Seena Mathew - Published Work
MODULATION OF INHIBITORY SYNAPTIC TRANSMISSION IN THE NEOCORTEX OF GLUR6 KNOCK-OUT MICE
by S.Mathew; J.J.Hablitz
There is a high level of kainate receptor expression in the neocortex, yet the role of individual subunits has not been determined. In the present study we used GluR6 knockout mice to determine the role of this subunit in kainate modulation of IPSCs in layer II/III pyramidal cells. To test the effect of kainate on pharmacologically isolated evoked IPSCs, EPSCs were blocked with 20 uM D-APV and 50 uM GYKI53655. GABAB receptors were blocked with 2 uM SCH50911. Layer II-III pyramidal neurons from prefrontal cortex were studied under voltage clamp conditions. We observed kainate induced an increase in the frequency of spontaneous IPSCs in both wild-type (6.1 +/- 0.4 Hz control, 8.1 +/- 0.8 KA) and GluR6 -/- mice (5.2 +/- 0.6 Hz control; 7.8 +/- 0.8 Hz KA) without a change in amplitude (31.6 +/- 10 pA control, 33.4+/-15 KA). Application of 250 nM kainic acid also increased the amplitude of evoked IPSCs in layer II/III pyramidal cells in wild-type and GluR6-/- mice. (82.8 % increase in wild-type n=7; 132.1 % increase in GluR6 -/-, n=7). Application of 1 uM ATPA, a GluR5 subunit agonist, significantly increased the amplitude of evoked IPSCs in GluR6 -/- mice (374 %, n=7). In addition, spontaneous and miniature IPSC frequency was significantly increased by ATPA in GluR6 -/- mice compared to wildtype mice (150 % sIPSC, 188 % mIPSC). The results indicate kainate receptor facilitation is not mediated by the GluR6 subunit in layer II/III pyramidal cells of the prefrontal cortex.
Source: S. Mathew, J.J. Hablitz. MODULATION OF INHIBITORY SYNAPTIC TRANSMISSION IN THE NEOCORTEX OF GLUR6 KNOCK-OUT MICE Program No. 40.8. 2005 Washington, DC: Society for Neuroscience, 2005.
2005 Copyright by the Society for Neuroscience all rights reserved.