, 2008, 2010). Although the assumption that ionotropic glutamate receptors are expressed by cholinergic Akt inhibitor terminals would provide a straightforward mechanism underlying these glutamatergic–cholinergic transient interactions, to our knowledge the presence of ionotropic glutamate receptors on cholinergic terminals has not been investigated. Thus, a more complex, multi-synaptic mechanism underlying the relationship between prefrontal cholinergic and glutamatergic signaling cannot be excluded. We will return
to the discussion of potential synaptic mechanisms further below following the discussion of the cognitive functions of cholinergic transients. Cholinergic inputs to the cortex are necessary for attentional performance and specifically for the detection and use of instructive cues to guide decisions about ongoing behavior (Muir et al., 1992; McGaughy et al.,
1996; Turchi & Sarter, 1997; Dalley et al., 2004; Botly & De Rosa, 2009). The use of cues to guide behavior IWR-1 research buy henceforth is termed ‘detection’, as defined in Posner et al. (1980). Importantly, this definition integrates the perceptual with the cognitive processes involved in the decision to report a signal – ‘By detection, we will mean the entry of information concerning the presence of a signal into a system that allows the subject to report the existence of the signal by an arbitrary response indicated by the experimenter’ (Posner et al., 1980, p. 162). Cholinergic activity in the cortex serves both neuromodulatory and deterministic functions, albeit via separate mechanisms. Our current model assumes that that the cholinergic neurons that modulate cortical circuitry form a separate population from those that generate the transient release events that are integrated into cortical information processing and exert deterministic functions (Hasselmo & Sarter, 2011; see also Hasselmo & Bower, 1992). This assumption awaits further testing, but separate cholinergic cell populations may be revealed based on, for example, their topographic organisation in the basal forebrain, differential
GPCR & G Protein inhibitor histological markers, and/or their differential cortical vs. subcortical afferent organisation (Unal et al., 2012; Zaborszky, 2002; Zaborszky et al., 2005, 2013; Fig. 1). In the present context, the neuromodulatory component of cholinergic activity is hypothesised to influence the probability and amplitude of cortical glutamatergic–cholinergic transients, primarily via stimulation of nAChRs (as described above). The level of this neuromodulatory influence has been shown to co-vary with demands on attentional control, not level of performance. That is, performance-associated increases are highest when performance is low as a result of distractors, extended time on task, or pharmacological challenges (Kozak et al., 2006; Sarter et al., 2006; St Peters et al., 2011).
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