Abstract
The modulation of frontal cortical EEG activation to noxious somatosensory (tail pressure) and olfactory (acetone) stimulation by the basal amygdala was examined in urethane-anesthetized rats. Mild tail pressure produced no EEG activation, while acetone (sniffed by freely breathing rats or drawn across the olfactory epithelium in tracheotomized rats) produced a moderate suppression of large-amplitude synchronized EEG patterns. Concurrent, low-intensity 100 Hz stimulation of the basal amygdala permitted EEG activation to tail pressure to occur, and strongly enhanced olfactory-induced cortical activation. These results indicate that excitation of the basal amygdala potentiates frontal cortical responsiveness to aversive sensory events. This may provide a mechanism to facilitate cortical excitability and processing by amygdaloid neuronal activity.
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