Acquired Dendritic Channelopathy in Temporal Lobe Epilepsy Export

@article{citeulike:359688, abstract = {Inherited channelopathies are at the origin of many neurological disorders. Here we report a form of channelopathy that is acquired in experimental temporal lobe epilepsy (TLE), the most common form of epilepsy in adults. The excitability of CA1 pyramidal neuron dendrites was increased in TLE because of decreased availability of A-type potassium ion channels due to transcriptional (loss of channels) and posttranslational (increased channel phosphorylation by extracellular signal-regulated kinase) mechanisms. Kinase inhibition partly reversed dendritic excitability to control levels. Such acquired channelopathy is likely to amplify neuronal activity and may contribute to the initiation and/or propagation of seizures in TLE.}, author = {Bernard, Christophe and Anderson, Anne and Becker, Albert and Poolos, Nicholas P. and Beck, Heinz and Johnston, Daniel}, citeulike-article-id = {359688}, citeulike-linkout-0 = {http://dx.doi.org/10.1126/science.1097065}, citeulike-linkout-1 = {http://www.sciencemag.org/cgi/content/full/305/5683/532}, day = {23}, doi = {10.1126/science.1097065}, journal = {Science}, keywords = {acquired, channelopathy, dendritic, epilepsy, in, lobe, temporal}, month = {July}, number = {5683}, pages = {532--535}, posted-at = {2005-10-21 10:51:25}, priority = {3}, title = {Acquired Dendritic Channelopathy in Temporal Lobe Epilepsy}, url = {http://dx.doi.org/10.1126/science.1097065}, volume = {305}, year = {2004} }

TY - JOUR ID - citeulike:359688 L3 - citeulike-article-id:359688 N2 - Inherited channelopathies are at the origin of many neurological disorders. Here we report a form of channelopathy that is acquired in experimental temporal lobe epilepsy (TLE), the most common form of epilepsy in adults. The excitability of CA1 pyramidal neuron dendrites was increased in TLE because of decreased availability of A-type potassium ion channels due to transcriptional (loss of channels) and posttranslational (increased channel phosphorylation by extracellular signal-regulated kinase) mechanisms. Kinase inhibition partly reversed dendritic excitability to control levels. Such acquired channelopathy is likely to amplify neuronal activity and may contribute to the initiation and/or propagation of seizures in TLE. IS - 5683 JF - Science EP - 535 TI - Acquired Dendritic Channelopathy in Temporal Lobe Epilepsy VL - 305 SP - 532 KW - acquired KW - channelopathy KW - dendritic KW - epilepsy KW - in KW - lobe KW - temporal AU - Bernard, Christophe AU - Anderson, Anne AU - Becker, Albert AU - Poolos, Nicholas AU - Beck, Heinz AU - Johnston, Daniel PY - 2004/07/23/ UR - http://dx.doi.org/10.1126/science.1097065 ER -