Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Expression of synaptopodin, an actin-associated protein, in the rat hippocampus after limbic epilepsy
Autore:
Roth, SU; Sommer, C; Mundel, P; Kiessling, M;
Indirizzi:
Univ Heidelberg, Inst Pathol, Abt Neuropathol, Dept Neuropathol, D-69120 Heidelberg, Germany Univ Heidelberg Heidelberg Germany D-69120 , D-69120 Heidelberg, Germany Albert Einstein Coll Med, Dept Med, Div Nephrol, Bronx, NY 10461 USA Albert Einstein Coll Med Bronx NY USA 10461 Nephrol, Bronx, NY 10461 USA
Titolo Testata:
BRAIN PATHOLOGY
fascicolo: 2, volume: 11, anno: 2001,
pagine: 169 - 181
SICI:
1015-6305(200104)11:2<169:EOSAAP>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
TEMPORAL-LOBE EPILEPSY; ACID-INDUCED SEIZURES; KAINIC ACID; DENTATE GYRUS; DENDRITIC SPINES; BINDING-SITES; MOSSY FIBERS; IN-VIVO; SYNAPTIC REORGANIZATION; NONPYRAMIDAL CELLS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
70
Recensione:
Indirizzi per estratti:
Indirizzo: Roth, SU Univ Heidelberg, Inst Pathol, Abt Neuropathol, Dept Neuropathol, Neuenheimer Feld 220, D-69120 Heidelberg, Germany Univ Heidelberg Neuenheimer Feld 220 Heidelberg Germany D-69120
Citazione:
S.U. Roth et al., "Expression of synaptopodin, an actin-associated protein, in the rat hippocampus after limbic epilepsy", BRAIN PATH, 11(2), 2001, pp. 169-181

Abstract

Synaptopodin, a 100 kD protein, associated with the actin cytoskeleton of the postsynaptic density and dendritic spines, is thought to play a role inmodulating actin-based shape and motility of dendritic spines during formation or elimination of synaptic contacts. Temporal lobe epilepsy in humans and in rats shows neuronal damage, aberrant sprouting of hippocampal mossy fibers and subsequent synaptic remodeling processes. Using kainic acid (KA)induced epilepsy in rats, the postictal hippocampal expression of synaptopodin was analyzed by in situ hybridization (ISH) and immunohistochemistry. Sprouting of mossy fibers was visualized by a modified Timm's staining. ISHshowed elevated levels of Synaptopodin mRNA in perikarya of CA3 principal neurons, dentate granule cells and in surviving hilar neurons these levels persisted up to 8 weeks after seizure induction. Synaptopodin immunoreactivity in the dendritic layers of CA3, in the hilus and in the inner molecularlayer of the dentate gyrus (DG) was initially reduced. Eight weeks after KA treatment Synaptopodin protein expression returned to control levels in dendritic layers of CA3 and in the entire molecular layer of the DG, The recovery of protein expression was accompanied by simultaneous supra- and infragranular mossy fiber sprouting. Postictal upregulation of Synaptopodin mRNA levels in target cell populations of limbic epilepsy-elicited damage and subsequent Synaptopodin protein expression largely co-localized with remodeling processes as demonstrated by mossy fiber sprouting. It may thus represent a novel postsynaptic molecular correlate of hippocampal neuroplasticity.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/07/20 alle ore 12:14:53