Figure 4.
Astrocytic and neuronal responses to SFLLRN-NH2 are modulated by glutamatergic pharmacological tools. Hindbrain slices containing the NST were pretreated with one of the following conditions for 10–15 min before stimulation with PAR1 agonist: control, dl-AP5, DNQX, or dl-AP3. The peak responses to SFLLRN-NH2 are represented as the (ΔF/F)%. The nonspecific NMDA receptor antagonist dl-AP5 significantly reduced both neuronal and glial responses to SFLLRN-NH2. Application of the AMPAR antagonist DNQX significantly reduced glial but not neuronal responses to the PAR1 agonist; 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.