Figure 2.

Optical activation of corticofugal fibers in the STN results in action potential-dependent AMPA synaptic transmission (a) Expression of mCherry following transfection of a ChR2-mCherry viral solution in the motor cortex. (b,c) mCherry-positive corticofugal fibers in the STN. The STN boundaries are delineated by the STN neuron-specific FoxP2 marker (in green). (d) Example of the current evoked by a 1 ms flash and descriptive parameters of the inward currents measured in a sample of 24 subthalamic neurons. Current peak amplitude and charge, onset latency, time required to decay from 80 to 20% of peak value, and jitter are reported as individual values (left) and mean ± sem (right). Flash duration and luminance ranges were 0.4 to 1 ms and 0.55 to 1.15 mW.mm⁻². (e,f) The light-induced inward currents were fully blocked by the specific AMPA/kainate receptor antagonist, DNQX (20 µM), or the sodium channel inhibitor, TTX (1 µM). The gray and black traces illustrate currents photo-evoked in controls and in the continued presence of the drugs, respectively. The graphs to the right of each recording display the summary data of current values before and after drug application. (g) Voltage-dependence and conductance of pharmacologically-isolated AMPA receptor EPSCs. Left: Representative traces of photo-induced EPSCs in the presence of the specific NMDA receptor antagonist, APV (50 µM). Holding voltage was changed from −90 to +50 mV in 20 mV steps. Right: Plot showing chord conductance against voltage. Conductance was significantly different from 1 at +30 and +50 mV, indicating rectifying AMPA receptors. (h) Naspm reduced the EPSC magnitude, indicating Ca²⁺-permeant, GluA2-lacking, as well as GluA2-containing, AMPA receptors. ^*Significantly different from the theoretical median = 1, two-tailed Wilcoxon signed rank test, p = 0.0313 for both +30 mV and +50 mV. ^**Indicates significant changes at p = 0.0156, one-tailed Wilcoxon matched-pairs signed rank test.