpolarization-activated cyclic nucleotide-gated (HCN) and calcium channels, and ligand-gated synaptic receptors, in particular GABA and glutamate receptors, have been reported in many types of both genetic and acquired epilepsies, in animal models and in humans. In this chapter we review these and discuss the potential pathogenic role they may play in the epilepsies.

Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 18 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 18 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 6 33%
Professor 3 17%
Professor > Associate Professor 2 11%
Student > Master 2 11%
Lecturer 1 6%
Other 0 0%
Unknown 4 22%
Readers by discipline Count As %
Psychology 4 22%
Biochemistry, Genetics and Molecular Biology 2 11%
Agricultural and Biological Sciences 2 11%
Neuroscience 2 11%
Medicine and Dentistry 1 6%
Other 1 6%
Unknown 6 33%