FENS Forum 2006

FENS Forum 2006 - Vienna

For lectures, symposia and workshops, time indicates the beginning of the session.
For posters, authors are expected to be in attendance at their posters at the time indicated.

First author: Magloczky, Zsofia (poster)

Poster board 502 - Sun 09/07, 11:30 - Hall Y
Session 024 - Epilepsy I
Abstract A024.24, published in FENS Forum Abstracts, vol. 3, 2006.
Ref.: FENS Abstr., vol.3, A024.24, 2006

Author(s) Magloczky Z. (1), Wittner L. (1), Katarova Z. (1), Rasonyi G. (2), Eross L. (3), Czirjak S. (3), Szabo G. (1), Halasz P. (2), Payne J. A. (4) & Freund T. F. (1)

Addresse(s) (1) Inst. Experimental Medicine, Hungarian Acad. Sci., Budapest, Hungary; (2) Epilepsy National Institute of Psychiatry and Neurology, Budapest, Hungary; (3) 3National Institute of Neurosurgery, Budapest, Hungary; (4) 4Dept. Human Physiol, School of Medicine, Univ. California, Davis, USA

Title Enhancement of type 2 potassium-chloride cotransporter (KCC2) expression correlates with synaptic reorganization in epileptic human hippocampi.

Text Type 2 K-Cl cotransporter (KCC2), a neuronal membrane protein is involved in the regulation of cell volume and the setting of chloride gradient required for GABAergic inhibition. GABA was shown to depolarize some neurons in the surgically removed temporal lobes of epileptic (TLE) patients. To shed light on the underlying mechanism, we examined the expression of the K-Cl cotransporter (KCC2) in 3 pathological groups of TLE patients showing different degrees of cell loss and fiber reorganization. Hippocampi of 6 control subjects (post mortem 2-4 hours) and 36 patients were immersion-fixed for immunochemistry against vesicular glutamate transporter1 (vGlut1) and KCC2. Part of the hippocampal blocks were snapped- frozen, run on Western blots and stained for KCC2 for quantification. The number, distribution and synaptic
connections of KCC2- immunolabelled elements were analysed in the pathological groups and compared to vGlut1-immunoreactivity and Western-blot of the same subjects. Western blots revealed an increase in KCC2 protein in TLE patients, which correlated with the degree of cell loss and synaptic reorganization. In control subjects some principal cell dendrites and spines were faintly, certain interneuron dendrites were strongly KCC2-immunoreactive. In the epileptic hippocampi, additional elements displayed KCC2-immunopositivity: somata and spines of surviving principal cells, as well as numerous interneuron dendrites and somata. The increased staining of the surviving neurons showed a positive correlation with the degree of epileptic cell loss and reorganization. The enhancement of KCC2-expression may be due to sprouting and epileptic hyperactivity, since it may protect cells against excitotoxic damage (swelling) via increased efficacy of volume regulation. It may also contribute to GABA-mediated excitation, if the chloride (and potassium) transport is reversed by the high extracellular potassium concentration during seizures.

Theme Neurological and psychiatric conditions
Epilepsy / Human studies and animal models

Close window

Author(s)	Magloczky Z. (1), Wittner L. (1), Katarova Z. (1), Rasonyi G. (2), Eross L. (3), Czirjak S. (3), Szabo G. (1), Halasz P. (2), Payne J. A. (4) & Freund T. F. (1)
Addresse(s)	(1) Inst. Experimental Medicine, Hungarian Acad. Sci., Budapest, Hungary; (2) Epilepsy National Institute of Psychiatry and Neurology, Budapest, Hungary; (3) 3National Institute of Neurosurgery, Budapest, Hungary; (4) 4Dept. Human Physiol, School of Medicine, Univ. California, Davis, USA
Title	Enhancement of type 2 potassium-chloride cotransporter (KCC2) expression correlates with synaptic reorganization in epileptic human hippocampi.
Text	Type 2 K-Cl cotransporter (KCC2), a neuronal membrane protein is involved in the regulation of cell volume and the setting of chloride gradient required for GABAergic inhibition. GABA was shown to depolarize some neurons in the surgically removed temporal lobes of epileptic (TLE) patients. To shed light on the underlying mechanism, we examined the expression of the K-Cl cotransporter (KCC2) in 3 pathological groups of TLE patients showing different degrees of cell loss and fiber reorganization. Hippocampi of 6 control subjects (post mortem 2-4 hours) and 36 patients were immersion-fixed for immunochemistry against vesicular glutamate transporter1 (vGlut1) and KCC2. Part of the hippocampal blocks were snapped- frozen, run on Western blots and stained for KCC2 for quantification. The number, distribution and synaptic connections of KCC2- immunolabelled elements were analysed in the pathological groups and compared to vGlut1-immunoreactivity and Western-blot of the same subjects. Western blots revealed an increase in KCC2 protein in TLE patients, which correlated with the degree of cell loss and synaptic reorganization. In control subjects some principal cell dendrites and spines were faintly, certain interneuron dendrites were strongly KCC2-immunoreactive. In the epileptic hippocampi, additional elements displayed KCC2-immunopositivity: somata and spines of surviving principal cells, as well as numerous interneuron dendrites and somata. The increased staining of the surviving neurons showed a positive correlation with the degree of epileptic cell loss and reorganization. The enhancement of KCC2-expression may be due to sprouting and epileptic hyperactivity, since it may protect cells against excitotoxic damage (swelling) via increased efficacy of volume regulation. It may also contribute to GABA-mediated excitation, if the chloride (and potassium) transport is reversed by the high extracellular potassium concentration during seizures.
Theme	Neurological and psychiatric conditions Epilepsy / Human studies and animal models