Fig. 5.

the PSC frequency that outlasted the duration of the agonist pulse, particularly at the highest concentrations of ACh (third and fourth traces).C, Traces shown in A were expanded for better visualization of the PSCs. Under control (first two traces), individual PSCs are well (Figure legend continues)separated. With choline (10 mm), the PSCs summated such that individual events could not be identified (third trace). In the presence of ACh (10 μm), individual PSCs could still be identified. However, in the presence of 100 μm and 1 mm ACh, the PSCs summated such that the frequency could not be analyzed.D, An example of an experiment in which charge analysis of the PSCs was performed. Traces shown in B were used for this analysis. Charge movement per 2 sec segment was calculated in the traces before, during, and after the end of pulse and plotted against time. The 10th sec in the time scale corresponds to activation of the agonist-delivery system. Membrane potential, +2 mV.Choline and ACh differ in their ability to trigger GABAergic PSCs. A, A 6 sec pulse of choline induced a burst of PSCs that did not outlast the agonist pulse (top trace). Note that the evoked PSCs were preceded by a small inward current that was induced by choline. In the same neuron, application of ACh induced a concentration-dependent increase in the PSC frequency (second, third, andfourth traces). The PSCs outlasted the ACh pulse. Membrane potential, −8 mV. B, In another neuron, a 12 sec pulse of choline (1 mm) also induced a burst of PSCs. The delay for the onset of the response was shortened by increasing the concentration of choline to 10 mm. In the same neuron, ACh induced a concentration-dependent increase in