This line of research examines the processes underlying the brain’s capacity to flexibly and dynamically enhance attentional processing. My theoretical framework distinguished the attentional function of boosting the relevant (signal) and reduce processing of the irrelevant (noise), both of which contribute to optimization of goal-directed behavior. We show acetylcholine is central to the latter attentional function and thus their differential degradation as we age.
While the cognitive mechanisms and functional neuroanatomy of attention have been well examined by the human cognitive literature, the neurochemistry and specific downstream neuroanatomical contributions of attention are less well-known. The basal forebrain provides cholinergic neuromodulatory input to the entire cortical mantle, including frontal and parietal cortices, and it has been implicated in attentional processing in nonhuman animals. We demonstrate across rats and humans that the cholinergic basal forebrain is a critical neural substrate for the regulation of attention.
Proactive interference (PI) is the impairing influence of past learning on the acquisition of new, related information. Using cholinergic pharmacology and cholinergic specific immunotoxic-lesion data, we demonstrate that efficient resolution of PI depends on adequate acetylcholine originating from the basal forebrain in a rodent model and using fMRI in humans.
The cholinergic basal forebrain, in particular the NBM, regulates subcortical targets, including the amygdala. We have examined how affective experience engages the amygdala in different ways to supports the regulation of attention. Affective states regulate activity in BF afferent structures, including the amygdala and medial OFC, which in conjunction are shown to alter the functional connectivity between primary and extrastriate visual cortices, simultaneously modulate both affective feelings and attention.
ACLAB