TY - JOUR
T1 - Neuroplasticity in the damaged dentate gyrus of the epileptic brain
AU - Ribak, Charles E.
AU - Dashtipour, Khashayar
N1 - Funding Information:
The authors gratefully acknowledge our collaborators on these studies Drs. Igor Spigelman, Xiao-Xin Yan, Andy Obenaus, Claude Wasterlain, J. Victor Nadler, Maxine Okazaki, Roy Bakay, Peter Weber, Laszlo Seress,C harles Epstein, Thomas Henry and Peter Tran. We also acknowledge Dr. Bao Xue, Angela X. Torres and Alan M. Wong for comments on the manuscript. This book chapter is dedicated to the victims of the New York City World Trade Center attack on September 11, 200 1. This work was supported by NM grant NS 38331 to C.E. Ribak.
PY - 2002
Y1 - 2002
N2 - Using Golgi preparations, Cajal described many cell types and connections of the dentate gyrus. He described granule cells as having a round or elliptical cell body with their long axis perpendicular to the granule cell layer, dendrites arising from one pole and an axon arising from the other. Cajal apparently never studied the brains from epileptic animals or humans, and thus did not report on changes in granule cell morphology after epilepsy. Several neuroplastic changes have been described in the dentate gyrus of epileptic mammals in the past decade or so using modern methods. Two changes involving their processes include mossy fiber sprouting of granule cell axons into the inner molecular layer of the dentate gyrus and the formation of hilar basal dendrites. Two changes associated with increased neurogenesis of granule cells in the epileptic brain include hilar ectopic granule cells and the dispersion of the granule cell layer. The significance of the first two changes is that granule cell axon collaterals establish additional synapses with apical and basal dendrites of granule cells, and these connections contribute to new recurrent excitatory circuitry. The significance of increased neurogenesis is that granule cells are migrating into inappropriate areas (deep hilus) or excessive numbers of granule cells accumulate in the layer (dispersion). These data on the epileptic dentate gyrus show that granule cells may change their axonal and dendritic arbors as well as their numbers and position to respond to altered activity possibly caused by decreased inhibition. These findings indicate that the dentate gyrus shows several neuroplastic changes following temporal lobe epilepsy.
AB - Using Golgi preparations, Cajal described many cell types and connections of the dentate gyrus. He described granule cells as having a round or elliptical cell body with their long axis perpendicular to the granule cell layer, dendrites arising from one pole and an axon arising from the other. Cajal apparently never studied the brains from epileptic animals or humans, and thus did not report on changes in granule cell morphology after epilepsy. Several neuroplastic changes have been described in the dentate gyrus of epileptic mammals in the past decade or so using modern methods. Two changes involving their processes include mossy fiber sprouting of granule cell axons into the inner molecular layer of the dentate gyrus and the formation of hilar basal dendrites. Two changes associated with increased neurogenesis of granule cells in the epileptic brain include hilar ectopic granule cells and the dispersion of the granule cell layer. The significance of the first two changes is that granule cell axon collaterals establish additional synapses with apical and basal dendrites of granule cells, and these connections contribute to new recurrent excitatory circuitry. The significance of increased neurogenesis is that granule cells are migrating into inappropriate areas (deep hilus) or excessive numbers of granule cells accumulate in the layer (dispersion). These data on the epileptic dentate gyrus show that granule cells may change their axonal and dendritic arbors as well as their numbers and position to respond to altered activity possibly caused by decreased inhibition. These findings indicate that the dentate gyrus shows several neuroplastic changes following temporal lobe epilepsy.
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U2 - 10.1016/S0079-6123(02)36027-8
DO - 10.1016/S0079-6123(02)36027-8
M3 - Article
C2 - 12143392
SN - 0079-6123
VL - 136
SP - 319
EP - 328
JO - Progress in Brain Research
JF - Progress in Brain Research
ER -