TY - JOUR
T1 - Status epilepticus induces region-specific changes in dendritic spines, dendritic length and TrkB protein content of rat brain cortex
AU - Ampuero, Estíbaliz
AU - Dagnino-Subiabre, Alexies
AU - Sandoval, Rodrigo
AU - Zepeda-Carreño, Rodrigo
AU - Sandoval, Soledad
AU - Viedma, Alejandra
AU - Aboitiz, Francisco
AU - Orrego, Fernando
AU - Wyneken, Ursula
N1 - Funding Information:
We are grateful to Mauricio Sandoval for careful reading of this manuscript. This work was supported by Farmacias Cruz Verde, by Fondecyt 1020257 (to U.W.) and by Universidad de los Andes.
PY - 2007/8/31
Y1 - 2007/8/31
N2 - Induction of status epilepticus (SE) with kainic acid results in a large reorganization of neuronal brain circuits, a phenomenon that has been studied primarily in the hippocampus. The neurotrophin BDNF, by acting through its receptor TrkB, has been implicated in such reorganization. In the present work we investigated, by Western blot and immunohistochemistry, whether regional changes of TrkB expression within the rat brain cortex are correlated with altered neuronal morphology and/or with apoptotic cell death. We found that the full-length TrkB protein decreased within the cortex when measured 24 h to 1 week after induction of SE. Analysis by immunohistochemistry revealed that TrkB staining diminished within layer V of the retrosplenial granular b (RSGb) and motor cortices, but not within the auditory cortex. In layer II/III, differential changes were also observed: TrkB decreased in the motor cortex, did not change within the RSGb but increased within the auditory cortex. Reduced TrkB was associated with dendritic atrophy and decreased spine density in pyramidal neurons within layer V of the RSGb. No correlation was observed between regional and cellular changes of TrkB protein and apoptosis, measured by the TdT-mediated dUTP nick end labeling (TUNEL) method. The global decrease of TrkB within the neocortex and the associated dendritic atrophy may counteract seizure propagation in the epileptic brain but may also underlie cognitive impairment after seizures.
AB - Induction of status epilepticus (SE) with kainic acid results in a large reorganization of neuronal brain circuits, a phenomenon that has been studied primarily in the hippocampus. The neurotrophin BDNF, by acting through its receptor TrkB, has been implicated in such reorganization. In the present work we investigated, by Western blot and immunohistochemistry, whether regional changes of TrkB expression within the rat brain cortex are correlated with altered neuronal morphology and/or with apoptotic cell death. We found that the full-length TrkB protein decreased within the cortex when measured 24 h to 1 week after induction of SE. Analysis by immunohistochemistry revealed that TrkB staining diminished within layer V of the retrosplenial granular b (RSGb) and motor cortices, but not within the auditory cortex. In layer II/III, differential changes were also observed: TrkB decreased in the motor cortex, did not change within the RSGb but increased within the auditory cortex. Reduced TrkB was associated with dendritic atrophy and decreased spine density in pyramidal neurons within layer V of the RSGb. No correlation was observed between regional and cellular changes of TrkB protein and apoptosis, measured by the TdT-mediated dUTP nick end labeling (TUNEL) method. The global decrease of TrkB within the neocortex and the associated dendritic atrophy may counteract seizure propagation in the epileptic brain but may also underlie cognitive impairment after seizures.
KW - Apoptosis
KW - Dendritic morphology
KW - Neocortex
KW - Seizure
KW - TrkB
UR - http://www.scopus.com/inward/record.url?scp=34247850712&partnerID=8YFLogxK
U2 - 10.1016/j.brainres.2007.02.089
DO - 10.1016/j.brainres.2007.02.089
M3 - Article
C2 - 17397806
AN - SCOPUS:34247850712
SN - 0006-8993
VL - 1150
SP - 225
EP - 238
JO - Brain Research
JF - Brain Research
IS - 1
ER -