RT Journal Article
SR Electronic
T1 Trial-to-Trial Variability and State-Dependent Modulation of Auditory-Evoked Responses in Cortex
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 10451
OP 10460
DO 10.1523/JNEUROSCI.19-23-10451.1999
VO 19
IS 23
A1 Michael A. Kisley
A1 George L. Gerstein
YR 1999
UL http://www.jneurosci.org/content/19/23/10451.abstract
AB Recent experimental work has provided evidence that trial-to-trial variability of sensory-evoked responses in cortex can be explained as a linear superposition of random ongoing background activity and a stationary response. While studying single trial variability and state-dependent modulation of evoked responses in auditory cortex of ketamine/xylazine-anesthetized rats, we have observed an apparent violation of this model.Local field potential and unit spike trains were recorded and analyzed during different anesthesia depths—deep, medium, and light—which were defined by the pattern of ongoing cortical activity. Estimation of single trial evoked response was achieved by considering whole waveforms, rather than just one or two peak values from each wave. Principal components analysis was used to quantitatively classify waveforms on the basis of their time courses (i.e., shapes).We found that not only average response but also response variability is modulated by depth of anesthesia. Trial-to-trial variability is highest under medium levels of anesthesia, during which ongoing cortical activity exhibits rhythmic population bursting activity. By triggering the occurrence of stimuli from the spontaneously occurring burst events, we show that the observed variability can be accounted for by the background activity. In particular, the ongoing activity was found to modulate both amplitude and shape (including latency) of evoked local field potentials and evoked unit activity in a manner not predicted by linear superposition of background activity and a stereotyped evoked response. This breakdown of the linear model is likely attributable to rapid transitions between different levels of thalamocortical excitability (e.g., spike-wave discharges), although brain “state” is relatively fixed.