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In 1969, H.H. Jasper, A.A. Ward, and A. Pope and the Public Health Service Advisory Committee on the Epilepsies of the National Institutes of Health published the first edition of Basic Mechanisms of the Epilepsies. The book was developed following a workshop held in Colorado Springs and an open symposium. Since then, basic and clinical researchers in epilepsy have gathered together about every 14 years to assess where epilepsy research has been, what it has accomplished, and where it should go. Each time a book was published. In a foreword written for the second edition of Basic Mechanisms of the Epilepsies, published in 1983, Jasper reminded us that the original and ultimate goal of the Public Health Service committee was to search for a “better understanding of the epilepsies and seek more rational methods of their prevention and treatment.” In 1999, the third edition was named in honor of H.H. Jasper. This fourth edition of Jasper’s Basic Mechanisms of the Epilepsies is based on a series of workshops held for four days at Yosemite National Park in March 2009. The book (1) synthesizes the role of interactions between neurons, synapses, and glia in the initiation, spread, and arrest of seizures; (2) examines the molecular, cellular, and network plasticity mechanisms that subserve excitability, seizure susceptibility, and ultimately epileptogenesis; (3) provides a framework for expanding the genome of rare Mendelian epilepsies and understanding the complex heredity responsible for common epilepsies; (4) explores cellular mechanisms of the two main groups of presently known Mendelian epilepsy genes, the ion channelopathies and developmental epilepsy genes; and (5) for the first time in the Jasper’s series describes the current efforts to translate the discoveries in epilepsy disease mechanisms into new therapeutic strategies. The editors were assisted in reviewing the chapters by an editorial advisory board consisting of Giuseppe Biagini, Amy Brooks-Kayal, Wolfgang Löscher, Helen Scharfman, Phil Schwartzkroin, John Swann, and Annamaria Vezzani.
Contents
- Introduction
- Herbert H. Jasper and the Basic Mechanisms of the EpilepsiesMassimo Avoli.
- Why – and How – Do We Approach Basic Epilepsy Research?Philip A Schwartzkroin.
- Herbert H. Jasper and the Basic Mechanisms of the Epilepsies
- Fundamentals of Neuronal Excitablility Relevant to Seizures and Epilepsy
- Voltage-Gated Na+ Channels: Structure, Function, and PathophysiologyMassimo Mantegazza and William A Catterall.
- Na+ CHANNEL SUBUNIT STRUCTURE
- Na+ CHANNEL GENES
- MOLECULAR BASIS OF Na+ CHANNEL FUNCTION
- THREE DIMENSIONAL STRUCTURE OF Na+ CHANNELS
- EXPRESSION, LOCALIZATION AND FUNCTION OF Na+ CHANNEL SUBTYPES IN THE NERVOUS SYSTEM
- Na+ CHANNEL PHARMACOLOGY
- Na+ CHANNEL AND EPILEPSY
- GENETIC Na+ CHANNELOPATHIES
- FUTURE DEVELOPMENTS AND CHALLENGES
- REFERENCES
- Potassium Channels (including KCNQ) and EpilepsyEdward C Cooper.
- Voltage-Gated Calcium Channels in EpilepsyStuart M Cain and Terrance P Snutch.
- Hyperpolarization-Activated Cyclic Nucleotide-Gated (HCN) Ion Channelopathy in EpilepsyNicholas P Poolos.
- Phasic GABAA-Mediated InhibitionEnrico Cherubini.
- Tonic GABAA Receptor-Mediated Signaling in EpilepsyMatthew C Walker and Dimitri M Kullmann.
- Glutamatergic Mechanisms Related to Epilepsy: Ionotropic ReceptorsRaymond Dingledine.
- Glutamate Receptors in Epilepsy: Group I mGluR-Mediated EpileptogenesisRiccardo Bianchi, Robert K S Wong, and Lisa R Merlin.
- THE mGluR MODEL OF EPILEPTOGENESIS
- KEY FEATURES RELEVANT TO INDUCTION OF GROUP I mGluR-DEPENDENT EPILEPTOGENESIS
- WHAT SUSTAINS THE ONGOING EXPRESSION OF THE GROUP I mGluR-INDUCED ICTAL DISCHARGES?
- ENDOGENOUS REGULATION OF GROUP I mGluR-DEPENDENT EPILEPTOGENESIS
- FRAGILE X SYNDROME: A CLINICAL CONDITION IN WHICH HYPEREXCITABLE GROUP I mGluRs UNDERLIE A PHENOTYPE THAT INCLUDES SEIZURES
- ADDITIONAL CLINICAL CONDITIONS IN WHICH GROUP I mGluR HYPEREXCITABILITY MAY PLAY A KEY ROLE
- REFERENCES
- Plasticity of Glutamate Synaptic MechanismsJ Victor Nadler.
- Neuronal Synchronization and Thalamocortical Rhythms in Sleep, Wake and EpilepsyIgor Timofeev, Maxim Bazhenov, Josée Seigneur, and Terrence Sejnowski.
- Limbic Network Synchronization and Temporal Lobe EpilepsyJohn G R Jefferys, Premysl Jiruska, Marco de Curtis, and Massimo Avoli.
- Imaging of Hippocampal Circuits in EpilepsyHajime Takano and Douglas A Coulter.
- Normal and Pathologic High-Frequency OscillationsRichard J Staba.
- Interictal Epileptiform Discharges in Partial Epilepsy: Complex Neurobiological Mechanisms Based on Experimental and Clinical EvidenceMarco de Curtis, John G R Jefferys, and Massimo Avoli.
- Different IED Patterns in Epileptic Patients: Spikes, Spike Bursts, Sharp Waves
- Interictal Spikes in Acute and Chronic Animal Models In Vivo
- IEDs in Acute Animal Models In Vitro
- High Frequency Oscillations as Interictal Events
- The Slow Component After the Interictal Discharges
- In Vitro Recordings of IEDs from Post-surgical Brain Tissue
- Conclusions
- References
- GABA-A Receptor Function in Typical Absence SeizuresVincenzo Crunelli, Nathalie Leresche, and David W Cope.
- GABAB Receptor and Absence EpilepsyHua A Han, Miguel A Cortez, and O Carter Snead, III.
- I. BACKGROUND ON GABAB RECEPTORS
- PHYSIOLOGY OF THE GABABR
- TYPICAL VS ATYPICAL ABSENCE SEIZURES
- ANIMAL MODELS OF TYPICAL ABSENCE SEIZURES
- ANIMAL MODELS OF ATYPICAL ABSENCE SEIZURES
- GABABR-MEDIATED MECHANISMS IN TYPICAL AND ATYPICAL ABSENCE SEIZURES
- TYPICAL AND ATYPICAL ABSENCE SEIZURES ARE CIRCUITRY-DEPENDENT
- IMPAIRMENT OF LEARNING AND MEMORY IN ATYPICAL ABSENCE SEIZURES
- CONCLUSION
- DISCLOSURE STATEMENT
- REFERENCES
- Brainstem Networks: Reticulo-Cortical Synchronization in Generalized Convulsive SeizuresCarl L Faingold.
- AUDIOGENIC SEIZURES AS GENERALIZED CONVULSIVE EPILEPSY MODELS
- NEURONAL NETWORK FOR AUDIOGENIC SEIZURES
- RETICULAR FORMATION IN CONVULSANT-INDUCED GENERALIZED SEIZURE INITIATION
- RETICULAR FORMATION PLASTICITY – CONDITIONAL MULTI-RECEPTIVE NEURONS
- SEIZURE REPETITION INDUCES NEURONAL NETWORK CHANGES
- INTERACTIONS BETWEEN NEURONAL NETWORKS
- RETICULO-CORTICAL SYNCHRONIZATION MECHANISMS
- CONCLUSIONS
- REFERENCES
- On the Basic Mechanisms of Infantile SpasmsJohn W Swann and Solomon L Moshe.
- Fast Oscillations and Synchronization Examined with In Vitro Models of EpileptogenesisRoger D Traub, Miles A Whittington, and Mark O Cunningham.
- Data indicating the existence of gap junctions between principal cortical neurons
- In vitro models of VFO suggest that chemical synapses are not required for their generation
- Brief VFO, generated by non-synaptic mechanisms, occurs during interictal bursts in human epileptogenic tissue in vitro
- Example of more sustained VFO prior to an electrographic seizure, in a patient’s brain in situ
- VFO can be elicited in neocortical slices in “non-synaptic” conditions, associated with spikelets in deep pyramidal neurons
- Spatial patterns of VFO in human epileptic brain are replicated with a simple model based on localized electrical coupling between pyramidal neurons
- Discussion: clinical implications
- Acknowledgements
- References
- Computer Modeling of EpilepsyMarianne J Case, Robert J Morgan, Calvin J Schneider, and Ivan Soltesz.
- Voltage-Gated Na+ Channels: Structure, Function, and Pathophysiology
- Mechanisms of Seizure Susceptibility and Epileptogenesis
- Traumatic Brain Injury and Posttraumatic EpilepsyDavid A. Prince, Isabel Parada, and Kevin Graber.
- Spectrum of potential epileptogenic mechanisms induced by traumatic brain injury
- Choice of models for research on posttraumatic epilepsy
- Partial neocortical isolation (“undercut”) model
- When does posttraumatic epileptogenesis begin?
- Prophylaxis of posttraumatic epileptogenesis
- Important unresolved issues affecting application of antiepileptogenic therapies for PTE
- Acknowledgements
- Reference List
- Head Trauma and EpilepsyAsla Pitkänen and Tamuna Bolkvadze.
- Fever, febrile seizures and epileptogenesisCéline M. Dubé, Shawn McClelland, ManKin Choy, Amy L. Brewster, Yoav Noam, and Tallie Z. Baram.
- Role of Blood-Brain Barrier Dysfunction in EpileptogenesisAlon Friedman and Uwe Heinemann.
- Cell death and survival mechanisms after single and repeated brief seizuresDavid C. Henshall and Brian S. Meldrum.
- INTRODUCTION
- MOLECULAR MECHANISMS OF CELL DEATH FOLLOWING SINGLE AND REPEATED BRIEF SEIZURES
- HUMAN CLINICO-PATHOLOGIC STUDIES: IS THERE DAMAGE PROGRESSION IN INTRACTABLE TEMPORAL LOBE EPILEPSY?
- MOLECULAR EVIDENCE OF APOPTOSIS-ASSOCIATED SIGNALLING IN HUMAN TEMPORAL LOBE EPILEPSY
- MITOCHONDRIAL DNA DAMAGE IN EPILEPSY
- CHAPTER SUMMARY AND FUTURE QUESTIONS
- References
- Programmed Necrosis After Status EpilepticusJerome Niquet, Maria-Leonor Lopez-Meraz, and Claude G. Wasterlain.
- Histopathology of Human EpilepsyNihal C. de Lanerolle, Tih-Shih Lee, and Dennis D. Spencer.
- INTRODUCTION
- HISTOPATHOLOGICAL VARIATIONS IN TLE HIPPOCAMPUS
- REORGANIZATION OF THE DENTATE GYRUS IN SCLEROTIC HIPPOCAMPUS
- CHANGES IN AMMON’S HORN AND THE ROLE OF ASTROCYTES
- GENE EXPRESSION IN SEIZURE FOCUS
- SUBICULUM
- ENTORHINAL CORTEX
- PROBABLE PATHOPHYSIOLOGICAL MECHANISMS OF SEIZURE GENERATION
- SPECULATION ON FUTURE CHALLENGES IN THE AREA
- IMPACT ON FINDING CURES AND REPAIRS FOR EPILEPSIES
- ACKNOWLEDMENTS
- BIBLIOGRAPHY
- The Time Course and Circuit Mechanisms of Acquired EpileptogenesisF. Edward Dudek and Kevin J. Staley.
- Mossy Fiber Sprouting in the Dentate GyrusPaul S. Buckmaster.
- Kainate and Temporal Lobe Epilepsies: 3 decades of progressYehezkel Ben-Ari.
- Abnormal dentate gyrus network circuitry in temporal lobe epilepsyRobert S. Sloviter, Argyle V. Bumanglag, Robert Schwarcz, and Michael Frotscher.
- WHY FOCUS ON TEMPORAL LOBE EPILEPSY AND THE DENTATE GYRUS?
- EPILEPTOGENIC NEURON LOSS AND IMMEDIATE GRANULE CELL HYPEREXCITABILITY; IS NEURON LOSS SUFFICIENT TO CAUSE EPILEPSY?
- MOSSY FIBER SPROUTING
- GRANULE CELL DISPERSION
- THE LATENT PERIOD AND EPILEPTOGENESIS
- A “GRID CELL” HYPOTHESIS OF TEMPORAL LOBE EPILEPTOGENESIS
- CONCLUSION
- ACKNOWLEDGEMENT
- LITERATURE CITED
- Alterations in synaptic function in epilepsyChristophe Bernard.
- Seizure-induced formation of basal dendrites on granule cells of the rodent dentate gyrusCharles E. Ribak, Lee A. Shapiro, Xiao-Xin Yan, Khashayar Dashtipour, J. Victor Nadler, Andre Obenaus, Igor Spigelman, and Paul S. Buckmaster.
- Perturbations of Dendritic Excitability in EpilepsyCha-Min Tang and Scott M. Thompson.
- A brief history of the active dendrite
- Electrical compartmentalization of dendrites: the intersection of form and function
- The terminal dendrite as an electrical compartment
- The apical trunk as an independent electrical compartment
- Coupling between different dendritic compartments
- The epileptic neuron vs the epileptic network
- References
- Neurogenesis and EpilepsyJack M. Parent and Michelle M. Kron.
- Temporal Lobe Epilepsy and the BDNF Receptor, TrkBJames O. McNamara and Helen E. Scharfman.
- INTRODUCTION
- MESIAL TEMPORAL LOBE EPILEPSY: A PROGRESSIVE DISORDER IN HUMANS AND ANIMAL MODELS
- SEIZURES: A PATHOLOGICAL FORM OF NEURONAL ACTIVITY
- BRAIN DERIVED NEUROTROPHIC FACTOR: AN ATTRACTIVE CANDIDATE GENE
- EVIDENCE IMPLICATING BDNF AND TRKB IN MTLE
- WHAT IS THE MOLECULAR MECHANISM MEDIATING TRKB ACTIVATION BY SEIZURES IN VIVO?
- THE POTENTIAL ROLE OF BDNF IN CATAMENIAL EPILEPSY
- CATAMENIAL EPILEPSY: DEFINITION AND POTENTIAL MECHANISMS
- ALTERNATE EXPLANATIONS FOR CATAMENIAL EPILEPSY BASED ON THE INTERPLAY BETWEEN ESTROGEN, PROGESTERONE, AND BDNF
- SUMMARY
- CONCLUDING REMARKS
- Acknowledgements
- REFERENCES
- Alterations in the Distribution of GABAA Receptors in EpilepsyCarolyn R. Houser, Nianhui Zhang, and Zechun Peng.
- MULTIPLE CHANGES IN GABAAR SUBUNITS IN EPILEPSY
- FRAMEWORK FOR VIEWING GABAAR SUBUNIT CHANGES IN EPILEPSY
- DECREASED EXPRESSION OF GABAAR SUBUNITS IN PRINCIPAL CELLS
- INCREASED EXPRESSION OF GABAAR SUBUNITS IN PRINCIPAL CELLS
- ALTERED GABAAR SUBUNIT EXPRESSION IN INTERNEURONS
- SUMMARY
- Acknowledgments
- References
- GABAA Receptor Plasticity During Status EpilepticusSuchitra Joshi and Jaideep Kapur.
- Animal models of SE
- Reduced GABAergic neurotransmission during SE
- GABARs
- GABAR-mediated inhibition is decreased during SE
- Increased internalization of synaptic GABARs during SE
- SE-induced dephosphorylation of GABARs decreases their cell surface stability
- Decreased benzodiazepine sensitivity with seizure progression in animal models of SE
- Tonic inhibition mediated by GABARs during SE
- GABAR function in catamenial epilepsy
- Conclusions
- Reference List
- Plasticity of GABAA receptors relevant to neurosteroid actionsIstvan Mody.
- GABAA Receptor Plasticity in Alcohol WithdrawalRichard W. Olsen and Igor Spigelman.
- Regulation of GABAA Receptor Gene Expression and EpilepsyAmy R. Brooks-Kayal and Shelley J. Russek.
- Chloride homeostasis and GABA signaling in temporal lobe epilepsyRichard Miles, Peter Blaesse, Gilles Huberfeld, Lucia Wittner, and Kai Kaila.
- Astrocytes and EpilepsyJerome Clasadonte and Philip G. Haydon.
- Astrocyte dysfunction in epilepsyChristian Steinhäuser and Gerald Seifert.
- Glia-neuronal interactions in ictogenesis and epileptogenesis: role of inflammatory mediatorsAnnamaria Vezzani, Stephan Auvin, Teresa Ravizza, and Eleonora Aronica.
- Glia-Neuron Interactions: Neurosteroids and EpileptogenesisGiuseppe Biagini, Carla Marinelli, Gabriella Panuccio, Giulia Puia, and Massimo Avoli.
- Traumatic Brain Injury and Posttraumatic Epilepsy
- Epilepsy Genes and Brain Development
- Genetic Epidemiology and Gene Discovery in EpilepsyRuth Ottman and Neil Risch.
- Strategies for Studying the Epilepsy GenomeThomas N. Ferraro, Dennis J. Dlugos, Hakon Hakonarson, and Russell J. Buono.
- Sodium Channel Mutations and EpilepsyWilliam A. Catterall.
- Introduction
- Voltage-gated sodium channels
- Sodium Channel Mutations in Generalized Epilepsy with Febrile Seizures Plus
- Severe Myoclonic Epilepsy of Infancy
- Potential Role of Mutations in NaV1.1 Channels in Febrile Seizures in Childhood
- A Unified Loss-of-Function Hypothesis for NaV1.1 Genetic Epilepsies
- Mutations of Other NaV Channels in Epilepsy
- References
- Potassium Channelopathies of EpilepsyRobert Brenner and Karen S. Wilcox.
- The Voltage-Gated Calcium Channel and Absence EpilepsyJeffrey L. Noebels.
- Tottering, its epileptogenic alleles, and interacting subunits
- How loss of function Cacna1a mutations impair neuronal networks
- Calcium channel regulatory subunit ‘reshuffling’ and emergent spike-wave networks
- Dysafferentation as a convergent pathway to absence epilepsy in developing brain
- Resculpting Thalamic Excitability: Involvement of T-type Currents
- Translational Advances toward the treatment of Inherited Calcium Channel Epilepsies
- Epistatic interactions
- Summary
- Acknowledgments
- References
- Mutated GABAA receptor subunits in idiopathic generalized epilepsyPatrick Cossette, Pamela Lachance-Touchette, and Guy A. Rouleau.
- INTRODUCTION AND HISTORICAL PERSPECTIVES
- DEFINITION AND CLASSIFICATION
- GENETIC EVIDENCES FOR IDIOPATHIC EPILEPSIES
- FAMILIAL FORMS OF IDIOPATHIC EPILEPSIES
- STRUCTURE AND FUNCTION OF GABAA RECEPTORS
- IMPAIRED FUNCTION OF MUTATED GABAA RECEPTORS
- MUTATIONS IN VOLTAGE-GATED CHLORIDE CHANNELS
- GABA EXERTS CRITICAL FUNCTIONS IN THE DEVELOPING BRAIN
- FUTURE PERSPECTIVES
- Acknowledgements
- REFERENCES
- The GABAAγ2(R43Q) mouse model of human genetic epilepsySteven Petrou and Christopher A. Reid.
- GABAA Receptor Subunit Mutations and Genetic EpilepsiesRobert L. Macdonald, Jing-Qiong Kang, and Martin J. Gallagher.
- INTRODUCTION
- GABAA RECEPTOR SUBUNIT GENES
- IES ASSOCIATED WITH GABAA RECEPTOR SUBUNIT MUTATIONS
- PATHOPHYSIOLOGY OF GABAA RECEPTOR SUBUNIT MUTATIONS ASSOCIATED WITH CAE AND JME
- PATHOPHYSIOLOGY OF GABAA RECEPTOR SUBUNIT MUTATIONS ASSOCIATED WITH FS WITH OR WITHOUT CAE
- PATHOPHYSIOLOGY OF GABAA RECEPTOR SUBUNIT MUTATIONS ASSOCIATED WITH GEFS+ AND DRAVET SYNDROME
- DISCUSSION
- REFERENCES
- Nicotinic acetylcholine receptor mutationsOrtrud K. Steinlein, Sunao Kaneko, and Shinichi Hirose.
- Introduction
- Clinical spectrum of ADNFLE
- EEG and brain imaging in ADNFLE patients
- ADNFLE mutations in nicotinic acetylcholine receptor subunits
- Neuronal nicotinic acetylcholine receptors
- In vitro expression of ADNFLE mutations
- Origin of seizures
- Genotype – phenotype correlations in ADNFLE
- Animal models of ADNFLE – what did we learn?
- Key question: Why do nAChR mutations cause epilepsy?
- Conclusions
- Acknowledgement
- REFERENCES
- Gene Interactions and Modifiers in EpilepsyMiriam H. Meisler and Janelle E. O’Brien.
- INTRODUCTION
- WITHIN-FAMILY HETEROGENEITY MAY REFLECT THE SEGREGATION OF GENETIC MODIFIERS
- LINKAGE EVIDENCE FOR DIGENIC INTERACTION IN HUMAN EPILEPSY
- INTERACTING ION CHANNEL MUTATIONS IN MOUSE MODELS
- INBRED STRAINS OF MICE PROVIDE ACCESS TO ADDITIONAL MODIFIERS OF EPILEPSY GENES
- FUTURE PROSPECTS FOR UNDERSTANDING GENE INTERACTION IN HUMAN EPILEPSY
- ACKNOWLEDGEMENTS
- REFERENCES
- Rare genetic causes of lissencephaly may implicate microtubule-based transport in the pathogenesis of cortical dysplasiasJudy S. Liu, Christian R. Schubert, and Christopher A. Walsh.
- INTRODUCTION
- IMPLICATIONS OF MICROTUBULE ASSEMBLY AND MICROTUBULE-BASED TRANSPORT FOR NEURONAL DEVELOPMENT
- LIS1 IS THE CAUSATIVE GENE ASSOCIATED WITH MILLER-DIEKER LISSENCEPHALY SYNDROME
- DCX MUTATIONS CAUSE BOTH X-LINKED LISSENCEPHALY AND SUBCORTICAL BAND HETEROTOPIA
- MUTATIONS IN αTUBULIN CAUSES LISSENCEPHALY
- MICROTUBULE FUNCTION AND THE PATHOGENESIS OF SEIZURES
- CORTICAL MALFORMATIONS ARE AN IMPORTANT CAUSE OF PEDIATRIC EPILEPSY
- REFERENCES
- The Generation of Cortical InterneuronsDiego M. Gelman, Oscar Marín, and John L. R. Rubenstein.
- Genes in infantile epileptic encephalopathiesChristel Depienne, Isabelle Gourfinkel-An, Stéphanie Baulac, and Eric LeGuern.
- Developing Models of Aristaless-related homeobox mutationsEric D. Marsh and Jeffrey A. Golden.
- Haploinsufficiency of STXBP1 and Ohtahara syndromeHirotomo Saitsu, Mitsuhiro Kato, and Naomichi Matsumoto.
- mTOR and Epileptogenesis in Developmental Brain MalformationsMichael Wong and Peter B. Crino.
- Major Susceptibility Genes for Common Idiopathic Epilepsies: ELP4 in Rolandic Epilepsy and BRD2 in Juvenile Myoclonic EpilepsyDeb K Pal and David A Greenberg.
- Myoclonin1/EFHC1 in cell division, neuroblast migration, synapse/dendrite formation in juvenile myoclonic epilepsyT. Grisar, B. Lakaye, L de Nijs, J. LoTurco, A. Daga, and A.V. Delgado-Escueta.
- EFHC1/MYOCLONIN1, A PROTEIN OF UNKNOWN FUNCTION
- EFHC1/MYOCLONIN1, A WIDELY DISTRIBUTED PROTEIN
- EFHC1/MYOCLONIN1 CALCIUM SIGNALLING AND APOPTOSIS
- EFHC1/MYOCLONIN1 IN MITOSIS AND CELL DIVISION
- EFHC1/MYOCLONIN1 AND EARLY NEUROBLAST MIGRATION
- EFHC1/MYOCLONIN1, A KEY CILIAR COMPONENT PLAYING A ROLE IN THE FUNCTION OF EPENDYMA
- THE MAP MYOCLONIN 1 IS ESSENTIAL FOR THE NORMAL DEVELOPMENT AND FUNCTION OF THE NEUROMUSCULAR JUNCTION SYNAPSE IN DROSOPHILA
- EFHC1 OR MYOCLONIN1 DEFECT CAUSES JME AS A DEVELOPMENTAL DISEASE AFFECTING THE PROPERTIES OF THE MICROTUBULES IN THE NEURONO-GLIAL PROCESSES AND CORTICAL SYNAPTIC FUNCTIONS (“MICROTUBULOPATHY”)
- CONCLUSIONS
- Acknowledgements
- REFERENCES
- Progressive myoclonus epilepsy of LaforaJosé M. Serratosa, Berge A. Minassian, and Subramaniam Ganesh.
- Progressive myoclonus epilepsy: Unverricht-Lundborg disease and Neuronal ceroid lipofuscinosesAnna-Elina Lehesjoki and Mark Gardiner.
- GABRB3, Epilepsy, and NeurodevelopmentMiyabi Tanaka, Timothy M. DeLorey, Antonio Delgado-Escueta, and Richard W. Olsen.
- Pathophysiology of Epilepsy in Autism Spectrum DisordersCarl E. Stafstrom, Paul J. Hagerman, and Isaac N. Pessah.
- Cognitive and Behavioral Co-Morbidities of EpilepsyJonathan K. Kleen, Rod C. Scott, Pierre-Pascal Lenck-Santini, and Gregory L. Holmes.
- Migraine and Epilepsy—Shared Mechanisms within the Family of Episodic DisordersMichael A. Rogawski.
- INTRODUCTION
- COMORBIDITY OF EPILEPSY AND MIGRAINE
- EPISODIC NEUROLOGICAL DISORDERS
- FEATURES THAT CHARACTERIZE EPISODIC DISORDERS
- ANTIEPILEPTIC DRUGS IN MIGRAINE
- CORTICAL SPREADING DEPRESSION
- HYPEREXCITABILITY IN CSD AND FOCAL SEIZURES
- ROLE OF GLUTAMATE
- REQUIREMENT FOR SYNAPTIC TRANSMISSION
- CORTICAL HYPERRESPONSIVITY IN MIGRAINE
- INSIGHTS FROM GENETICS
- CONCLUSIONS
- ACKNOWLEDGMENT
- REFERENCES
- Neurobiology of Depression as a Comorbidity of EpilepsyRaman Sankar and Andrey Mazarati.
- Depression in Animal Models of Epilepsies
- Depression in an animal model of genetic absence epilepsy
- Depression in animal models of limbic epilepsy
- Depression after kindling epileptogenesis
- Depression accompanies epileptogenesis following status epilepticus
- Epileptogenesis is accompanied by changes in serotonin turnover and evoked serotonin release
- Epileptic state affects the hypothalamo-pituitary-adrenocortical (HPA) axis to produce effects on serotonin release
- Inflammation contributes to HPA axis dysregulation, impaired serotonergic function, and prolongs immobility time in the FST
- Conclusions
- Acknowledgment
- References
- Genetic Epidemiology and Gene Discovery in Epilepsy
- Epilepsy Therapeutics
- Calcium channel α2δ subunits in epilepsy and as targets for antiepileptic drugsAnnette C Dolphin.
- Targeting SV2A for Discovery of Antiepileptic DrugsRafal M. Kaminski, Michel Gillard, and Henrik Klitgaard.
- Neurosteroids — Endogenous Regulators of Seizure Susceptibility and Role in the Treatment of EpilepsyDoodipala Samba Reddy and Michael A. Rogawski.
- INTRODUCTION
- DIVERSITY OF NEUROSTEROIDS AND THEIR BIOSYNTHESIS
- PRODUCTION OF NEUROSTEROIDS IN THE BRAIN AND THEIR LOCALIZATION TO PRINCIPAL NEURONS
- NEUROSTEROID MODULATION OF GABAA RECEPTORS
- ANTICONVULSANT AND ANTIEPILEPTOGENIC EFFECTS OF NEUROSTEROIDS
- ROLE OF ENDOGENOUS NEUROSTEROIDS IN THE MODULATION OF SEIZURES
- GANAXOLONE AS A NOVEL NEUROSTEROID-BASED ANTIEPILEPTIC DRUG
- CONCLUSIONS
- ACKNOWLEDGMENTS AND DISCLOSURES
- REFERENCES
- Mechanisms of Ketogenic Diet ActionSusan A. Masino and Jong M. Rho.
- Deep Brain Stimulation for Epilepsy: Animal ModelsKevin D. Graber and Robert S. Fisher.
- Animal Models for Evaluating AntiepileptogenesisH. Steve White.
- Strategies for antiepileptogenesis: Antiepileptic drugs versus novel approaches evaluated in post-status epilepticus models of temporal lobe epilepsyWolfgang Löscher.
- Neonatal Seizures and Neuronal Transmembrane Ion TransportKristopher T. Kahle and Kevin J. Staley.
- THE EFFECTS OF GABA ARE LAREGLY DETERMINED BY THE INTRACELLULAR CONCENTRATION OF CHLORIDE
- NKCC1 AND KCC2 ARE ESSENTIAL CATION-CHLORIDE COTRANSPORTERS IN THE NERVOUS SYSTEM
- A DEVELOPMENTAL SWITCH IN NKCC1:KCC2 EXPRESSION RENDERS GABA HYPERPOLARIZING DURING NEURONAL DEVELOPMENT
- THE ROLE OF NKCC1-DEPENDENT CHLORIDE ACCUMULATION IN NEONATAL SEIZURES
- TARGETING NKCC1 AND OTHER CCCs AS AN ANTIEPILEPTIC STRATEGY
- SUMMARY
- REFERENCES
- Antiepileptogenesis, Plasticity of AED Targets, Drug resistance, and Targeting the Immature BrainHeinz Beck and Yoel Yaari.
- Drug ResistanceJan A. Gorter and Heidrun Potschka.
- Neural Stem Cell Therapy for Temporal Lobe EpilepsyAshok K. Shetty.
- Embryonic Stem Cell Therapy for Intractable EpilepsyJanice R. Naegele, Mohan C. Vemuri, and Lorenz Studer.
- Might Stem Cell Therapies be Effective for Controlling Seizures in Epilepsy?
- Repairing Dysfunctional Neural Circuitry in Temporal Lobe Epilepsy
- Stem Cells for Neurodegeneration and Epilepsy
- Pluripotent Stem Cells
- Induced Pluripotent Stem Cells
- Directed Differentiation of ESCS and IPSCS
- Bacterial Artificial Chromosome Transgenesis
- Clinical Grade Pluripotent Stem Cells In Xeno and Feeder-Free Culture Systems
- Transplant Studies of Fetal NSC for Seizure Suppression in Experimental Models
- Challenges in Cell Therapy Approaches to Treat Epilepsy
- CONCLUSIONS AND THE PATH FORWARD
- ACKNOWLEDGEMENTS
- REFERENCES
- Cell Therapy Using GABAergic Neural ProgenitorsStewart A. Anderson and Scott C. Baraban.
- Reversing Disorders of Neuronal Migration and Differentiation in Animal ModelsJean-Bernard Manent and Joseph LoTurco.
- Gene therapy of focal onset epilepsy using adeno-associated virus vector-mediated overexpression of neuropeptide YFrancesco M. Noe’, Andreas T. Sørensen, Merab Kokaia, and Annamaria Vezzani.
- Adenosine Augmentation TherapyDetlev Boison.
- Calcium channel α2δ subunits in epilepsy and as targets for antiepileptic drugs
Published concurrently on July 2, 2012 as Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Contemporary Neurology Series 80) (J.L. Noebels, M. Avoli, M.A. Rogawski, R.W. Olsen and A.V. Delgado-Escueta, eds.) by Oxford University Press, USA | ISBN-10: 0199746540 | ISBN-13: 978-0199746545.
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- "Jasper's Basic Mechanisms of the Epilepsies" Workshop.[Epilepsia. 2010]"Jasper's Basic Mechanisms of the Epilepsies" Workshop.Noebels JL, Avoli M, Rogawski M, Olsen R, Delgado-Escueta AV. Epilepsia. 2010 Dec; 51 Suppl 5(0 5):1-5.
- Review Herbert H. Jasper and the Basic Mechanisms of the Epilepsies.[Jasper's Basic Mechanisms of t...]Review Herbert H. Jasper and the Basic Mechanisms of the Epilepsies.Avoli M. Jasper's Basic Mechanisms of the Epilepsies. 2012
- Abstracts of Jasper’s Basic Mechanisms of the Epilepsies Workshop. March 23-27, 2009. Yosemite National Park, California, USA.[Epilepsia. 2010]Abstracts of Jasper’s Basic Mechanisms of the Epilepsies Workshop. March 23-27, 2009. Yosemite National Park, California, USA.. Epilepsia. 2010 Dec; 51 Suppl 5:1-97.
- Review New wave of research in the epilepsies.[Adv Neurol. 1986]Review New wave of research in the epilepsies.Delgado-Escueta AV, Ward AA Jr, Woodbury DM, Porter RJ. Adv Neurol. 1986; 44:3-55.
- Review Idiopathic focal epilepsies: the "lost tribe".[Epileptic Disord. 2016]Review Idiopathic focal epilepsies: the "lost tribe".Pal DK, Ferrie C, Addis L, Akiyama T, Capovilla G, Caraballo R, de Saint-Martin A, Fejerman N, Guerrini R, Hamandi K, et al. Epileptic Disord. 2016 Sep 1; 18(3):252-88.
- Jasper's Basic Mechanisms of the EpilepsiesJasper's Basic Mechanisms of the Epilepsies
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