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Simulated ischaemia induces Ca(2+)-independent glutamatergic vesicle release through actin filament depolymerization in area CA1 of the hippocampus
Transient, non-catastrophic brain ischaemia can induce either a protected state against subsequent episodes of ischaemia (ischaemic preconditioning) or delayed, selective neuronal death. Altered glutamatergic signalling and altered Ca(2+) homeostasis have been implicated in both processes. Here we u...
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| Main Authors: | , |
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| Formáid: | Artigo |
| Teanga: | Inglês |
| Foilsithe: |
Blackwell Science Inc
2010
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| Ábhair: | |
| Rochtain Ar Líne: | https://ncbi.nlm.nih.gov/pmc/articles/PMC2876805/ https://ncbi.nlm.nih.gov/pubmed/20211977 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1113/jphysiol.2010.187609 |
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