Despite the fact that glutamate this website receptor antagonists caused map expansion and increased overlap between Mab and Mad, movement topography was not abolished. The Mab and Mad maps could still be distinguished in the presence of glutamate receptor antagonists (Figure 6B), with no significant reduction in the separation between their centers of gravity (Figure 6D). Application

of glutamate receptor antagonists did not cause a significantly greater shift in map centers from their baseline positions than application of saline for Mab (0.5 ± 0.09 versus 0.5 ± 0.1 mm, respectively, p = 0.96, n = 9 versus n = 5, t test) or Mad (0.5 ± 0.09 versus 0.2 ± 0.04 mm, respectively, p = 0.06). Although the increased movement durations (Figure 5C) and expansion of motor maps (Figure 6C) caused by disruption of excitatory synaptic transmission were unexpected, this may be explained

by PD-1/PD-L1 assay a loss of disynaptic inhibition (Helmstaedter et al., 2009, Murayama et al., 2009, Adesnik and Scanziani, 2010, Silberberg and Markram, 2007 and Kapfer et al., 2007). To test this hypothesis, we repeated these experiments with GABAA receptor antagonists (gabazine 1 μM n = 4 or picrotoxin 100 μM n = 2, Figure S6). GABA receptor antagonists diminished differences between Mab and Mad movement trajectories, but had no significant effect on movement kinematics (Figure S6), and generally did not degrade functional subdivisions of the motor cortex. Disrupting GABAergic transmission

did reproduce the increases in map amplitude (Figure S7C) and area (Figure S7D) seen during blockade of excitatory transmission. As with the delayed increase in movement speeds (Figure 5C), this effect was restricted to Mad. These effects are consistent with disinhibition causing the selective expansion of the Mad subregion. The separation between Mab and Mad and the region of overlap between them was unchanged (Figure S7E). Like glutamate receptor antagonists, GABA receptor antagonists did not cause greater displacement of map centers than saline treatment for Mab (0.6 ± 0.1 versus 0.5 ± 0.1 mm, p = 0.37, n = 6 versus n = 5, t test) or Mad Axenfeld syndrome (0.4 ± 0.1 versus 0.2 ± 0.04 mm, p = 0.24). The observation that disrupting intracortical synaptic transmission can impair the expression of diverse complex movements without abolishing the topography of movement maps was initially surprising, but may be explained by differences between the roles of intracortical and corticofugal circuits. It is possible that cortical application of receptor antagonists interferes with local circuit function and the generation of complex movements by prolonged stimulation, but does not alter the movement maps generated by the output of corticofugal cells directly activated by brief pulses of optogenetic excitation.