Table 4.
PAR1-dependent increases in calcium influx are diminished by glutamate receptor antagonists
| Condition | (ΔF/F)% | n |
|---|---|---|
| Neurons | ||
| Control | 14.1 ± 1.3 | 39 |
| dl-AP5 | 4.4 ± 0.8* | 27 |
| DNQX | 10.2 ± 0.9 | 45 |
| dl-AP3 | 11.4 ± 1.6 | 8 |
| Astrocytes | ||
| Control | 25.7 ± 1.5 | 121 |
| dl-AP5 | 9.8 ± 1.6** | 27 |
| DNQX | 17.5 ± 1.4** | 87 |
| dl-AP3 | 24.7 ± 2.7 | 40 |
Slices were pretreated with glutamate receptor antagonists dl-AP5, DNQX, or dl-AP3 before being stimulated with SFLLRN-NH2. Peak responses were determined for each cell type. The NMDAR antagonist dl-AP5 significantly inhibited both neuronal and glial responses to SFLLRN-NH2. However, the AMPAR antagonist DNQX significantly reduced glial but not neuronal responses to SFLLRN-NH2 and the broad spectrum metabotropic glutamate receptor antagonist dl-AP3 had no effect (one-way ANOVA with Tukey's post hoc test;
* p < 0.05 compared with the control neuronal response;
** p < 0.05 compared with the control glial response). These data suggest that glutamate gliotransmitter release after PAR1 stimulation activates NST-neuronal NMDA receptors as well as NST-astrocytic NMDA and AMPA receptors, which further enhances the astrocytic activation.