Differential cortical acetylcholine release in rats performing a sustained attention task versus behavioral control tasks that do not explicitly tax attention

Arnold, H. Moore; Burk, Joshua A.; Hodgson, E.M; Sarter, Martin; Bruno, John P.

doi:10.1016/s0306-4522(02)00292-0

Cited by 160 publications

(121 citation statements)

References 33 publications

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“…Thus, the effects of repeated AMPH exposure and AMPH-challenge on ACh release did not differ between the two collections taken before task onset and the four collections taken during task performance (see Figure 4). Similar to the results from previous experiments (Arnold et al, 2002;Himmelheber et al, 2000;Kozak et al, 2006), performance of the attention task increased ACh release in the mPFC over baseline. In SAL/SAL animals, ACh release increased by 158.28718.49% over basal ACh levels during the performance of the task (F(1,6) ¼ 66.98; po0.001; see Figure 4).…”

Section: Effects Of Repeated Amph On Ach Release In Performing Ratssupporting

confidence: 88%

“…For example, cortical ACh release in rats performing a fixed interval 9 s schedule of reinforcement increased only by about 50% over baseline, despite a lever-pressing rate that was almost 10-fold the rate observed in sustained attention task-performing rats (Arnold et al, 2002). Likewise, operant procedures controlling for the effects of reward rate and the sensory effects of stimuli indicated that these variables do not account for the increases in ACh release observed in attentional task-performing rats (Dalley et al, 2001;Himmelheber et al, 1997).…”

Section: Discussionmentioning

confidence: 88%

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Toward a Neuro-Cognitive Animal Model of the Cognitive Symptoms of Schizophrenia: Disruption of Cortical Cholinergic Neurotransmission Following Repeated Amphetamine Exposure in Attentional Task-Performing, but Not Non-Performing, Rats

Kozak

Martı́nez

Young

et al. 2007

Neuropsychopharmacol

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Impairments in attentional functions and capacities represent core aspects of the cognitive symptoms of schizophrenia. Attentional performance has been demonstrated to depend on the integrity and activity of cortical cholinergic inputs. The neurobiological, behavioral, and cognitive effects of repeated exposure to psychostimulants model important aspects of schizophrenia. In the present experiment, prefrontal acetylcholine (ACh) release was measured in attentional task-performing and non-performing rats pretreated with an escalating dosing regimen of amphetamine (AMPH) and following challenges with AMPH. In non-performing rats, pretreatment with AMPH did not affect the increases in ACh release produced by AMPH-challenges. In contrast, attentional task performanceassociated increases in ACh release were attenuated in AMPH-pretreated and AMPH-challenged rats. This effect of repeated AMPH exposure on ACh release was already present before task-onset, suggesting that the loss of cognitive control that characterized these animals' performance was a result of cholinergic dysregulation. The findings indicate that the demonstration of repeated AMPH-induced dysregulation of the prefrontal cholinergic input system depends on interactions between the effects of repeated AMPH exposure and cognitive performance-associated recruitment of this neuronal system. Repeated AMPH-induced disruption of prefrontal cholinergic activity and attentional performance represents a useful model to investigate the cholinergic mechanisms contributing to the cognitive impairments of schizophrenia.

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Section: Effects Of Repeated Amph On Ach Release In Performing Ratssupporting

confidence: 88%

Section: Discussionmentioning

confidence: 88%

Toward a Neuro-Cognitive Animal Model of the Cognitive Symptoms of Schizophrenia: Disruption of Cortical Cholinergic Neurotransmission Following Repeated Amphetamine Exposure in Attentional Task-Performing, but Not Non-Performing, Rats

Kozak

Martı́nez

Young

et al. 2007

Neuropsychopharmacol

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“…The blockade of ionotropic glutamate receptors situated in the region containing the cell bodies of the cholinergic neurons projecting to the cortex produced little effect on basal cortical ACh release but, as would be expected, attenuated the increases in release that are normally produced by a simple conditioned cue eliciting behavioral activation and orientation (Fadel et al, 2001). Contrasting effects on release were found in animals performing a task, which taxes attentional functions and is known to depend on the integrity and activity of the cortical cholinergic input system (Arnold et al, 2002;McGaughy et al, 1996). Specifically, in task-performing animals, blockade of these same ionotropic glutamate receptors resulted in the augmentation of the increases in transmitter release normally observed as a function of task performance (Kozak et al, 2006a).…”

Section: Neurotransmitter Dysregulation In Recruited Circuits: the Simentioning

confidence: 69%

Abnormal Neurotransmitter Release Underlying Behavioral and Cognitive Disorders: Toward Concepts of Dynamic and Function-Specific Dysregulation

Sarter

Bruno

Parikh

2006

Neuropsychopharmacol

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Abnormalities in the regulation of neurotransmitter release and/or abnormal levels of extracellular neurotransmitter concentrations have remained core components of hypotheses on the neuronal foundations of behavioral and cognitive disorders and the symptoms of neuropsychiatric and neurodegenerative disorders. Furthermore, therapeutic drugs for the treatment of these disorders have been developed and categorized largely on the basis of their effects on neurotransmitter release and resulting receptor stimulation. This perspective stresses the theoretical and practical implications of hypotheses that address the dynamic nature of neurotransmitter dysregulation, including the multiple feedback mechanisms regulating synaptic processes, phasic and tonic components of neurotransmission, compartmentalized release, differentiation between dysregulation of basal vs activated release, and abnormal release from neuronal systems recruited by behavioral and cognitive activity. Several examples illustrate that the nature of the neurotransmitter dysregulation in animal models, including the direction of drug effects on neurotransmitter release, depends fundamentally on the state of activity of the neurotransmitter system of interest and on the behavioral and cognitive functions recruiting these systems. Evidence from evolving techniques for the measurement of neurotransmitter release at high spatial and temporal resolution is likely to advance hypotheses describing the pivotal role of neurotransmitter dysfunction in the development of essential symptoms of major neuropsychiatric disorders, and also to refine neuropharmacological mechanisms to serve as targets for new treatment approaches. The significance and usefulness of hypotheses concerning the abnormal regulation of the release of extracellular concentrations of primary messengers depend on the effective integration of emerging concepts describing the dynamic, compartmentalized, and activitydependent characteristics of dysregulated neurotransmitter systems.

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“…The dynamics of cholinergic signalling in the cortex during ongoing behaviour has long remained enigmatic. Due to low temporal resolution of classical techniques such as microdialysis, cholinergic modulation was considered to occur on a timescale of minutes [11,58]. However, recently it was shown that cholinergic signalling involved in attention has a much faster temporal dynamics,…”

Section: Nicotine's Modes Of Actionmentioning

confidence: 99%

Nicotinic actions on neuronal networks for cognition: General principles and long-term consequences

Poorthuis

Goriounova

Couey

et al. 2009

Biochemical Pharmacology

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Differential cortical acetylcholine release in rats performing a sustained attention task versus behavioral control tasks that do not explicitly tax attention

Cited by 160 publications

References 33 publications

Toward a Neuro-Cognitive Animal Model of the Cognitive Symptoms of Schizophrenia: Disruption of Cortical Cholinergic Neurotransmission Following Repeated Amphetamine Exposure in Attentional Task-Performing, but Not Non-Performing, Rats

Toward a Neuro-Cognitive Animal Model of the Cognitive Symptoms of Schizophrenia: Disruption of Cortical Cholinergic Neurotransmission Following Repeated Amphetamine Exposure in Attentional Task-Performing, but Not Non-Performing, Rats

Abnormal Neurotransmitter Release Underlying Behavioral and Cognitive Disorders: Toward Concepts of Dynamic and Function-Specific Dysregulation

Nicotinic actions on neuronal networks for cognition: General principles and long-term consequences

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