摘要
In the mammalian central nervous system（CNS）coupling of neurons by gap junctions and the expression of neuronal gap junction protein,connexin 36（Cx36）rapidly increases（usually during 1–2 hours）following a wide range of neuronal injuries,including ischemia,traumatic brain injury（TBI）,spinal cord injury and epilepsy（reviewed in Belousov and Fontes,2013）.Pharmacological blockade or genetic elimi-nation of Cx36-containing gap junctions dramatically re- duce neuronal death in animal models of ischemia, TBI and epilepsy and prevent NMDA receptor （NMDAR）-mediated excitotoxicity （Belousov and Fontes, 2014）.
In the mammalian central nervous system（CNS）coupling of neurons by gap junctions and the expression of neuronal gap junction protein,connexin 36（Cx36）rapidly increases（usually during 1–2 hours）following a wide range of neuronal injuries,including ischemia,traumatic brain injury（TBI）,spinal cord injury and epilepsy（reviewed in Belousov and Fontes,2013）.Pharmacological blockade or genetic elimi-nation of Cx36-containing gap junctions dramatically re- duce neuronal death in animal models of ischemia, TBI and epilepsy and prevent NMDA receptor （NMDAR）-mediated excitotoxicity （Belousov and Fontes, 2014）.
基金
supported by NIH (R21 NS076925)
the University of Kansas Medical Center funds to A.B.B
supported in part by NIH P20 GM104936, P30 AG035982 and UL1 TR000001
Core support was provided by NIH HD002528
