Figure 4.

AVP-elicited inward currents depend on PLCβ and depletion of PIP₂, but do not require the functions of intracellular Ca²⁺ release and PKC activity. A, Current trace recorded from a DG GC in response to bath application of AVP alone. B, Current trace recorded from a DG GC in response to bath application of AVP in a slice pretreated with the PLC inhibitor U73122 (5 μm). C, Current trace recorded from a DG GC before, during, and after bath application of AVP in the intracellular solution containing heparin (0.5 mg/ml). D, Current trace recorded from a DG GC in response to bath application of AVP in the intracellular solution supplemented with thapsigargin (10 μm). E, AVP-induced inward current recorded from a DG GC in a slice pretreated with Bis II (2 μm). The extracellular solution continuously contained the same concentration of Bis II. F, AVP-elicited inward current trace recorded from a DG GC in a slice pretreated with RHC 80267 (25 μm), a DAG lipase inhibitor. The extracellular solution contained the same concentration of RHC 80267. G, Current trace recorded from a DG GC dialyzed with the intracellular solution containing diC8-PIP₂ (50 μm). H, Summary graph. The shaded bar was the averaged inward currents evoked by AVP in control condition pooled from the control experiment conducted for each individual pharmacological experiment. **p = 0.002, ***p = 0.0002 versus AVP alone, one-way ANOVA followed by Dunnett’s test.