Prefrontal cortical modulation of acetylcholine release in posterior parietal cortex

Nelson, Christopher Lee; Sarter, Martin; Bruno, John P.

doi:10.1016/j.neuroscience.2004.12.007

Cited by 112 publications

(87 citation statements)

References 60 publications

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“…The diminished ability of ACh-LX rats to adjust to the change in the relationship between the tone and event timing suggests compromised top-down control. Top-down processing of stimuli in the presence of increased attentional demands is hypothesized to result from high levels of prefrontal acetylcholine activating descending glutamatergic pathways from the cortex to the nbm and ultimately augmenting cholinergic efflux in PPC (Nelson et al, 2005). The loss of PFC acetylcholine in the present study would prevent increased cholinergic efflux in PPC Bruno, 1997, 1999;Sarter et al, , 2001bSarter et al, , 2005, impeding discrimination of targets from distractors.…”

mentioning

confidence: 73%

“…Acetylcholine in PFC is hypothesized to control top-down allocation of attentional resources (Sarter et al, 2001a. Increases in prefrontal ACh stimulates cholinergic efflux in the posterior parietal cortex (PPC) (Nelson et al, 2005). The parietal cortex controls spatial (Posner et al, 1987) and temporal (Coull and Nobre, 1998) orientation of attention and maintains focus in the presence of distraction Yantis, 2004, 2006).…”

Section: Introductionmentioning

confidence: 99%

“…The parietal cortex controls spatial (Posner et al, 1987) and temporal (Coull and Nobre, 1998) orientation of attention and maintains focus in the presence of distraction Yantis, 2004, 2006). The recruitment of PPC by PFC is hypothesized to result from increased attentional demand (Nelson et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

“…First, cholinergic deafferentation of PFC may decrease top-down attentional control and prohibit filtering of irrelevant stimuli. Specifically, damage to the PFC disrupts descending control of the cholinergic basal forebrain to prevent augmented cholinergic efflux in PPC that aids in resolving targets from distractors (Sarter et al, 2001aNelson et al, 2005;Buschman and Miller, 2007). Alternatively, decreased acetylcholine in PFC produces a shift in circuit dynamics to ultimately increase the influence of corticocortical circuits, specifically PPC to PFC, that mediate bottom-up processing of stimuli (Hasselmo and McGaughy, 2004;Buschman and Miller, 2007).…”

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confidence: 99%

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Cholinergic Deafferentation of Prefrontal Cortex Increases Sensitivity to Cross-Modal Distractors during a Sustained Attention Task

Newman¹,

McGaughy²

2008

J. Neurosci.

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The effects of restricted cholinergic deafferentation of prefrontal cortex in rats on sustained attention were assessed. Attentional demands were increased by presentation of distractor stimuli in a different modality (auditory) or the same modality (visual) as target stimuli. Additionally, the effects of the regularity of the distractor on rats' ability to disregard this stimulus were assessed by testing different frequencies of stimuli for each modality. Cholinergically lesioned rats were more sensitive to the effects of auditory distractors than nonlesioned rats, whereas visual distractors of any frequency potently impaired the performance of all subjects. The effects of the auditory stimuli on attentional performance varied depending on the frequency of the tone. A tone with a predictable pattern enhanced signal detection in all rats. An irregular tone selectively impaired performance of rats with cholinergic lesions. Additional tests suggest that rats use the regular tone to time when to attend. Lesioned rats were impaired when the regular tone was presented with a more variable intertrial interval in a subsequent testing session, suggesting impairments in top-down control. In addition to changes in top-down control of attention, differential effects on performance based on the regularity of the tone suggest that stimulus properties encoded by bottom-up processes are also altered after lesioning. The current data suggest that cholinergic deafferentation of prefrontal cortex alters top-down and bottom-up processing of stimuli.

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confidence: 73%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

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Cholinergic Deafferentation of Prefrontal Cortex Increases Sensitivity to Cross-Modal Distractors during a Sustained Attention Task

Newman¹,

McGaughy²

2008

J. Neurosci.

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“…In contrast, cholinergic inputs to other cortical regions may primarily be activated to optimize signal detection and input processing under challenging conditions. For example, to attenuate declining attentional performance, the prefrontal cortex may activate cholinergic inputs to other cortical, including parietal (Nelson et al, 2005), regions, thereby improving the detection and processing of signals . Ongoing experiments are designed to test the role of prefrontal cholinergic inputs in the regulation of parietal cholinergic inputs in situations that impede the detection process.…”

Section: Discussionmentioning

confidence: 99%

Increased Capacity and Density of Choline Transporters Situated in Synaptic Membranes of the Right Medial Prefrontal Cortex of Attentional Task-Performing Rats

et al. 2005

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Glutamate receptors in nucleus accumbens mediate regionally selective increases in cortical acetylcholine release

Zmarowski

Sarter

Bruno

2006

Synapse

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The basal forebrain cortical cholinergic system (BFCS) is critical for the regulation of attentional information processing. BFCS activity is regulated by several cortical and subcortical structures, including the nucleus accumbens (NAC) and prefrontal cortex (PFC). GABAergic projection neurons from NAC to basal forebrain are modulated by Glu receptors within NAC. We previously reported that intra-NAC perfusions of NMDA or its antagonist CPP stimulate ACh release in PFC. In this experiment we determined whether this trans-synaptic modulation of cortical ACh release is evident in multi-sensory associational areas like the posterior parietal cortex (PPC). Artificial cerebrospinal fluid (aCSF, control), NMDA (250 or 400 muM), or CPP (200 or 400 muM) were perfused into the NAC shell and ACh was measured in the ipsilateral PPC. Amphetamine (2.0 mg/kg, i.p), was systemically administered as a positive control in a fourth session, since it also stimulates cortical ACh release but via mechanisms known to not necessitate transmission within the NAC. Neither NMDA nor CPP increased ACh efflux in the PPC, yet both drugs increased ACh release in PFC, suggesting that NMDA receptor modulation in the NAC increases ACh in the cortex in a regionally-specific manner. Systemic amphetamine administration significantly increased (100-200%) ACh in the PPC, suggesting that levels of ACh in the PPC can be increased following certain pharmacological manipulations. The cortical region-specific modulation of ACh by NAC may underlie the linkage of motivational information with top-down controls of attention as well as guide appropriate motor output following exposure to salient and behaviorally relevant stimuli.

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Prefrontal cortical modulation of acetylcholine release in posterior parietal cortex

Cited by 112 publications

References 60 publications

Cholinergic Deafferentation of Prefrontal Cortex Increases Sensitivity to Cross-Modal Distractors during a Sustained Attention Task

Cholinergic Deafferentation of Prefrontal Cortex Increases Sensitivity to Cross-Modal Distractors during a Sustained Attention Task

Increased Capacity and Density of Choline Transporters Situated in Synaptic Membranes of the Right Medial Prefrontal Cortex of Attentional Task-Performing Rats

Glutamate receptors in nucleus accumbens mediate regionally selective increases in cortical acetylcholine release

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