The effects of seizures on the connectivity and circuitry of the developing brain.
Recurring seizures in infants and children are often associated with cognitive deficits, but the reason for the learning difficulties is unclear. Recent studies in several animal models suggest that seizures themselves may contribute in important ways to these deficits. Other studies in animals have shown that recurring seizures result in dendritic spine loss. This change, coupled with a down-regulation in NMDA receptor subunit expression, suggests that repetitive seizures may interrupt the normal development of glutamatergic synaptic transmission. We hypothesize that homeostatic, neuroprotective processes are induced by recurring early-life seizures. These processes, by diminishing glutamatergic synaptic transmission, are aimed at preventing the continuation of seizures. However, by preventing the normal development of glutamatergic synapses, and particularly NMDA receptor-mediated synaptic transmission, such homeostatic processes also reduce synaptic plasticity and diminish the ability of neuronal circuits to learn and store memories.
Swann
John W
JW
The Cain Foundation Laboratories, Department of Pediatrics, Division of Neuroscience, Baylor College of Medicine, Houston, Texas 77030, USA. jswann@bcm.tmc.edu
D001921:Brain / Q000254:growth & development* / Q000503:physiopathology*; D002648:Child; D002658:Developmental Disabilities / Q000503:physiopathology; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D016202:N-Methylaspartate / Q000378:metabolism; D009415:Nerve Net / Q000503:physiopathology*; D009473:Neuronal Plasticity / Q000502:physiology; D012640:Seizures / Q000503:physiopathology*; D013569:Synapses / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology
D018698:Glutamic Acid; D016202:N-Methylaspartate