Monoaminergic modulation of behavioural and electrophysiological indices of error processing

Barnes, J. J.; O’Connell, Redmond G; Nandam, L. Sanjay; Dean, Angela J.; Bellgrove, Mark A.

doi:10.1007/s00213-013-3246-y

Cited by 37 publications

(24 citation statements)

References 85 publications

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“…Our null finding was consistent with other performance monitoring studies that used acute doses of citalopram in humans (70,134,159). The finding that acute low doses of SSRIs actually lower central serotonin levels due to activation of 5-HT 1A autoreceptors may explain these null results (194).…”

Section: Summary Of Resultssupporting

confidence: 82%

“…Methylphenidate, as detailed later, could facilitate this L. Sanjay Nandam Page 30 of 62 process by increasing dopamine concentrations within specific regions of the basal ganglia (187). The dACC activation is also in keeping with the finding that methylphenidate increases ERN amplitudes following error awareness in the EAT, as the dACC is thought to be the neural generator of the ERN (8,134). The concomitant activity in the IPL is consistent with a proposal that the parietal cortex, along with the IFG and pre supplementary motor area, form an 'executive control network' that responds to events deemed salient by the ACC and insula (188).…”

Section: Summary Of Resultssupporting

confidence: 50%

“…Accordingly, the reporting of errors was binary and time limited, in that, unless the subject pressed the awareness button before the next trial commenced, it was assumed that they had been unaware of an error. Since its inception the EAT has been examined with a number of modalities, including event related potentials (ERP) and fMRI, in an attempt to probe the specific neurobiology of error awareness (133,134). Nonetheless, this investigation remains critically informed by and situated within its larger context, the neurobiology of human performance monitoring.…”

Section: The Neuropsychology Of Error Awarenessmentioning

confidence: 99%

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Neurochemical and neurophysiological bases of executive control

Nandam¹

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The aim of this work is to further understanding into the biological bases of human executive control through an integration of neuropsychology, psychopharmacology and functional imaging. Executive control includes the prototypical executive functions of response inhibition and error awareness.Response inhibition can be further divided into action cancellation and action restraint, which were assayed with the stop signal (SST) and Error Awareness (EAT) tasks, respectively. The EAT, which is a modified go-no go paradigm, was also used to measure error awareness behaviour. Monoamine neurotransmitters, specifically dopamine, noradrenaline and serotonin, were modulated during task performance with acute doses of methylphenidate (a dopamine and noradrenaline reuptake inhibitor), atomoxetine (a noradrenaline reuptake inhibitor), citalopram (a serotonin reuptake inhibitor) and cabergoline (a D 2 agonist). The pharmacoimaging correlates of task performance were also examined with functional magnetic resonance imaging (fMRI). All experiments adhered to a randomised, double blind, placebo-controlled, crossover design and were limited to 18-35 year old healthy right-handed male participants.In Chapter 1, twenty-four (24) participants received acute doses of methylphenidate (30mg), atomoxetine (60mg), citalopram (30mg) and placebo and performed the SST. Methylphenidate, but not atomoxetine or citalopram, led to a reduction in response time variability and stop-signal reaction time indicating enhanced action cancellation compared with the other drug conditions. This enhancement occurred without change to overall response speed suggesting that methylphenidate was modulating core response inhibition processes rather than simply augmenting overall processing speed.This result argued for the prominence of dopaminergic, rather than adrenergic or serotonergic, mechanisms in action cancellation.In Chapter 2, the pharmacoimaging correlates of action restraint aspect were explored. Twenty-seven (27) males received acute doses of methylphenidate (30mg), atomoxetine (60mg), citalopram (30mg) and placebo whilst undertaking the EAT during fMRI. No-go related BOLD activations were then correlated for each of the drug conditions. Although Inhibitory performance under methylphenidate was numerically superior to the other drug conditions, this difference did not achieve statistical significance. On fMRI, methylphenidate activated, versus placebo, the anterior cingulate cortex, right inferior frontal, left middle frontal, left angular and right superior temporal gyri and right caudate. Atomoxetine activated a broad network of cortical regions.Both methylphenidate and atomoxetine, but not citalopram, activated superior temporal, right inferior frontal and left middle frontal clusters. Citalopram only activated the left inferior occipital lobe. Taking each condition's activations as functionally defined regions of interest, the specificity of no-go related activity was compared across the four conditions. Only methylphenidate demonstrat...

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Section: Summary Of Resultssupporting

confidence: 82%

Section: Summary Of Resultssupporting

confidence: 50%

Section: The Neuropsychology Of Error Awarenessmentioning

confidence: 99%

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Neurochemical and neurophysiological bases of executive control

Nandam¹

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“…Barnes et al (2014) (11). plasma levels for each of the study drugs (12)(13)(14) and doses were selected based upon 84 clinical relevance (15)(16)(17) and demonstrated cognitive effects (18)(19)(20).…”

Section: Processes 35 36mentioning

confidence: 99%

The Effects of Methylphenidate on the Neural Signatures of Sustained Attention

Dockree

Barnes

Matthews

et al. 2017

Biological Psychiatry

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“…Error-correction is an integral part of this predictive coding strategy for both the accurate propagation of representations and the adjustments to model structure. The monoaminergic system is exquisitely implicated in error processing and awareness of performance errors, which is especially important for adaptive goal-directed behavior [32, 33]. The major monoamine (MA) neuromodulators include histamine (HA), the catecholamines norepinephrine (NE) and dopamine (DA), and the indoleamine 5-hydroxytryptamine (5-HT) [34].…”

Section: Role Of the Monoaminergic System In Behavior And Its Relevanmentioning

confidence: 99%

Monoaminergic Control of Cellular Glucose Utilization by Glycogenolysis in Neocortex and Hippocampus

et al. 2015

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Brainstem nuclei are the principal sites of monoamine (MA) innervation to major forebrain structures. In the cortical grey matter, increased secretion of MA neuromodulators occurs in response to a wealth of environmental and homeostatic challenges, whose onset is associated with rapid, preparatory changes in neural activity as well as with increases in energy metabolism. Blood-borne glucose is the main substrate for energy production in the brain. Once entered the tissue, interstitial glucose is equally accessible to neurons and astrocytes, the two cell types accounting for most of cellular volume and energy metabolism in neocortex and hippocampus. Astrocytes also store substantial amounts of glycogen, but non-stimulated glycogen turnover is very small. The rate of cellular glucose utilization in the brain is largely determined by hexokinase, which under basal conditions is more than 90% inhibited by its product glucose-6-phosphate (Glc-6-P). During rapid increases in energy demand, glycogen is a primary candidate in modulating the intracellular level of Glc-6-P, which can occur only in astrocytes. Glycogenolysis can produce Glc-6-P at a rate higher than uptake and phosphorylation of glucose. MA neurotransmitter are released extrasinaptically by brainstem neurons projecting to neocortex and hippocampus, thus activating MA receptors located on both neuronal and astrocytic plasma membrane. Importantly, MAs are glycogenolytic agents and thus they are exquisitely suitable for regulation of astrocytic Glc-6-P concentration, upstream substrate flow through hexokinase and hence cellular glucose uptake. Conforming to such mechanism, Gerald A. Dienel and Nancy F. Cruz recently suggested that activation of noradrenergic locus coeruleus might reversibly block astrocytic glucose uptake by stimulating glycogenolysis in these cells, thereby anticipating the rise in glucose need by active neurons. In this paper, we further develop the idea that the whole monoaminergic system modulates both function and metabolism of forebrain regions in a manner mediated by glycogen mobilization in astrocytes.

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Monoaminergic modulation of behavioural and electrophysiological indices of error processing

Cited by 37 publications

References 85 publications

Neurochemical and neurophysiological bases of executive control

Neurochemical and neurophysiological bases of executive control

The Effects of Methylphenidate on the Neural Signatures of Sustained Attention

Monoaminergic Control of Cellular Glucose Utilization by Glycogenolysis in Neocortex and Hippocampus

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