Figure 8.

Chronic haloperidol treatment slows intrinsic pacemaker activity by increasing A-type K⁺ current. A, Whole-cell current-clamp recording showing the effect of 100 nm HpTx₃ on spontaneous firing activity of DA neurons from a rat chronically treated with haloperidol. Spontaneous activity was recorded after releasing the current clamp from a holding potential of -80 mV. HpTx₃ increases spike frequency and decreases first spike latency and first interspike interval in DA neurons. Broken lines indicate -80 mV. B, Summary of 100 nm HpTx₃ effects on spike frequency, first spike latency, and first interspike interval of spontaneous activity in haloperidol-treated DA neurons (chronic Hal, n = 7; +HpTx₃, n = 7; -HpTx₃, n = 5). Note that acutely reversing the haloperidol effect on A-type current with HpTx₃ normalizes pacemaker activity. ^**p < 0.01; ^*p < 0.05; NS, no significance. C, The effect of 100 nm HpTx₃ on tonic firing activity by a chronic haloperidol-treated DA neuron.