TY - JOUR
T1 - Modulation of dendritic spines in epilepsy
T2 - Cellular mechanisms and functional implications
AU - Wong, Michael
N1 - Funding Information:
The author thanks Dr. Steven Rothman for helpful comments on the article. This work was supported in part by NIH K02 NS045583.
PY - 2005/12
Y1 - 2005/12
N2 - Epilepsy patients often suffer from significant neurological deficits, including memory impairment, behavioral problems, and psychiatric disorders. While the causes of neuropsychological dysfunction in epilepsy are multifactorial, accumulating evidence indicates that seizures themselves may directly cause brain injury. Although seizures sometimes result in neuronal death, they may also cause more subtle pathological changes in neuronal structure and function, including abnormalities in synaptic transmission. Dendritic spines receive a majority of the excitatory synaptic inputs to cortical neurons and are critically involved in synaptic plasticity and learning. Studies of human epilepsy and experimental animal models demonstrate that seizures may directly affect the morphological and functional properties of dendritic spines, suggesting that seizure-related changes in spines may represent a mechanistic basis for cognitive deficits in epilepsy. Novel therapeutic strategies directed at modulation of spine motility may prevent the detrimental effects of seizures on cognitive function in epilepsy.
AB - Epilepsy patients often suffer from significant neurological deficits, including memory impairment, behavioral problems, and psychiatric disorders. While the causes of neuropsychological dysfunction in epilepsy are multifactorial, accumulating evidence indicates that seizures themselves may directly cause brain injury. Although seizures sometimes result in neuronal death, they may also cause more subtle pathological changes in neuronal structure and function, including abnormalities in synaptic transmission. Dendritic spines receive a majority of the excitatory synaptic inputs to cortical neurons and are critically involved in synaptic plasticity and learning. Studies of human epilepsy and experimental animal models demonstrate that seizures may directly affect the morphological and functional properties of dendritic spines, suggesting that seizure-related changes in spines may represent a mechanistic basis for cognitive deficits in epilepsy. Novel therapeutic strategies directed at modulation of spine motility may prevent the detrimental effects of seizures on cognitive function in epilepsy.
KW - Actin
KW - Dendritic spine
KW - Epilepsy
KW - Learning disability
KW - Long-term potentiation
KW - Mental retardation
KW - Seizure
KW - Synaptic transmission
UR - http://www.scopus.com/inward/record.url?scp=29544439385&partnerID=8YFLogxK
U2 - 10.1111/j.1467-9892.2005.00420.x
DO - 10.1111/j.1467-9892.2005.00420.x
M3 - Review article
C2 - 16246628
AN - SCOPUS:29544439385
SN - 1525-5050
VL - 7
SP - 569
EP - 577
JO - Epilepsy and Behavior
JF - Epilepsy and Behavior
IS - 4
ER -