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Neuronal gap junctions play a role in the secondary neuronal death following controlled cortical impact
In the mammalian CNS, excessive release of glutamate and overactivation of glutamate receptors are responsible for the secondary (delayed) neuronal death following neuronal injury, including ischemia, traumatic brain injury (TBI) and epilepsy. Recent studies in mice showed a critical role for neuron...
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| Main Authors: | , , , , , |
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| Format: | Artigo |
| Sprog: | Inglês |
| Udgivet: |
2012
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| Fag: | |
| Online adgang: | https://ncbi.nlm.nih.gov/pmc/articles/PMC3414632/ https://ncbi.nlm.nih.gov/pubmed/22781494 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.neulet.2012.06.065 |
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