Figure 4.

Effects of BAPTA on the AHP_slow and on the excitability of an acutely dissociated rabbit nodose neuron. (A) Bath-applied BAPTA/acetomethylester (10 μM) blocks the AHP_slow within 5 min without changing the resting membrane potential or membrane input resistance. APs were evoked by transmembrane depolarizing current pulses (4 nA, 1.5 ms, 10 Hz) and are truncated. (B) Responses recorded at a faster sweep speed to illustrate the kinetics of the AHP_fast and AHP_medium, which precede the AHP_slow. The AHP_fast is unaffected by 10 μM BAPTA/acetomethylester (compare a with b). The Ca²⁺ dependence of the AHP_medium is illustrated in c, where the neuron is superfused with 100 μM CdCl₂ for 30 s, which blocks most of the AHP_medium. The residual component of the AHP recorded in CdCl₂ is the AHP_fast, which is mediated by delayed rectifier K⁺ channels. (C) Depression of the AHP_slow markedly increases neuronal excitability. The average AP firing frequency induced by a current ramp protocol (1 nA, 2 s) increased from 1 to 5.5 Hz when the AHP_slow was blocked. Similar loss of spike-frequency adaptation was observed with bradykinin, prostaglandin D₂, histamine, and other inflammatory autacoids (see Table 2). The scale bar represents 3 mV, 2 s in A; 15 mV, 0.25 s in B; and 15 mV, 0.5 s in C. The dashed line represents the resting membrane potential (−60 mV). Resting membrane input resistance was 70 MΩ. Data is from ref. 19 with permission from the American Physiological Society.