Figure 10.

Coexistence of KAR-mediated ionotropic and metabotropic pathways. A, Traces showing mIPSC activity before and during bath application of UBP302 in untreated slices from unstimulated rats, either in the presence of both U73122 and PhTx or only U73122. B, Summary histogram illustrating the percentage of change in mIPSC frequency induced by UBP302 in the presence of both U73122 and PhTx (gray bars; n = 6) or only U73122 (black bars; n = 10). For comparison purpose, the action of UBP302 under control conditions is illustrated (dotted bars). Inhibiting the PLC pathway in control conditions did not affect GluK1-mediated facilitatory effect. C, Traces showing mIPSC activity before and during bath application of UBP302 in TBOA-treated slices from unstimulated rats either in the presence of both PhTx and U73122 or only PhTx. D, Summary histogram illustrating in TBOA-treated slices the percentage of change in mIPSC frequency induced by UBP302 in the presence of both PhTx and U73122 (gray bars; n = 6) or only PhTx (black bars; n = 5). For comparison purpose, the effect of UBP302 under control conditions is illustrated (dotted bars, from Fig. 6A). Inhibiting Ca²⁺ entry through GluK1 in high extracellular glutamate levels, did not affect KAR-mediated inhibitory effect. Blocking the ionotropic and the metabotropic pathways in untreated and TBOA-treated slices completely inhibited GluK1 effect on GABA release, suggesting that these two modes of action coexist on the same GABAergic terminals. *p < 0.05.