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. Author manuscript; available in PMC: 2014 Feb 20.
Published in final edited form as: Neuron. 2013 Feb 20;77(4):736–749. doi: 10.1016/j.neuron.2012.12.032

Figure 6.

Figure 6

A comparison of AMPA vs. NMDAR blockade on the task-related firing of Delay cells in the primate dlPFC. A. Left graph: The percentage of neurons showing significant reduction in firing rate following iontophoresis of the NMDA antagonist, MK801 compared to the AMPA antagonists CNQX or NBQX. Right graph: The maximal degree of reduction in delay-related firing induced by the NMDA antagonist MK801 compared to the AMPA antagonists CNQX or NBQX. The reduction in firing rate was measured by the following ratio: (control-drug)/control. B. An example of an individual Delay cell treated with NMDA vs. AMPA antagonists. Under control conditions, the neuron showed prominent, spatially-tuned, delay-related firing (dark blue). Subsequent iontophoresis of the NMDA NR2B antagonist, Ro25-6981 (25nA; red), led to a large reduction in task-related firing. The iontophoretic current was then turned off and the neuron recovered normal rates of firing (light blue). Following recovery, the AMPA antagonist CNQX (40nA, green) was iontophoresed onto the neuron. CNQX had little effect on firing early in the delay epoch, but reduced firing in the later portion of the delay epoch. C. Average response showing the mean±SEM firing patterns of the 8 dlPFC Delay cells under control conditions (dark blue), during iontophoresis of Ro25-6981 (25nA; red), and during iontophoresis CNQX (40nA; green). Ro25-6981 produced a marked reduction in task-related firing, CNQX had more subtle effects, reducing firing only in the later aspects of the delay epoch. D. A comparison of mean±SEM firing rates in the five successive 0.5s epochs of the 2.5s delay period under control, MK801 and CNQX conditions. * p<0.05; ** p<0.01