Granule cell dispersion is not accompanied by enhanced neurogenesis in temporal lobe epilepsy patients.

Alexander Fahrner; Gunda Kann; Armin Flubacher; Christophe Heinrich; Thomas M Freiman; Josef Zentner; Michael Frotscher; Carola A Haas

Granule cell dispersion is not accompanied by enhanced neurogenesis in temporal lobe epilepsy patients.

Standard

Granule cell dispersion is not accompanied by enhanced neurogenesis in temporal lobe epilepsy patients. / Fahrner, Alexander; Kann, Gunda; Flubacher, Armin; Heinrich, Christophe; Freiman, Thomas M; Zentner, Josef; Frotscher, Michael; Haas, Carola A.

in: EXP NEUROL, Jahrgang 203, Nr. 2, 2, 2007, S. 320-332.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Fahrner, A, Kann, G, Flubacher, A, Heinrich, C, Freiman, TM, Zentner, J, Frotscher, M & Haas, CA 2007, 'Granule cell dispersion is not accompanied by enhanced neurogenesis in temporal lobe epilepsy patients.', EXP NEUROL, Jg. 203, Nr. 2, 2, S. 320-332. <http://www.ncbi.nlm.nih.gov/pubmed/17049346?dopt=Citation>

APA

Fahrner, A., Kann, G., Flubacher, A., Heinrich, C., Freiman, T. M., Zentner, J., Frotscher, M., & Haas, C. A. (2007). Granule cell dispersion is not accompanied by enhanced neurogenesis in temporal lobe epilepsy patients. EXP NEUROL, 203(2), 320-332. [2]. http://www.ncbi.nlm.nih.gov/pubmed/17049346?dopt=Citation

Vancouver

Fahrner A, Kann G, Flubacher A, Heinrich C, Freiman TM, Zentner J et al. Granule cell dispersion is not accompanied by enhanced neurogenesis in temporal lobe epilepsy patients. EXP NEUROL. 2007;203(2):320-332. 2.

Bibtex

@article{b9350c4a7dbc4f9291320f01e42a55cc,

title = "Granule cell dispersion is not accompanied by enhanced neurogenesis in temporal lobe epilepsy patients.",

abstract = "Granule cell dispersion (GCD) in the dentate gyrus is a frequent feature of Ammon's horn sclerosis (AHS) which is often associated with temporal lobe epilepsy (TLE). It has been hypothesized that GCD may be caused by an abnormal migration of newly born granule cells. To test this hypothesis, we used markers of proliferation and neurogenesis and immunocytochemical methods as well as quantitative Western blot and real-time RT-PCR analyses in surgically resected hippocampi from TLE patients and controls. Below the age of 1 year, Ki-67-immunopositive nuclei were detected in the subgranular zone of the dentate gyrus, but not in the dentate of TLE patients independent of age. The expression of the proliferation marker minichromosome maintenance protein 2 (mcm2) and of doublecortin (DCX) decreased significantly with age in controls and in TLE patients, but the expression of both proteins was independent of the degree of AHS and GCD. Quantitative real-time RT-PCR confirmed these findings at the level of gene expression. In contrast, immunocytochemistry for glial fibrillary acidic protein (GFAP) and vimentin as well as Golgi staining revealed a radially aligned glial network in the region of GCD. GFAP-positive fiber length significantly increased with the severity of GCD. These results indicate that epileptic activity does not stimulate neurogenesis in the human dentate gyrus and that GCD probably does not result from a malpositioning of newly generated granule cells, but rather from an abnormal migration of mature granule cells along a radial glial scaffold.",

keywords = "Adult, Humans, Male, Female, Middle Aged, Adolescent, Child, Immunohistochemistry, Infant, development, Reverse Transcriptase Polymerase Chain Reaction, Cell Nucleus metabolism, Neurons physiology, Glial Fibrillary Acidic Protein metabolism, Blotting, Western, Brain Neoplasms pathology, Cytoplasmic Granules pathology, Dentate Gyrus growth, Epilepsy, Temporal Lobe pathology, Glioblastoma pathology, Hippocampus growth, Ki-67 Antigen immunology, Microtubule-Associated Proteins biosynthesis, Mitosis physiology, Neuroglia physiology, Neuropeptides biosynthesis, Vimentin metabolism, Adult, Humans, Male, Female, Middle Aged, Adolescent, Child, Immunohistochemistry, Infant, development, Reverse Transcriptase Polymerase Chain Reaction, Cell Nucleus metabolism, Neurons physiology, Glial Fibrillary Acidic Protein metabolism, Blotting, Western, Brain Neoplasms pathology, Cytoplasmic Granules pathology, Dentate Gyrus growth, Epilepsy, Temporal Lobe pathology, Glioblastoma pathology, Hippocampus growth, Ki-67 Antigen immunology, Microtubule-Associated Proteins biosynthesis, Mitosis physiology, Neuroglia physiology, Neuropeptides biosynthesis, Vimentin metabolism",

author = "Alexander Fahrner and Gunda Kann and Armin Flubacher and Christophe Heinrich and Freiman, {Thomas M} and Josef Zentner and Michael Frotscher and Haas, {Carola A}",

year = "2007",

language = "Deutsch",

volume = "203",

pages = "320--332",

journal = "EXP NEUROL",

issn = "0014-4886",

publisher = "Academic Press Inc.",

number = "2",

}

RIS

TY - JOUR

T1 - Granule cell dispersion is not accompanied by enhanced neurogenesis in temporal lobe epilepsy patients.

AU - Fahrner, Alexander

AU - Kann, Gunda

AU - Flubacher, Armin

AU - Heinrich, Christophe

AU - Freiman, Thomas M

AU - Zentner, Josef

AU - Frotscher, Michael

AU - Haas, Carola A

PY - 2007

Y1 - 2007

N2 - Granule cell dispersion (GCD) in the dentate gyrus is a frequent feature of Ammon's horn sclerosis (AHS) which is often associated with temporal lobe epilepsy (TLE). It has been hypothesized that GCD may be caused by an abnormal migration of newly born granule cells. To test this hypothesis, we used markers of proliferation and neurogenesis and immunocytochemical methods as well as quantitative Western blot and real-time RT-PCR analyses in surgically resected hippocampi from TLE patients and controls. Below the age of 1 year, Ki-67-immunopositive nuclei were detected in the subgranular zone of the dentate gyrus, but not in the dentate of TLE patients independent of age. The expression of the proliferation marker minichromosome maintenance protein 2 (mcm2) and of doublecortin (DCX) decreased significantly with age in controls and in TLE patients, but the expression of both proteins was independent of the degree of AHS and GCD. Quantitative real-time RT-PCR confirmed these findings at the level of gene expression. In contrast, immunocytochemistry for glial fibrillary acidic protein (GFAP) and vimentin as well as Golgi staining revealed a radially aligned glial network in the region of GCD. GFAP-positive fiber length significantly increased with the severity of GCD. These results indicate that epileptic activity does not stimulate neurogenesis in the human dentate gyrus and that GCD probably does not result from a malpositioning of newly generated granule cells, but rather from an abnormal migration of mature granule cells along a radial glial scaffold.

AB - Granule cell dispersion (GCD) in the dentate gyrus is a frequent feature of Ammon's horn sclerosis (AHS) which is often associated with temporal lobe epilepsy (TLE). It has been hypothesized that GCD may be caused by an abnormal migration of newly born granule cells. To test this hypothesis, we used markers of proliferation and neurogenesis and immunocytochemical methods as well as quantitative Western blot and real-time RT-PCR analyses in surgically resected hippocampi from TLE patients and controls. Below the age of 1 year, Ki-67-immunopositive nuclei were detected in the subgranular zone of the dentate gyrus, but not in the dentate of TLE patients independent of age. The expression of the proliferation marker minichromosome maintenance protein 2 (mcm2) and of doublecortin (DCX) decreased significantly with age in controls and in TLE patients, but the expression of both proteins was independent of the degree of AHS and GCD. Quantitative real-time RT-PCR confirmed these findings at the level of gene expression. In contrast, immunocytochemistry for glial fibrillary acidic protein (GFAP) and vimentin as well as Golgi staining revealed a radially aligned glial network in the region of GCD. GFAP-positive fiber length significantly increased with the severity of GCD. These results indicate that epileptic activity does not stimulate neurogenesis in the human dentate gyrus and that GCD probably does not result from a malpositioning of newly generated granule cells, but rather from an abnormal migration of mature granule cells along a radial glial scaffold.

KW - Adult

KW - Humans

KW - Male

KW - Female

KW - Middle Aged

KW - Adolescent

KW - Child

KW - Immunohistochemistry

KW - Infant

KW - development

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Cell Nucleus metabolism

KW - Neurons physiology

KW - Glial Fibrillary Acidic Protein metabolism

KW - Blotting, Western

KW - Brain Neoplasms pathology

KW - Cytoplasmic Granules pathology

KW - Dentate Gyrus growth

KW - Epilepsy, Temporal Lobe pathology

KW - Glioblastoma pathology

KW - Hippocampus growth

KW - Ki-67 Antigen immunology

KW - Microtubule-Associated Proteins biosynthesis

KW - Mitosis physiology

KW - Neuroglia physiology

KW - Neuropeptides biosynthesis

KW - Vimentin metabolism