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Prepulse Inhibition Study and Event-related Oscillations from Evoked Potentials: (P300 EEG, EMG & ERP)

Mid-latency evoked responses are so designated to differentiate them from the earlier sensory potentials and later ERPs that
are more affected by cognitive processing. The ERP measures that appear most important are the three most examined midlatency components in the auditory modality that are designated P50 (a positive component occurring between 35 and 80 ms
after stimulus onset), N100 (a negative component occurring between 80 and 150 ms after stimulus onset), and P200 (a
positive component occurring between 150 and 250 ms after stimulus onset). These components share the characteristic that
their amplitude decreases with repetition (habituation or sensory gating).

The P50 and N100 components have been studied extensively in psychiatric patients. Sensory gating of P50 is a potentially
useful endophenotype of psychosis or latent psychosis. Evidence for an inhibitory abnormality (i.e., sensory gating deficit) in
schizophrenic patients has been around for almost 25 years. The magnitude of the deficit is similar to the most robust
findings reported in neuroimaging and neuropsychology in schizophrenia. The N100 electrode component has also been
recently shown to exhibit a similar deficit in habituation in schizophrenic patients.

It is now firmly established that anomalies in the P300 response are associated with a wide variety of psychiatric conditions,
including substance abuse. It has repeatedly been shown that the offspring of alcoholics demonstrate P300 amplitude
reduction despite their lack of exposure to alcohol, thus suggesting that this anomaly is an endophenotype tapping the
underlying genetic risk for alcoholism.

Research with this putative endophenotype also is helping to explain patterns of psychiatric comorbidity often observed with
other substance use disorders. To the extent that amplitude reduction indexes underlying genetic risk, the pattern observed in
the figure is consistent with the hypothesis that the covariation among these disorders reflects shared genetic influences.
There is ample evidence to support this notion, including twin and family studies showing that shared genes account for most
of the covariance among these disorders.

Consistent with the notion that P300 provides a neurobiological representation of the underlying genetic risk, P300 amplitude
also covaries with these disinhibitory disorders, with shared genes accounting for the association.

Because ERPs are derived from the EEG, it is possible to use time frequency analysis to identify the constituent EEG waves,
which, because they are time locked to the stimulus presentation, compose the ERP waveform. This type of analysis makes it
possible to determine the amount of each EEG frequency present at each point in time elapsing from the onset of a stimulus
to the resolution of the associated ERP. These event-related oscillations (EROs) can be partitioned into the same frequency
bands identified for spontaneous EEG, but these stimulus-elicited rhythms are likely to be functionally different from the
frequency bands that compose resting EEG. With respect to P300, specific neural activity have different responses during
elicitation of P300.

Event-related oscillations also are beginning to provide insights regarding brain dynamics and psychopathology, especially
regarding the development of drug dependence. Reduced delta and theta EROs have been associated with risk for the
development of alcoholism over and above the risk associated with reduced P300 amplitude, suggesting that they add
important predictive information not tapped by measures of the P300 endophenotype.
These EROs have been linked to gene variants involved in cholinergic and GABAergic neurotransmitter systems, systems
that have been implicated in the neurochemical pathways involved in substance use and P300 generation. Collectively, this
line of ERP/ERO research highlights the evolving potential of electrophysiological correlates of human information
processing to identify those at genetic risk for the development of alcoholism and related comorbidities.




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