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Excitotoxicity neurotransmitter-mediated

The mechanisms of secondary injury include neurotransmitter-mediated excitotoxicity free-radical injury to cell membranes, electrolyte imbalances, mitochondrial dysfunction, inflammatory responses, apoptosis, secondary ischemia from vasospasm, focal microvascular occlusion, and vascular injury (Werner and Engelhard, 2007). These events can lead to cerebral edema and further increases in ICR The detailed molecular mechanisms of these events are described later in this chapter. [Pg.695]

Glutamate is the neurotransmitter which mediates excitatory neurotransmission as well as excitotoxicity. True or False. [Pg.613]


See other pages where Excitotoxicity neurotransmitter-mediated is mentioned: [Pg.323]    [Pg.20]    [Pg.464]    [Pg.20]    [Pg.563]    [Pg.88]    [Pg.386]    [Pg.174]    [Pg.262]    [Pg.3]    [Pg.338]    [Pg.409]    [Pg.127]    [Pg.20]    [Pg.464]    [Pg.515]    [Pg.157]    [Pg.157]    [Pg.152]    [Pg.23]    [Pg.273]    [Pg.454]    [Pg.519]    [Pg.544]    [Pg.21]    [Pg.385]    [Pg.152]    [Pg.334]    [Pg.425]    [Pg.368]    [Pg.609]   
See also in sourсe #XX -- [ Pg.695 ]




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