Poster board 511 - Sun 09/07, 12:15 - Hall Y
Session 024 - Epilepsy I
Abstract A024.33, published in FENS Forum Abstracts, vol. 3, 2006.
Ref.: FENS Abstr., vol.3, A024.33, 2006
|Author(s)||Tóth K. (1), Eross L. (1), Czirják S. (2), Vajda J. (2), Halász P. (2), Freund T. F. (3) & Maglóczky Z. (1)|
|(1) Inst. Exp. Med., Budapest, Hungary; (2) Nat. Inst. Neurosurgery, Budapest, Hungary; (3) Nat. Inst. Psych. and Neurol. Epilepsy Center, Budapest, Hungary|
|Title||Calretinin-immunoreactive interneurons degenerate in epileptic human hippocampi.|
|Text||Changes of the hippocampal GABAergic interneuronal circuits are known to play a central role in epileptogenesis. A subset of GABAergic inhibitory cells containing calretinin were shown to be vulnerable to ischaemic and epileptic injury both in animal models and humans. Therefore we aimed to reveal the fate of this cell type in human epileptic hippocampi. In the rat CA1 region, CR-containing cells are interneuron specific (IS) inhibitory cells, they selectively terminate on other interneurons mostly those that contain calbindin. In the human hippocampus, they are more heterogeneous participating in dendritic inhibition and the innervation of other interneurons. The IS cells containing CR are in an ideal position to synchronize the activity of dendritic inhibitory interneurons. Surgically removed hippocampi of drug-resistant temporal lobe epileptic patients were examined and compared with control samples with different post mortem delays. The samples were immunostained for CR and the changes in the distribution and density of CR-immunopositive cells were analysed. Post mortem delays longer than 6 hours of control samples resulted in a reduced number of immunolabeled cells. The number of CR-positive cells in the epileptic tissue is considerably decreased in parallel with the severity of principal cell loss in all regions. Preserved cells had segmented and shortened dendrites. This suggests that CR-containing interneurons are sensitive to epileptic activity, thus, inhibition and synchronization of dendritic inhibitory cells by interneuron-specific interneurons might be impaired in human epileptic hippocampi, which may lead to abnormal plasticity of excitatory inputs. Long post mortem delays of control samples can also cause significant loss of immunostaining, therefore examination of changes of the density of CR- immunopositive cells can be carried out only in carefully selected human samples with short post mortem delays and high quality fixation.
|Theme||Neurological and psychiatric conditions
Epilepsy / Human studies and animal models