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. Author manuscript; available in PMC: 2011 Jan 28.
Published in final edited form as: Eur J Neurosci. 2009 Apr;29(8):1711–1722. doi: 10.1111/j.1460-9568.2009.06713.x

Fig. 8.

Fig. 8

Detection-related PPC neurons respond similarly on hit and miss trials following cholinergic lesions. (A, left) Stimulus-locked population peri-event time histograms (PETHs) for hit and miss trials (20-ms bins, Gaussian filtered over three bins) of 36 cue-evoked neurons from pre-lesion recordings. Peak activation of these neurons on hit trials occur at an average of 220 ms following the cue, and the firing rate remains elevated through the 1-s delay and response. (A, right) The average firing rate of each neuron during the 1-s epoch following the cue, with hit trials plotted against miss trials; 28/36 neurons (green dots) have a significantly higher firing rate on hit trials (all P < 0.05). Only 2/36 neurons (red dots) have a significantly higher firing rate on miss trials. (B, left) A stimulus-locked PETH from 18 cholinergically lesioned cue-driven neurons. PPC neurons are activated on both hit and miss trials. (B, right) The average firing rate of each neuron during the 1-s epoch following the cue; 6/18 neurons have a higher firing rate on hit trials than on miss trials, and 3/18 neurons have a higher firing rate on miss trials. (C, left) Following saline infusions, PPC neurons are activated on hit trials, but not miss trials. Right: 10/15 neurons have a higher firing rate in the 1-s epoch following the cue on hit trials than on miss trials.