Role of neuronal gap junctions in NMDA receptor-mediated excitotoxicity and ischemic neuronal death
نویسندگان
چکیده
منابع مشابه
Neuronal gap junctions are required for NMDA receptor-mediated excitotoxicity: implications in ischemic stroke.
N-methyl-D-aspartate receptors (NMDARs) play an important role in cell survival versus cell death decisions during neuronal development, ischemia, trauma, and epilepsy. Coupling of neurons by electrical synapses (gap junctions) is high or increases in neuronal networks during all these conditions. In the developing CNS, neuronal gap junctions are critical for two different types of NMDAR-depend...
متن کاملNeuronal Gap Junctions Are Required for NMDA Receptor - Mediated 1
19 20 21 2 ABSTRACT 22 23 NMDA receptors (NMDAR) play an important role in cell survival versus cell 24 death decisions during neuronal development, ischemia, trauma and epilepsy. 25 Coupling of neurons by electrical synapses (gap junctions) is high or increases in 26 neuronal networks during all these conditions. In the developing CNS, neuronal gap 27 junctions are critical for two different t...
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BACKGROUND AND PURPOSE Activation of NMDA subtypes of glutamate receptors is implicated in cell damage induced by ischemia as well as for the establishment of ischemic tolerance after ischemic preconditioning in animal models. We investigated the contributions of NR2A- and NR2B-containing NMDA receptors to ischemic cell death and ischemic tolerance in a rat model of transient global ischemia. ...
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Epilepsy is a recurrent, often progressive neurological disorder with a chronic evolution, affecting 1 to 2 % of the world population. Research with experimental models and imaging analysis of diseased patients have been used to show that recurrent episodes produce oxidative stress, most of which is related to neuronal excitability phenomena. It is known that the excessive stimulation of glutam...
متن کاملDeath of Neurons following Injury Requires Conductive Neuronal Gap Junction Channels but Not a Specific Connexin
Pharmacological blockade or genetic knockout of neuronal connexin 36 (Cx36)-containing gap junctions reduces neuronal death caused by ischemia, traumatic brain injury and NMDA receptor (NMDAR)-mediated excitotoxicity. However, whether Cx36 gap junctions contribute to neuronal death via channel-dependent or channel-independent mechanism remains an open question. To address this, we manipulated c...
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ژورنال
عنوان ژورنال: Neural Regeneration Research
سال: 2016
ISSN: 1673-5374
DOI: 10.4103/1673-5374.169630