Figure 2.

Bath-applied CabPK peptide elicits a sustained, subthreshold depolarization in the isolated LG neuron by activating the voltage-dependent I_MI. A, With Int1 neuron activity suppressed by hyperpolarizing current injection, bath-applied CabPK elicited a sustained, subthreshold depolarization in the LG neuron. B, With Int1 neuron exhibiting its normal pyloric-timed burst pattern, thereby providing rhythmic inhibition to LG, bath-applied CabPK initially caused a gradual increase in the amplitude of the subthreshold, pyloric-timed oscillations in LG. Note that the oscillation peaks became more depolarized, while the membrane potential of the trough was not changed. CabPK superfusion was begun immediately before the start of this trace. Subsequently, the gastric mill rhythm commenced. C, I–V plots of CabPK-influenced current in LG, obtained using TEVC and a voltage ramp protocol, during focal pressure application (5 psi, 1 s) of CabPK (10⁻⁴ m) under control conditions (black) and during CCAP (10⁻⁶ m) bath application (red). Each curve represents the difference current (CabPK − control or CCAP condition) as indicated. Solid curves represent the mean values for each condition; broken lines represent three individual experiments. D, Injection of artificial I_MI (g_MI = 100 nS) into LG, via the dynamic-clamp, in a preparation where Int1 activity was weak (<5 Hz) caused a sustained depolarization comparable to that resulting from CabPK application.