了解早期癫痫对认知的影响-猫眼课题宝

了解早期癫痫对认知的影响

批准号：

7681264

负责人：

Frances E Jensen

金额：

$84.5万

依托单位：

BOSTON CHILDREN'S HOSPITAL

依托单位国家：

美国

项目类别：

财政年份：

2007

资助国家：

美国

项目状态：

已结题

起止时间：

2007-09-30 至 2012-07-31

来源：

https://reporter.nih.gov/project-details/7681264

关键词：

A Mouse AMPA Receptors Academy Acute Address Adult Affect Age American Amygdaloid structure Animal Model Animals Anoxic Encephalopathy Antiepileptic Agents Antiepileptogenic Anxiety Asphyxia Attenuated Autistic Disorder Autopsy Award Behavior Behavior Disorders Behavioral Biological Assay Biopsy Boston Brain Brain Injuries Bumetanide Calcineurin Calcium Cells Cerebrum Child Chloride Ion Chlorides Chronic Clinical Clinical Treatment Clinical Trials Cognition Cognition Disorders Cognitive Cognitive deficits Communities Comorbidity Cortical Dysplasia Data Development Disease Down-Regulation Education Elderly Electroencephalography Electrophysiology (science)Emotional Emotional disorder Encephalopathies Epidemiology Epilepsy Epileptogenesis Event Excision Excitatory Amino Acid Antagonists Exhibits Experimental Animal Model FDA approved Faculty Fellowship Female Functional disorder Funding GABA Receptor Gene Abnormality Gene Proteins Genes Genetic Genetic Transcription Genets Glutamate Receptor Glutamates Growth Hereditary Disease Hippocampus (Brain)Hour Human Hypoxia Impaired cognition In Vitro Incidence Individual Infant Injury Interruption Intervention Investigation Isoxazoles Kainic Acid Receptors Knockout Mice Laboratories Lead Leadership Learning Learning Disabilities Learning Disorders Life Link Long-Term Potentiation Love Maintenance Mediating Medical Memory Mental Retardation Mental disorders Mentors Methods Methyl-CpG-Binding Protein 2 Minnesota Modeling Modification Molecular Mood Disorders Motor Mus Mutation N-Methyl-D-Aspartate Receptors N-Methylaspartate Nature Neocortex Neonatal Neurobiology Neurologic Neurologic Deficit Neurology Neuronal Injury Neurons Neurosciences Neurotransmitter Receptor Neurotransmitters Newborn Infant Operative Surgical Procedures Pathway interactions Patients Pattern Pediatric Hospitals Pediatrics Perinatal Perinatal Hypoxia Phenobarbital Phenotype Phenytoin Philadelphia Phosphoric Monoester Hydrolases Phosphorylation Phosphorylation Site Phosphotransferases Physicians Physiological Pilot Projects Population Positioning Attribute Postdoctoral Fellow Predisposition Preparation Prevention Process Propionic Acids Prosencephalon Prospective Studies Protein Analysis Protein Dephosphorylation Proteins Protocols documentation Psychiatry Qualifying Rattus Recording of previous events Recruitment Activity Refractory Regulation Reporting Repressor Proteins Research Research Design Research Ethics Committees Resistance Resources Rett Syndrome Risk Rodent Rodent Model Rolandic Epilepsy Role Schizophrenia Scientist Seizures Sensory Signal Pathway Signal Transduction Signaling Protein Sirolimus Slice Societies Stimulus Stroke Structure Synapses Synaptic Receptors Synaptic Transmission Synaptic plasticity Syndrome Systems Biology TSC1 gene Talampanel Techniques Term Birth Testing Therapeutic Therapeutic Clinical Trial Therapy Clinical Trials Time Tissue Banking Tissue Banks Tissue Sample Tissues Transcription Repressor/Corepressor Translating Translational Research Translations Tuberous Sclerosis United States National Institutes of Health Up-Regulation Vertebral column Visual Western Blotting Work abstracting age related autism spectrum disorder base behavioral impairment brain tissue career clinical practice clinically relevant college depression design effective therapy extracellular frontier gain of function mutation hippocampal pyramidal neuron human FRAP1 protein human tissue hypoxia neonatorum immunocytochemistry in vivo infancy inhibitor/antagonist innovation interest loss of function mTOR protein meetings mouse model myelination neonatal human neonate nervous system disorder neurobehavior neuron loss neuronal excitability neuropathology neurophysiology new therapeutic target novel overexpression postnatal postsynaptic prevent programs protein expression pup rat methyl CpG binding protein 2 receptor receptor expression relating to nervous system research study symposium synaptic function synaptogenesis therapeutic target tool topiramate trafficking translational study treatment strategy trend white matter

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Epilepsy is a disorder that involves far more than the occurrence of seizures, and seizures can cause neuronal network disturbances that result in a wide range of cognitive and behavioral impairment. To date, most work in the epilepsy field has centered on the mechanism or prevention of the ictal events themselves. The focus of my laboratory has been on the impact of early life seizures on brain development and epileptogenesis. The present proposal extends our work to determine whether these mechanisms also induce alterations that could lead to cognitive dysfunction manifesting in early life, such as autism. There is clinical evidence that early life seizures may be one of many precedents for autism, and epilepsy is common in patients with autism, suggesting an interaction between the two processes. Our prior and recent work suggests that at least in the immature brain, where baseline synaptic plasticity is enhanced, seizures appear to directly activate specific plasticity-associated signaling pathways. We hypothesize that seizure induced dysplasticity may occlude normal plasticity involved in cognition, and induce abnormal patterns of synapse development similar to those observed in autism and other forms of neurodevelopmental delay. Using electrophysiological techniques, we will first examine the time course of seizure-induced interruption of normal synaptic plasticity in the immature brain. We will then determine whether specific activity-dependent signaling abnormalities known to be associated with autism occur de novo following seizures in the immature brain. Next, we will identify seizure induced mechanisms for their activation and test whether post-seizure intervention attenuates the altered structure and function of neuronal networks. Finally, we will determine whether similar alterations in signaling, regulatory, and synaptic proteins also are observed in human tissue following seizures and in cases of autism associated with neonatal or infantile seizures.

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