bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cell death after single and repeated brief seizures
Authors: Henshall David C. , Meldrum Brian S. 
Published: December 2010

SummaryWe review the experimental evidence from animal models that suggest that brief, evoked seizures can result in neuronal death while spontaneous seizures normally do not, as well as human data showing damage may progress in certain patients, and we describe the cell death and survival pathways regulating these processes. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AC, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Circuit mechanisms of acquired epileptogenesis
Authors: Dudek F. Edward , Staley Kevin J. 
Published: December 2010

SummaryThe time course of development of spontaneous recurrent seizures is a sigmoid function of time after status epilepticus or perinatal stroke, which reflects underlying mechanisms of epileptogenesis. The increase in recurrent excitation after axon sprouting, along with death of specific γγ‐aminobutyric acid (GABA)ergic interneurons, may contribute to this temporal pattern of epileptogenesis. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Abnormal dentate gyrus network circuitry in temporal lobe epilepsy
Authors: Sloviter Robert S. , Bumanglag Argyle V. , Schwarcz Robert , Frotscher Michael 
Published: December 2010

SummaryPatients with temporal lobe epilepsy exhibit developmental and acquired hippocampal abnormalities that include abnormally developed structure, neuron loss, aberrant neurogenesis, synaptic reorganization, granule cell dispersion, and gliosis. Determining which features play causal roles in epileptogenesis, and which features affect other aspects of the disorder, is a central challenge of epilepsy research. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Seizure‐induced basal dendrites on granule cells
Authors: Ribak Charles E. , Shapiro Lee A. , Yan Xiao‐Xin , Dashtipour Khashayar , Nadler J. Victor , Obenaus Andre , Spigelman Igor , Buckmaster Paul S. 
Published: December 2010

SummarySeizure‐induced hilar basal dendrites on dentate granule cells are observed in several rodent models of temporal lobe epilepsy. Ultrastructural evidence showed that basal dendrites receive predominantly excitatory synapses, including many from mossy fibers. Such highly interconnected granule cells with basal dendrites are suggested to enhance hyperexcitability within the dentate network. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Neurogenesis and epilepsy
Authors: Parent Jack M. , Kron Michelle M. 
Published: December 2010

SummaryPersistent neural stem cells generate dentate granule cells (DGCs) throughout life. Evidence suggests that aberrant neurogenesis contributes to epileptic structural abnormalities, but that normally integrating adult‐born DGCs may restore inhibition. Current research focuses on how epileptogenic insults alter neurogenesis, and whether restoring normal neurogenesis will attenuate epilepsy or its comorbidities. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Temporal lobe epilepsy and the BDNF receptor, TrkB
Authors: McNamara James O. , Scharfman Helen E. 
Published: December 2010

SummaryBrain derived neurotrophic factor (BDNF) regulates diverse neuronal functions and plasticity, and its expression is increased by seizures. Here we review the evidence that actions of BDNF at TrkB receptors contribute to temporal lobe epilepsy. In addition, regulation of BDNF by steroid hormones might explain syndromes such as catamenial epilepsy. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
GABAA receptor plasticity in status epilepticus
Authors: Joshi Suchitra , Kapur Jaideep 
Published: December 2010

SummarySeizures become self‐sustaining during status epilepticus (SE) in part due to altered inhibitory neurotransmission mediated by γ‐aminobutyric acid (GABAA) receptors (GABAARs). This chapter reviews mechanisms of altered GABAAR function during SE. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Plasticity of GABAA receptors relevant toneurosteroid actions
Authors: Mody Istvan 
Published: December 2010

SummaryIt is now widely accepted that phasic (synaptic) and tonic (extrasynaptic) γ‐aminobutyric acid (GABA)ergic influences on neuronal excitability are mediated by different receptors with different pharmacologic profiles. This article focuses on the plasticity of the neurosteroid‐sensitive δ subunit containing GABAA receptors(δ‐GABAARs) in animal models of temporal lobe epilepsies (TLEs) and its possible consequences for modulating the excitability of the dentate gyrus. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Regulation of GABAA receptor gene expression and epilepsy
Authors: Brooks‐Kayal Amy R. , Russek Shelley J. 
Published: December 2010

SummaryAlthough multiple genes drive epileptogenesis, uncovering the mechanisms controlling expression of GABAA receptors (GABAARs), the brain’s major inhibitory receptors, may have far‐reaching therapeutic implications. In this review, we describe how seizure‐induced changes in GABAARs result from brain‐derived neurotrophic factor (BDNF)‐induced changes in Janus kinase/Signal Transducer and Activators of Transcription (JAK/STAT), cAMP response element binding protein/inducible cAMP early repressor (CREB/ICER), and early growth factor (Egr3) signaling, and discuss implications for prevention and treatment. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Study of the genetically complex epilepsies
Authors: Ottman Ruth , Risch Neil 
Published: December 2010

SummaryIdentifying the genes that influence risk for genetically complex epilepsies is a major challenge for the next decade. This chapter reviews possible biologic mechanisms, methodologic approaches, and findings from recent studies aimed at gene identification in complex epilepsies, and approaches for clarifying phenotype definition for genetic research on the epilepsies. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Potassium channelopathies of epilepsy
Authors: Brenner Robert , Wilcox Karen S. 
Published: December 2010

SummaryThe potassium channel family represents a large group with diverse functional roles. Not surprisingly, the list of potassium channelopathies contributing to human epilepsy has greatly expanded. The focus of this chapter will be the causative role in epilepsy of mutations in potassium channels and associated regulatory proteins. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Nicotinic acetylcholine receptor mutations
Authors: Steinlein Ortrud K. , Kaneko Sunao , Hirose Shinichi 
Published: December 2010

SummaryAutosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is characterized by clusters of brief motor seizures. This rare syndrome is caused by mutations in at least two subunit genes of the neuronal nicotinic acetylcholine receptor (nAChR). Some of these mutations seem to increase the risk for additional neurologic symptoms. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Gene interactions and modifiers in epilepsy
Authors: Meisler Miriam H. 
Published: December 2010

SummaryThe onset, progression, and severity of epilepsy vary between family members with identical mutations in primary disease genes. The background of genetic variation unique to each individual genome contributes to clinical variation. Known examples of gene interactions in human families and mouse models provide insight into underlying molecular mechanisms. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press. (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Rare genetic causes of lissencephaly may implicate microtubule‐based transport in the pathogenesis of cortical dysplasias
Authors: Liu Judy S. , Walsh Christopher A. 
Published: December 2010

SummaryThe causative genes for lissencephaly—including LIS1, DCX, and TUBA1A—highlight the importance of a microtubule‐based transport pathway in cortical development and potentially in pathogenesis of focal cortical dysplasias. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
The generation of cortical interneurons
Authors: Rubenstein John L.R. 
Published: December 2010

SummaryThe developmental origins of cortical and hippocampal interneurons in the rodent are discussed, in addition to a description of the transcriptional mechanisms that control their specification and differentiation. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Genes in infantile epileptic encephalopathies
Authors: Depienne Christel , Gourfinkel‐An Isabelle , Baulac Stéphanie , LeGuern Eric 
Published: December 2010

SummaryPatients with infantile epileptic encephalopathies are often isolated cases with or without a limited familial history of epilepsy, suggesting a complex mode of inheritance. However, recent data, for example regarding Dravet syndrome, show that these sporadic rare diseases can result from a monogenic cause. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Haploinsufficiency of STXBP1 and Ohtahara syndrome
Authors: Saitsu Hirotomo , Kato Mitsuhiro , Matsumoto Naomichi 
Published: December 2010

SummaryOhtahara syndrome (OS) is one of the most severe and earliest forms of epilepsy. De novo heterozygous mutations and a microdeletion of STXBP1 have been found in individuals with OS. STXBP1 encodes MUNC18‐1, which is essential in synaptic vesicle release, highlighting aberration of synaptic vesicle release in pathogenesis of epilepsy. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press. (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
mTOR and epileptogenesis in developmental brain malformations
Authors: Wong Michael , Crino Peter B. 
Published: December 2010

SummaryTuberous sclerosis complex and related malformations of cortical development represent common developmental causes of intractable epilepsy. Abnormalities in the mammalian target of rapamycin pathway may be central to the pathophysiology of epilepsy and other neurologic deficits in these disorders and serve as a rational target for antiepileptogenic or disease‐modifying therapies. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
ELP4 in rolandic epilepsy and BRD2 in juvenile myoclonic epilepsy
Authors: Pal Deb K. , Strug Lisa J. , Veliskova Jana , Chachua Tamar , Velisek Libor , Greenberg David A. 
Published: December 2010

SummaryThe common forms of idiopathic epilepsies have complex genetic inheritance and are likely to include genes in biologic pathways other than “channelopathies,” the most frequent cause of their rare Mendelian counterparts. Recent analyses of ELP4 and BRD2 indicate that subtle genetically determined neurodevelopmental deviations may play a part in the pathogenesis of rolandic epilepsy and juvenile myoclonic epilepsy. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Epilepsy in autism spectrum disorders
Authors: Stafstrom Carl E. , Hagerman Paul J. , Pessah Isaac N. 
Published: December 2010

SummaryEpilepsy occurs frequently in individuals with autism spectrum disorders (ASDs). However, the mechanisms responsible for increased seizure susceptibility in ASDs are largely unknown. Clues to neural hyperexcitability in the autistic brain might be derived from disorders in which single gene mutations cause both epilepsy and an autistic phenotype, such as fragile X syndrome. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Calcium channel α2δ subunits in epilepsy and as targets for antiepileptic drugs
Authors: Dolphin Annette C. 
Published: December 2010

SummaryThe α2δ proteins are auxiliary subunits of voltage‐gated calcium channels, but may also have other functions. Four mammalian α2δ genes have been cloned. There are several links between α2δ proteins and disease, including mice with mutated α2δ‐2, which exhibit spike‐wave epilepsy. Furthermore, the gabapentinoid drugs bind to α2δ‐1 and α2δ‐2. For an expanded treatment of this topic see Jasper’s basic mechanisms of the epilepsies. 4th ed. (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Neurosteroids as endogenous regulators of seizure susceptibility and use in the treatment of epilepsy
Authors: Reddy Doodipala S. , Rogawski Michael A. 
Published: December 2010

SummaryNeurosteroids such as allopregnanolone are positive allosteric modulators of γ‐aminobutyric acid (GABA)A receptors with powerful antiseizure activity in diverse animal models. Neurosteroids may be endogenous regulators of seizure susceptibility, for example, in catamenial epilepsy. Clinical trials with the synthetic neurosteroid analog ganaxolone in the treatment of refractory partial seizures and infantile spasms have been encouraging. Neurosteroids and analogs such as ganaxolone show promise in the treatment of diverse forms of epilepsy. For an expanded treatment of this topic see Jasper’s basic mechanisms of the epilepsies. 4th ed. (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Animal models for evaluating antiepileptogenesis
Authors: White H. Steve 
Published: December 2010

SummaryThe development of any new therapy for the treatment of a human disorder or disease depends heavily on the demonstration of efficacy in a validated animal model. The need for finding a therapy that would prevent or delay the development of epilepsy in the susceptible individual is evident, and many of the required tools have been developed in recent years. However, there are many practical challenges and hurdles that must be overcome before a “cure” can be realized. For an expanded treatment of this topic see Jasper’s basic mechanisms of the epilepsies. 4th ed. (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
A treatment paradigm for neonatal seizures based on the ontogeny of neuronal chloride/cation cotransporter expression in the human cortex
Authors: Kahle Kristopher T. , Staley Kevin J. 
Published: December 2010

SummaryNeonatal seizures are a common problem inadequately treated with standard γ‐aminobutyric acid (GABA)ergic anticonvulsants. Understanding how the ontogeny of neuronal cation/chloride cotransporter expression renders GABAergic signaling excitatory in the neonatal brain has helped explain the increased seizure propensity and poor efficacy of GABAergic anticonvulsants in newborns, and is the rational underlying the polypharmaceutical approach to treating neonatal seizures with bumetanide and phenobarbital. For an expanded treatment of this topic see Jasper’s basic mechanisms of the epilepsies. 4th ed. (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Drug resistance in epilepsy
Authors: Gorter Jan , Potschka Heidrun 
Published: December 2010

SummaryDrug resistance remains one of the major challenges in epilepsy therapy. Identification of factors that contribute to therapeutic failure is crucial for future development of novel drugs and therapeutic strategies for difficult‐to treat epilepsies. For an expanded treatment of this topic see Jasper’s basic mechanisms of the epilepsies. 4th ed. (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Neural stem cell therapy for temporal lobe epilepsy
Authors: Shetty Ashok K. 
Published: December 2010

SummaryNeural stem cells (NSCs) are one of the candidates for grafting in the realm of cell‐based therapy for temporal lobe epilepsy (TLE). Because NSCs can produce neurons synthesizing the inhibitory neurotransmitter γ‐aminobutyric acid (GABA) and cells secreting multiple neurotrophic factors, NSC grafting therapy has promise for restraining seizures and easing cognitive dysfunction in TLE. For an expanded treatment of this topic see Jasper’s Basic Mechanisms of the Epilepsies, Fourth Edition (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Embryonic stem cell therapy for intractable epilepsy
Authors: Naegele Janice R. , Vemuri Mohan C. , Studer Lorenz 
Published: December 2010

SummaryStem cell therapies are envisioned for severe neurologic disorders and intractable epilepsy. Methods to maintain and derive neural cells from embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) are providing insights into human nervous system development from stem cells and the future of stem cell therapy for epilepsy. For an expanded treatment of this topic see Jasper’s basic mechanisms of the epilepsies. 4th ed. (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Restarting arrested neurodevelopment
Authors: Manent Jean‐Bernard , LoTurco Joseph J. 
Published: December 2010

SummaryMalformations of cortical development (MCDs) are common causes of seizures and developmental delay. Although considered to be irreversible, recent observations in animal models suggest that MCDs may remain responsive to corrective manipulations during prolonged time periods after malformations are formed. These findings may change our understanding of MCDs and open new therapeutic avenues. For an expanded treatment of this topic, see Jasper’s basic mechanisms of the epilepsies. 4th ed. (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).
Adenosine augmentation therapy for epilepsy
Authors: Boison Detlev 
Published: December 2010

SummaryDeficiency of the brain’s endogenous anticonvulsant adenosine is a pathologic hallmark of epilepsy. Consequently, focal adenosine augmentation therapies (AATs) constitute a rational approach for seizure suppression. Focal adenosine augmentation and resulting seizure suppression can be realized by implanting adenosine‐releasing stem cells or polymers into epileptogenic brain regions. For an expanded treatment of this topic see Jasper’s basic mechanisms of the epilepsies. 4th ed. (Noebels JL, Avoli M, Rogawski MA, Olsen RW, Delgado‐Escueta AV, eds) published by Oxford University Press (available on the National Library of Medicine Bookshelf [NCBI] at http://www.ncbi.nlm.nih.gov/books).