UNIVERSI
TÄ
TS-
BIBLIOTHEK
P
ADERBORN
Anmelden
Menü
Menü
Start
Hilfe
Blog
Weitere Dienste
Neuerwerbungslisten
Fachsystematik Bücher
Erwerbungsvorschlag
Bestellung aus dem Magazin
Fernleihe
Einstellungen
Sprache
Deutsch
Deutsch
Englisch
Farbschema
Hell
Dunkel
Automatisch
Sie befinden Sich nicht im Netzwerk der Universität Paderborn. Der Zugriff auf elektronische Ressourcen ist
gegebenenfalls
nur via VPN oder Shibboleth (DFN-AAI) möglich.
mehr Informationen...
Universitätsbibliothek
Katalog
Suche
Details
Zur Ergebnisliste
Ergebnis 7 von 21
Datensatz exportieren als...
BibTeX
Kainate-induced toxicity in the hippocampus: potential role of lithium
Bipolar disorders, 2010-06, Vol.12 (4), p.425-436
Crespo-Biel, Natalia
Camins, Antoni
Canudas, Anna M
Pallàs, Mercè
2010
Details
Autor(en) / Beteiligte
Crespo-Biel, Natalia
Camins, Antoni
Canudas, Anna M
Pallàs, Mercè
Titel
Kainate-induced toxicity in the hippocampus: potential role of lithium
Ist Teil von
Bipolar disorders, 2010-06, Vol.12 (4), p.425-436
Ort / Verlag
Oxford, UK: Blackwell Publishing Ltd
Erscheinungsjahr
2010
Link zum Volltext
Quelle
MEDLINE
Beschreibungen/Notizen
Crespo‐Biel N, Camins A, Canudas AM, Pallàs M. Kainate‐induced toxicity in the hippocampus: potential role of lithium. Bipolar Disord 2010: 12: 425–436. © 2010 The Authors. Journal compilation © 2010 John Wiley & Sons A/S. Objectives: We investigated the neuroprotective effects of lithium in an experimental neurodegeneration model gated to kainate (KA) receptor activation. Methods: The hippocampus from KA‐treated mice and hippocampal cell cultures were used to evaluate the pathways regulated by chronic lithium pretreatment in both in vivo and in vitro models. Results: Treatment with KA, as measured by fragmentation of α‐spectrin and biochemically, induced the activation of calpain resulting in p35 cleavage to p25, indicating activation of cyclin‐dependent kinase 5 (cdk5) and glycogen synthase kinase‐3ß (GSK‐3ß) and an increase in tau protein phosphorylation. Treatment with lithium reduced calpain activation and reduced the effects of cdk5 and GSK‐3ß on tau. KA treatment of cultures resulted in neuronal demise. According to nuclear condensed cell counts, the addition of lithium to neuronal cell cultures (0.5–1 mM) a few days before KA treatment had neuroprotective and also antiapoptotic effects. The action of lithium on calpain/cdk5 and GSK‐3ß pathways produced similar results in vivo. As calpain is activated by an increase in intracellular calcium, we showed that lithium reduced calcium concentrations in basal and KA‐treated hippocampal cells, which was accompanied by an increase in NCX3, a Na+/Ca2+ exchanger pump. Conclusion: A robust neuroprotective effect of lithium in the excitotoxic process induced by KA in mouse hippocampus was demonstrated via modulation of calcium entry and the subsequent inhibition of the calpain pathway. These mechanisms may act in an additive way with other mechanisms previously described for lithium, suggesting that it may be useful as a possible therapeutic strategy for Alzheimer’s disease.
Sprache
Englisch
Identifikatoren
ISSN: 1398-5647
eISSN: 1399-5618
DOI: 10.1111/j.1399-5618.2010.00825.x
Titel-ID: cdi_proquest_miscellaneous_745937670
Format
–
Schlagworte
Animals
,
calcium
,
Calcium - metabolism
,
calpain
,
Calpain - metabolism
,
cdk5
,
Cell Survival - drug effects
,
Cells, Cultured
,
Cyclin-Dependent Kinase 5 - metabolism
,
Disease Models, Animal
,
excitotoxicity
,
Glycogen Synthase Kinases - metabolism
,
GSK-3
,
Hippocampus - metabolism
,
Hippocampus - pathology
,
Kainic Acid - toxicity
,
Lithium Chloride - pharmacology
,
Male
,
Mice
,
Mice, Inbred Strains
,
Neurodegenerative Diseases - chemically induced
,
Neurodegenerative Diseases - drug therapy
,
Neuroprotective Agents - pharmacology
,
p25
,
p35
,
Phosphorylation
,
tau Proteins - metabolism
Weiterführende Literatur
Empfehlungen zum selben Thema automatisch vorgeschlagen von
bX