Skip to main content
. Author manuscript; available in PMC: 2013 Jun 1.
Published in final edited form as: Hippocampus. 2011 Nov 10;22(6):1438–1450. doi: 10.1002/hipo.20984

Fig. 4.

Fig. 4

CCK-mediated augmentation of NMDA currents requires the functions of PLC, intracellular Ca2+ and PKC. A, Pretreatment of cells with and continuous bath application of U73122 blocked CCK-induced increases in NMDA currents (n=7) whereas application of U73343 (the inactive analog, n=6) in the same fashion had no effects on NMDA currents. B, Application of CCK did not increase NMDA currents in granule cells (n=11 cells) isolated from PLCβ1(-/-) mice but still enhanced NMDA currents in granule cells (n=9 cells) isolated from WT mice. C, Inclusion of BAPTA (10 mM) in the recording pipettes blocked CCK-mediated enhancement of NMDA currents (n=6 cells). D, Pretreatment of cells with and inclusion of GF109203X (0.5 μM) in the recording pipettes blocked CCK-induced increases in NMDA currents (n=7 cells). E, Application of CCK induced a significantly smaller scale of increase in NMDA currents in dentate granule cells (n=12 cells) isolated from PKCγ KO mice compared with CCK-induced facilitation of NMDA currents (n=11 cells) in granule cells from WT mice.