Central Gating Mechanisms That Regulate Event-Related Potentials and Behavior

Abstract

Previous work in our laboratory showed that the mesencephalic reticular formation (MRF) and frontal granular cortex (FC) jointly regulate the activity in the thalamic reticular nucleus (R). The R neurons project specifically into relay nuclei and, when activated, inhibit the specific transmission of sensory information through the thalamus to primary receptive cortex. The MRF has a generalized inhibitory effect on the R cells and can produce generalized disinhibition of sensory channels, as is known to occur during orienting responses. The frontal cortex, on the other hand, provides specific and tonic excitation of individual R cells and can selectively turn off specific sensory channels, as is known to occur during selective attention. Our more recent work has focused on the cellular mechanisms in the frontal cortex that result in the specific sensory gating that occurs during operationally defined states of behavioral attention. The occurrence of the event-related potential (ERSP) in the FC seems to be the harbinger of both EEG desynchronization and sensory channel selection. Both of these latter event-related activities are explainable by FC effects on R cells. We have found that during an ERSP in the FC, in the underlying tissue: (a) norepinephrine (NE) is released, (b) cAMP is activated, (c) extracellular potassium ion activity is reduced, and (d) slow membrane potential shifts occur in some of the neurons. These results suggest that the same neuromodulatory mechanism exists in the cortex as is known to operate in a model preparation, the sympathetic ganglion.