Principal component analysis of evoked responses and the effects of alcohol on the geniculo-striate system of the monkey.

Abstract

This study was designed to test the effects of alcohol on visual evoked potentials in nonhuman primates performing a cognitive task. Flash evoked potentials were recorded from monkeys involved in a delayed matching-to-sample (DMS) paradigm in which the flash served as an alerting signal before each trial. Event-related potentials were recorded from the lateral geniculate nucleus and homolateral striate cortex before, during, and after intravenous administration of saline or ethanol (0.25, 0.5, 1.0, and 2.0 g/kg). Average evoked potentials (AEPs) were computed. Residual waveforms were obtained by subtracting the predrug AEP from postdrug AEPs. A principal component analysis was employed to define the alcohol alterations on the evoked responses. In the analysis each AEP was represented by 40 time points spaced 12 msec apart. These reduced representations of the AEP were entered in the variance-covariance matrix calculations. The first five eigenvectors were computed and plotted. Alcohol produced the greatest variance in the AEPs at the two highest dose levels. So the data were grouped together into three experimental categories: saline, low-dose (0.25-0.5 g/kg) and high-dose (1.0-2.0 g/kg). A correlation template, representing each category, was computed by correlating individual eigenvectors with each sequential average composed of 10 individual evoked potentials in the 200 trials of an experimental session. Alcohol affected the state vector from the brain by loading the correlation coefficient in the opposite direction following alcohol administration in two principal components. One or two of the eigenvectors significantly (P less than 0.01) shifted in geniculate nucleus, indicating that either the nucleus or a previous station was affected by alcohol. In comparison, three or more eigenvectors from striate cortex were shifted significantly following alcohol injection. This difference may be explained by the effect of alcohol on multisynaptic brain structures, including the brain-stem reticular formation, which in turn influenced the cortex.