FIG. 4.

Outward current induced by CAR was caused by the activation of M2 receptors mainly via opening the inwardly rectifying potassium channels in the Pf. A: outward current induced by CAR in the presence of TTX (recording I) was blocked by pretreatment with methoctramine (MTO) (recording II) in this Pf neuron. B: input resistance (R_in) change during recordings in A. CAR decreased the R_in from ∼700 to ∼300 MΩ in the presence of TTX, which recovered to ∼600 MΩ after wash with artificial cerebrospinal fluid (ACSF) (recording I). In the presence of MTO, CAR failed to decrease R_in (recording II). C: I-V relationship obtained in recordings (A). Subtraction of current ramp at the peak CAR effect (b) from that in control condition (a) showed that the CAR-induced outward current reversed at approximately −72 mV (b − a); however, in the presence of MTO, subtraction of control from CAR (d − c) showed no deviation from the voltage axis at 0 pA, suggesting that no current was activated. D: the CAR-induced outward current in the presence of TTX (recording I) was significantly reduced by Ba²⁺ (recording II). E: R_in change during recordings in D. Note that Ba²⁺ slightly increased R_in and significantly reduced the R_in decrease induced by CAR. F: subtractions of current ramps in different conditions indicated that the CAR-induced outward current reversed at approximately −72 mV in the presence of TTX (b − a), Ba²⁺ induced a small inward current reversing at approximately −87 mV (d − c), and almost completely blocked the current induced by CAR (e − d). Black bars show the period when drugs were applied. Horizontal scale bars are 100 s, and vertical bars are 10 pA.