2012
DOI: 10.1523/jneurosci.1267-12.2012
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Anoxia-Induced NMDA Receptor Activation Opens Pannexin Channels via Src Family Kinases

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Cited by 198 publications
(268 citation statements)
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“…Taken together, it appears that P2X 7 possesses the ability to undergo pore dilation and thus, in the absence of Px1, allow for permeation of fluorescent dyes. Although P2X 7 receptors have the capability to function independently of Px1, our data by no means preclude that Px1 may be activated by other receptors, as has been demonstrated for ␣-adrenergic and NMDA receptors (78,79).…”
Section: Ref 30)mentioning
confidence: 47%
“…Taken together, it appears that P2X 7 possesses the ability to undergo pore dilation and thus, in the absence of Px1, allow for permeation of fluorescent dyes. Although P2X 7 receptors have the capability to function independently of Px1, our data by no means preclude that Px1 may be activated by other receptors, as has been demonstrated for ␣-adrenergic and NMDA receptors (78,79).…”
Section: Ref 30)mentioning
confidence: 47%
“…To date, only a few studies have investigated the role of pannexin channels in vascular functions, and it is now clear that they participate in the adrenergic signaling pathway in SMCs as well as in the thrombin signaling pathway in ECs Godecke et al, 2012). Lastly, although pannexins have not been identified in any clear microdomains and are not localized within caveoli, as demonstrated in a rat mammary tumor cell line (Gehi et al, 2011), they have been associated with a number of receptors that can initiate their opening, including the a1D-adrenergic receptor, the NMDA receptor, and PAR-1 Godecke et al, 2012;Weilinger et al, 2012). Ongoing and future studies of these channels could provide interesting clues into Panx1 integration in signaling microdomains in the blood vessel wall.…”
Section: A Gap Junction Channelsmentioning
confidence: 99%
“…Conditions of oxygen deprivation in neural tissue lead to anoxic depolarization (AD, also referred to as peri-infarct depolarization) of membrane potentials, which results from overstimulation of glutamate receptors and a large glutamate-mediated inward current, referred to as either the AD current or ischemiainduced anoxic current (3,4). However, the source and mechanism of production of excitotoxic glutamate, which mediates oxygen and glucose deprivation-induced (OGD-induced) neuronal damage, are not well defined.…”
mentioning
confidence: 99%