Figure 3.

NT increases AP firing frequency via the activation of NTS1 receptors. (A₁,A₂) Application of the NTS1 antagonist, SR48692 (1 µm), almost completely blocked NT-induced facilitation of AP firing frequency. (A₁) APs recorded before, during, and after the application of NT in the presence of SR48692. (A₂) Pooled time course of the AP firing frequency in response to NT in the presence of SR48692. Data were shown in the same fashion thereafter. (B₁,B₂) Bath application of the NTS1 agonist, PD149163 (0.5 µm), significantly increased AP firing frequency. (C₁,C₂) Pretreatment of slices with and continuous bath application of the NTS2 antagonist, levocabastine (30 µm), did not alter significantly NT-induced transient enhancement of AP firing frequency. (D₁,D₂) Bath application of NT to slices cut from NTS1 KO mice failed to augment AP firing frequency. (E₁,E₂) Bath application of NT to slices cut from NTS2 KO mice still augmented AP firing frequency. (F) The dentate gyrus expressed NTS1 receptors. Upper left: immunostaining for NTS1 in the dentate gyrus GCs of rats; upper middle: immunostaining for the specific neuronal marker, NeuN, in rats; upper right: merged micrograph to show the expression of NTS1 in the dentate gyrus GCs of rats; lower left: no immunoreactivity was detected in the dentate gyrus of rats when NTS1 antibody was pre-adsorbed with the specific blocking peptide. Lower middle: immunostaining for NTS1 in the dentate gyrus GCs of WT mice. Lower right: no immunoreactivity was detected in the dentate gyrus GCs of NTS1 KO mice. Scale bar: 50 µm.