Activity-evoked capacitative Ca2+ entry: implications in synaptic plasticity.
J Neurosci
; 23(21): 7737-41, 2003 Aug 27.
Article
en En
| MEDLINE
| ID: mdl-12944501
ABSTRACT
The Ca2+ influx controlled by intracellular Ca2+ stores, called store-operated Ca2+ entry (SOC), occurs in various eukaryotic cells, but whether CNS neurons are endowed with SOC capability and how they may operate have been contentious issues. Using Ca2+ imaging, we present evidence for the presence of SOC in cultured hippocampal pyramidal neurons. Depletion of internal Ca2+ stores by thapsigargin caused intracellular Ca2+ elevation, which was prevented by SOC channel inhibitors 2-aminoethoxydiphenyl borate (2-APB), SKF96365, and La3+. Interestingly, these inhibitors also accelerated the decay of NMDA-induced Ca2+ transients without affecting their peak amplitude. In addition, SOC channel inhibitors attenuated tetanus-induced dendritic Ca2+ accumulation and long-term potentiation at Schaffer collateral-CA1 synapses in hippocampal slice preparations. These data suggest a novel link between ionotropic receptor-activated SOC and neuroplasticity.
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Calcio
/
Células Piramidales
/
Potenciación a Largo Plazo
Límite:
Animals
Idioma:
En
Revista:
J Neurosci
Año:
2003
Tipo del documento:
Article
País de afiliación:
Japón