Cognitive inhibition is an integral component of normal cognitive functioning. This thesis represents a significant step towards a greater understanding of the neural circuits underlying cognitive inhibition. In Chapter 1, we established a novel rodent version of the stop signal task (SST), linking a powerful behavioral paradigm for studying a form of cognitive inhibition to the advantages of rodent models. We utilized this novel rodent SST in Chapters 2 and 3 to examine a novel node in the neuronal circuits underlying stopping, the basal forebrain (BF). In Chapter 2, we examined whether age-related slowing of processing speed and SSRT were independent in a naturally-occurring rodent model of normal cognitive aging, and whether these changes related to altered BF integrity. We find that aging is associated with substantial nonoverlapping impairment in stopping, spatial navigation, and processing speed, and that altered sustained attention in aged animals is accompanied by changes in the integrity of the BF cholinergic population. In Chapter 3 we utilized this rodent SST and in vivo electrophysiological recording to study the role of putative non-cholinergic bursting neurons in the BF in stopping. We find substantial causal evidence that this population of BF neurons is capable of controlling the latency of cognitive inhibition, stop signal reaction time (SSRT). Together, these studies make several critical advances towards the study of cognitive inhibition and broaden the scope of existing proposed neuronal circuits underlying stopping to include the cortically-projecting basal forebrain.
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The Role of the Basal Forebrain in Cognitive Inhibition
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