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Effects of Glutamate on Glycerophospholipid Degradation

5 Excitatory Amino Acid Receptors and Neural Membrane [Pg.80]

6-cyano-7-nitroquinoxaline (CNQX) block this release in a dose-dependent manner (Table 5.2). As pH shifts from 7.2 to 7.8, the glutamate-mediated release of arachi-donic acid is enhanced 3-fold (Stella et al., 1995). Quinacrine, a CPLA2 non-specific inhibitor (Sanfeliu et al., 1990 Kim et al., 1995 Farooqui et al., 2003b), as well as arachidonoyl trifluoromethylketone, a potent inhibitor of CPLA2, also inhibit this increase in CPLA2 activity mediated by glutamate (Table 5.3). [Pg.80]

Systemic administration of KA into adult rats markedly increases CPLA2 immunoreactivity in neurons at 1 and 3 days after injection (Sandhya et al., 1998). KA injection increases the CPLA2 immunoreactivity in astrocytes after 1, 2, 4, 11 weeks. Increased CPLA2 activity in neurons in KA-mediated toxicity may be involved in neurodegeneration, whereas the elevation of CPLA2 immunoreactivity in astrocytes is associated with gliosis (Sandhya et al., 1998 Farooqui et al., 1997c) [Pg.80]

CPLA2 activity was determined by procedure described earlier. Results are the means SEM for three different cultures. APV, 2-amino-5- phosphonovalerate and CNQX, 6-cyano-7-nitroquinox aline. [Pg.80]


See other pages where Effects of Glutamate on Glycerophospholipid Degradation is mentioned: [Pg.78]    [Pg.79]    [Pg.81]    [Pg.83]    [Pg.85]    [Pg.87]    [Pg.78]    [Pg.79]    [Pg.81]    [Pg.83]    [Pg.85]    [Pg.87]    [Pg.75]   


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