Fig. 2.

Intracellular recordings from five different ventral pallidal neurons demonstrating typical responses to subthalamic nucleus (STN) stimulation. In Aand B, the resting membrane potential was −80 mV, and current was injected through the intracellular microelectrode to depolarize the membrane potential to the value indicated on theleft side of each trace. A, STN stimulation (1 Hz, 1.0 mA) evoked an EPSP (onset latency = 14.2 msec) when the membrane potential was −80 mV. The EPSP resulted in a spike when the cell was depolarized to −75 mV, and multiple spiking occurred with more positive potentials. B, In another ventral pallidal neuron, the EPSP (latency = 4.3 ± 0.6 msec) evoked by STN stimulation (1 Hz, 1.0 mA) was followed by an IPSP when this cell was depolarized. With further depolarization, a spike was generated during the EPSP, and the duration and amplitude of the IPSP were enhanced. C, This ventral pallidal neuron was depolarized to −65 mV. When the STN was stimulated with 0.7 mA (1 Hz), an EPSP was evoked (left trace). When the stimulation current for the STN was increased to 1.0 mA (stimulus artifacts are identified byarrows), an action potential was generated during the EPSP (middle and right traces). The mean onset of this spike was 2.7 ± 0.7 msec, but because it was riding on an EPSP and exhibited variable latencies with repeated stimulus presentations (compare the middle and right traces), it likely was mediated orthodromically.D, Stimulation of the STN at higher frequencies (4 Hz, 0.8 mA; 4 consecutive traces overlaid) evoked EPSPs in this ventral pallidal neuron that had a relatively consistent latency (latency = 4.2 ± 0.1 msec), and EPSP failures were not observed.E, With increasing STN stimulus strength (1 Hz, 0.4, 0.6, 0.8, and 1.0 mA), the EPSP (latency = 3.7 ± 0.7 msec) exhibited a linear increase in amplitude. The properties illustrated inD and E are consistent with monosynaptically mediated events.