The DOI matches its Crossref record; 137 of the 139 references it cites were found in a registry or an index; 10 of the 73 sources its claims cite were checked for support.
Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks
Open accessAbstract
The symptoms of attention-deficit/hyperactivity disorder (ADHD) involve impairments in prefrontal cortical top-down regulation of attention and behavior. All current pharmacological treatments for ADHD facilitate catecholamine transmission, and basic research suggests that these compounds have prominent actions in the prefrontal cortex (PFC). The dorsolateral PFC is especially sensitive to levels of norepinephrine and dopamine, whereby either too little or too much markedly impairs PFC function. Recent physiological studies have shown that norepinephrine strengthens PFC network connectivity and maintains persistent firing during a working memory task through stimulation of postsynaptic α(2A)-adrenoceptors on PFC neurons. Conversely, dopamine acts at D1 receptors to narrow spatial tuning, sculpting network inputs to decrease noise (i.e., stabilization of the representation). The stimulant medications and atomoxetine appear to enhance PFC function by indirectly increasing these catecholamine actions through blockade of norepinephrine and/or dopamine transporters. In contrast, guanfacine mimics the enhancing effects of norepinephrine at postsynaptic α(2A)-receptors in the PFC, strengthening network connectivity. Stronger PFC regulation of attention, behavior, and emotion likely contributes to the therapeutic effects of these medications for the treatment of ADHD.
Overview
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Written from the paper’s full text.
TL;DR
This review argues that dorsolateral prefrontal cortex function depends on an inverted-U level of norepinephrine and dopamine, with norepinephrine α2A receptors strengthening network connectivity and dopamine D1 receptors narrowing spatial tuning. ADHD medications likely work by indirectly increasing or mimicking these catecholamine actions to improve prefrontal top-down regulation.
Key findings
- Norepinephrine and dopamine both show inverted-U effects on dorsolateral prefrontal working memory: moderate arousal-related release improves function, while depletion/fatigue or stress-level release impairs it. Norepinephrine α2A stimulation enhances delay-period firing for preferred directions by inhibiting cAMP-HCN signaling, whereas α1/β1 stimulation under stress impairs prefrontal function.
- Dopamine D1/5 stimulation has a complementary sculpting role: optimal levels suppress firing to nonpreferred directions and sharpen spatial tuning, while high D1/5 stimulation suppresses all firing and impairs working memory. D2 receptors mainly affect response-related firing rather than delay-period firing.
- ADHD medications act through catecholamine mechanisms: methylphenidate blocks norepinephrine and dopamine transporters and is more potent for norepinephrine than dopamine in rat prefrontal cortex; atomoxetine blocks the norepinephrine transporter and raises both norepinephrine and dopamine in prefrontal cortex; guanfacine directly mimics norepinephrine at postsynaptic α2A receptors. Atomoxetine at 40 mg increased right inferior prefrontal activity during a stop-signal task, while a much higher dose impaired go/no-go performance.
- Blocking α2 receptors in monkey dorsolateral prefrontal cortex reproduces ADHD-like symptoms: yohimbine infusions induced locomotor hyperactivity, no-go commission errors, and working memory deficits. Genetic variants in dopamine β-hydroxylase and the α2A receptor have been associated with ADHD and impaired prefrontal executive function.
Methods
- Narrative review synthesizing basic and clinical literature on catecholamine modulation of dorsolateral prefrontal cortical networks, with emphasis on working memory circuits.
- Evidence base includes monkey electrophysiology and iontophoresis during spatial working memory tasks, rodent biochemistry and slice physiology, and human pharmacological, imaging, and genetic studies.
- Main analysis is conceptual integration of receptor-specific mechanisms (α2A, α1, β, D1/5, D2) and medication effects; no systematic search or meta-analysis is described.
Limitations
- Stated in the paper: PET imaging cannot detect dopamine interactions with receptors in prefrontal cortex; available D1 drugs act at both D1 and D5, so pharmacological studies cannot separate these mechanisms; D2 response-cell microcircuitry is less understood and it is unknown whether GABA interneurons influence response cells; D1 agonists likely cannot reproduce the dynamic range of endogenous dopamine; the proposed atomoxetine dose-response hypothesis remains to be tested.
- Stated in the paper: human guanfacine evidence is mixed, with some studies showing cognitive improvement and at least one (Muller et al.) finding no effects on executive or memory functions in healthy volunteers.
- Evident from the text: this is a narrative review rather than a primary study, with much mechanistic evidence from nonhuman animals and a focus on dorsolateral prefrontal spatial working memory; human causal and prefrontal receptor imaging data are limited.
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Claims the paper makes
31 No full text of the sources · 11 Own interpretation · 6 Partly supported · 2 Supported · 1 Supported so far · 1 Not checked yet · 1 No basis given · accuracy not yet measured
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“The stimulant medications and atomoxetine appear to enhance PFC function by indirectly increasing these catecholamine actions through blockade of norepinephrine and/or dopamine transporters.”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > Abstract
What the sources say
- Not checked — no full text of the sourcecites [83] Berridge, 2006, Methylphenidate preferentially increases catecholamine neurotransmission within the prefrontal cortex at low doses that enhance cognitive function, Biol Psychiatry source
- Supportedcites [90] Bymaster, 2002, Atomoxetine increases extracellular levels of norepinephrine and dopamine in prefrontal cortex of rat: A potential mechanism for efficacy in attention deficit/hyperactivity disorder, Neuropsychopharmacology source
The Discussion proposes that enhanced prefrontal catecholamine neurotransmission contributes to the efficacy of both psychostimulants and atomoxetine. It identifies atomoxetine as an NE-transporter inhibitor and reports that methylphenidate, a psychostimulant with affinity for the DA transporter, also raises prefrontal NE and DA. The paper presents improved PFC function as a proposed mechanism, consistent with the citing sentence’s hedge. Page numbers were not available in our copy. (LLM, conf=0.90)
hedgedconditional- Asserted: passes — The authors put it forward as true.
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Every source the paper cites for this claim was checked and supports it.
In the paper
“Research in rodent medial PFC has shown that D2 receptor stimulation can reduce GABAergic inputs to pyramidal cells (130).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > D2 Receptor Mechanisms
What the sources say
- Supportedcites [130] Seamans, 2001, Bidirectional dopamine modulation of GABAergic inhibition in prefrontal cortical pyramidal neurons, J Neurosci source
The Materials and Methods describe recordings from pyramidal neurons in rat prelimbic–infralimbic PFC slices, matching rodent medial PFC. The Discussion reports that D2 receptor activation reduced evoked GABAergic inhibitory currents in those neurons. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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- Supported
In the paper
“In contrast to α2A receptors, infusion of an α1 agonist directly into the dorsolateral PFC impairs working memory performance (42).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > The Underappreciated Role of Norepinephrine
What the sources say
- Not checked — no full text of the sourcecites [42] Mao, 1999, Local infusion of an alpha-1 adrenergic agonist into the prefrontal cortex impairs spatial working memory performance in monkeys, Biol Psychiatry source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Guanfacine administration to children with ADHD and tics improved performance of a Conners’ Continuous Performance Test task that requires sustained attention, working memory, and behavioral inhibition (95).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > NE Mechanisms and ADHD Medications
What the sources say
- Not checked — no full text of the sourcecites [95] Scahill, 2001, A placebo-controlled study of guanfacine in the treatment of children with tic disorders and attention deficit hyperactivity disorder, Am J Psychiatry source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“This research began with the landmark discovery that depletion of catecholamines from the dorsolateral PFC was as detrimental as ablation of the cortical tissue itself (4).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > The Strength of Network Connections Is Rapidly Altered by the Neurochemical Environment: Integrating Arousal and Cognition
What the sources say
- Not checked — no full text of the sourcecites [4] Brozoski, 1979, Cognitive deficit caused by regional depletion of dopamine in prefrontal cortex of rhesus monkey, Science source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Dopamine has an inverted U-shaped influence on working memory abilities via actions at the D1 receptor family in both animals (100) and humans (105).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > D1/5 Receptor Mechanisms
What the sources say
- Not checked — no full text of the sourcecites [100] Arnsten, 2009, Dopamine's influence on prefrontal cortical cognition: Actions and circuits in behaving primates source
- Not checked — no full text of the sourcecites [105] Gibbs, 2006, A functional magnetic resonance imaging study of the effects of pergolide, a dopamine receptor agonist, on component processes of working memory, Neuroscience source
plaindirect- Asserted: passes — The authors put it forward as true.
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A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“In contrast, guanfacine mimics the enhancing effects of norepinephrine at postsynaptic α2A-receptors in the PFC, strengthening network connectivity.”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > Abstract
What the sources say
- Not checked — no full text of the sourcecites [35] Arnsten, 1985, Alpha 2-adrenergic mechanisms in prefrontal cortex associated with cognitive decline in aged nonhuman primates, Science source
- Not checked — no full text of the sourcecites [41] Cai, 1993, Reserpine impairs spatial working memory performance in monkeys: Reversal by the alpha 2-adrenergic agonist clonidine, Brain Res source
- Not checked — no full text of the sourcecites [42] Mao, 1999, Local infusion of an alpha-1 adrenergic agonist into the prefrontal cortex impairs spatial working memory performance in monkeys, Biol Psychiatry source
- Not checked — no full text of the sourcecites [43] Ramos, 2006, Alpha2A-adrenoceptor stimulation improves prefrontal cortical regulation of behavior through inhibition of cAMP signaling in aging animals, Learn Mem source
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Stronger PFC regulation of attention, behavior, and emotion likely contributes to the therapeutic effects of these medications for the treatment of ADHD.”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > Abstract
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Biochemical studies in rats have consistently shown that both DA and NA release are increased in the medial PFC during acute stress exposure (30–32).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > The Strength of Network Connections Is Rapidly Altered by the Neurochemical Environment: Integrating Arousal and Cognition
What the sources say
- Not checked — no full text of the sourcecites [30] Roth, 1988, Stress and the mesocorticolimbic dopamine systems, Ann NY Acad Sci source
- Not checked — no full text of the sourcecites [31] Deutch, 1990, The determinants of stress-induced activation of the prefrontal cortical dopamine system, Prog Brain Res source
- Not checked — no full text of the sourcecites [32] Finlay, 1995, Increased dopamine and norepinephrine release in medial prefrontal cortex induced by acute and chronic stress: Effects of diazepam, Neuroscience source
boosteddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Recent physiological studies have shown that norepinephrine strengthens PFC network connectivity and maintains persistent firing during a working memory task through stimulation of postsynaptic α2A-adrenoceptors on PFC neurons.”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > Abstract
What the sources say
- Not checked — no full text of the sourcecites [57] Wang, 2007, Alpha2A-adrenoceptors strengthen working memory networks by inhibiting cAMP-HCN channel signaling in prefrontal cortex, Cell source
plaindirect- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 20
- Probably not a substantial claim. 1
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Systemic administration of an α1 agonist that crosses the blood brain barrier also impairs working memory performance, while administration of an α1 antagonist, e.g., prazosin, can protect working memory performance during stress (37,50,51).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > The Underappreciated Role of Norepinephrine
What the sources say
- Partly supportedcites [37] Birnbaum, 1999, A role for norepinephrine in stress-induced cognitive deficits: Alpha-1-adrenoceptor mediation in the prefrontal cortex, Biol Psychiatry sourceExperimental — accuracy not yet measured
The Discussion reports that α1 stimulation in the prefrontal cortex impairs spatial working memory and that intra-PFC urapidil reversed a pharmacological stressor’s effect on response accuracy in rats (page not available in our copy). It does not establish that a blood–brain-barrier-crossing α1 agonist was administered systemically, or that prazosin protected working memory during stress; its prazosin example concerns performance under nonstress conditions. (LLM, conf=0.86)
- Partly supportedcites [50] Arnsten, 1997, The alpha-1 adrenergic agonist, cirazoline, impairs spatial working memory performance in aged monkeys, Pharmacol Biochem Behav sourceExperimental — accuracy not yet measured
The Drug Administration and Results sections report systemic cirazoline treatment in aged monkeys, impaired spatial working memory, and reversal of that impairment by prazosin (page numbers unavailable). The Discussion proposes that α1 mechanisms may contribute to cognitive impairment during stress, but the paper does not show that prazosin protects working memory during stress. It describes cirazoline's brain penetrance as purported rather than directly demonstrating it. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [51] Arnsten, 1999, Alpha-1 noradrenergic receptor stimulation impairs prefrontal cortical cognitive function, Biol Psychiatry source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Like methylphenidate, atomoxetine also blocks the NE transporter (Figure 2E), and as the NE transporter clears both NE and DA in the PFC, this increases extracellular levels of both catecholamines (90).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > NE Mechanisms and ADHD Medications
What the sources say
- Partly supportedcites [90] Bymaster, 2002, Atomoxetine increases extracellular levels of norepinephrine and dopamine in prefrontal cortex of rat: A potential mechanism for efficacy in attention deficit/hyperactivity disorder, Neuropsychopharmacology sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) reports that atomoxetine inhibits the NE transporter, that this transporter takes up dopamine in the PFC, and that atomoxetine increases extracellular NE and dopamine there. It presents transporter-mediated dopamine clearance as a proposed explanation, however, and says other interactions may also contribute; the citing sentence states that causal explanation more definitively than the paper does. (LLM, conf=0.82)
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“A common misconception is that methylphenidate is a selective DA transporter blocker, when in actuality it blocks both NE and DA transporters. Indeed, methylphenidate has more potent effects on NE than DA in the rat PFC (83) (84).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > NE Mechanisms and ADHD Medications
What the sources say
- Not checked — no full text of the sourcecites [83] Berridge, 2006, Methylphenidate preferentially increases catecholamine neurotransmission within the prefrontal cortex at low doses that enhance cognitive function, Biol Psychiatry source
- Partly supportedcites [84] Berridge, 2011, Psychostimulants as cognitive enhancers: The prefrontal cortex, catecholamines, and attention-deficit/hyperactivity disorder, Biol Psychiatry sourceExperimental — accuracy not yet measured
The section “Neurochemical Actions of Low-Dose Psychostimulants” (page not supplied) states that methylphenidate blocks both NE and DA reuptake and increases both in the rat PFC. It does not say that its effects on NE are more potent than its effects on DA in the rat PFC. (LLM, conf=0.86)
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Data from studies of monkey dorsolateral PFC demonstrate an inverted-U dose-response: moderate levels of NE released during alert, nonstressed waking improve working memory performance by engaging postsynaptic, α2A receptors (35,36), whereas high levels of NE released during stress impair PFC function via stimulation of lower affinity α1 (37) and β1 receptors (38).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > The Underappreciated Role of Norepinephrine
What the sources say
- Not checked — no full text of the sourcecites [35] Arnsten, 1985, Alpha 2-adrenergic mechanisms in prefrontal cortex associated with cognitive decline in aged nonhuman primates, Science source
- Not checked — no full text of the sourcecites [36] Li, 1994, Delayed-response deficit induced by local injection of the alpha 2-adrenergic antagonist yohimbine into the dorsolateral prefrontal cortex in young adult monkeys, Behav Neural Biol source
- Partly supportedcites [37] Birnbaum, 1999, A role for norepinephrine in stress-induced cognitive deficits: Alpha-1-adrenoceptor mediation in the prefrontal cortex, Biol Psychiatry sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Not checked — no full text of the sourcecites [38] Ramos, 2005, The beta-1 adrenergic antagonist, betaxolol, improves working memory performance in rats and monkeys, Biol Psychiatry source
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
Every source the paper cites for this claim was checked and supports it.
In the paper
“Norepinephrine has the highest affinity for α2 adrenergic receptors and lower affinity for α1 and β receptors (34).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > The Underappreciated Role of Norepinephrine
What the sources say
- Supportedcites [34] Arnsten, 2000, Through the looking glass: Differential noradenergic modulation of prefrontal cortical function, Neural Plast source
The discussion and Fig. 4 caption (pp. 141–142) state that norepinephrine has higher affinity for α2A receptors than for α1 or β receptors. The claim paraphrases this comparison, using the broader α2 label for the α2A subtype specified in the paper. (LLM, conf=0.93)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Cognitive studies in animals have shown that either blockade of D1/5 receptors or excessive stimulation of D1/5 receptors in the PFC impairs spatial working memory (106–108).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > D1/5 Receptor Mechanisms
What the sources say
- Not checked yetcites [106] Arnsten, 1990, Stress impairs prefrontal cortex cognitive function in monkeys: Role of dopamine, Soc Neurosci Abstr
- Not checked — no full text of the sourcecites [107] Sawaguchi, 1991, D1 dopamine receptors in prefrontal cortex: Involvement in working memory, Science source
- Partly supportedcites [108] Zahrt, 1997, Supranormal stimulation of D1 dopamine receptors in the rodent prefrontal cortex impairs spatial working memory performance, J Neurosci sourceExperimental — accuracy not yet measured
The paper reports that excessive D1 receptor stimulation in rat PFC impaired delayed-alternation performance, a spatial working-memory task. Its introduction also describes evidence that insufficient D1 stimulation impairs PFC cognition, but this study’s antagonist dose alone did not impair performance (Experiment 2, page unavailable). The passages identify D1 receptors, not D1/5 receptors, so the D5 part of the claim is not established by this source. (LLM, conf=0.86)
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The D2 receptors are less prevalent in monkey dorsolateral PFC and are concentrated on layer V neurons, the layer that projects to striatum and the superior colliculus (98,122,123).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > D2 Receptor Mechanisms
What the sources say
- Not checked — no full text of the sourcecites [98] Lidow, 1998, Layer V neurons bear the majority of mRNAs encoding the five distinct dopamine receptor subtypes in the primate prefrontal cortex, Synapse source
- Partly supportedcites [122] Lidow, 1989, Dopamine D2 receptors in the cerebral cortex: Distribution and pharmacological characterization with [3H]raclopride, Proc Natl Acad Sci U S A sourceExperimental — accuracy not yet measured
The Discussion reports that D2 binding sites are considerably less concentrated in primate cortex than in the neostriatum, and the Results report binding in monkey prefrontal cortex. The paper does not establish that receptors are concentrated on layer V neurons or identify layer V projections to the striatum and superior colliculus; it measures binding by cortical region, not neuronal layer. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites [123] Lidow, 1991, Distribution of dopaminergic receptors in the primate cerebral cortex: quantitative autoradiographic analysis using [3H]raclopride, [3H]spiperone and [3H]SCH23390, Neuroscience source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
In the paper
“Dopamine neurons have not been followed as methodically with regard to states of arousal but have been shown to fire related to prediction of reward (28).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > The Strength of Network Connections Is Rapidly Altered by the Neurochemical Environment: Integrating Arousal and Cognition
What the sources say
- Not checked — no full text of the sourcecites [28] Schultz, 1998, The phasic reward signal of primate dopamine neurons, Adv Pharmacol source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Stimulation of α2A receptors increases delay-related firing of PFC neurons via inhibition of cyclic adenosine mono-phosphate (cAMP) (57), while stimulation of α1 receptors decreases delay-related firing via activation of phosphatidylinositol protein kinase C signaling (58).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > The Underappreciated Role of Norepinephrine
What the sources say
- Not checked — no full text of the sourcecites [57] Wang, 2007, Alpha2A-adrenoceptors strengthen working memory networks by inhibiting cAMP-HCN channel signaling in prefrontal cortex, Cell source
- Not checked — no full text of the sourcecites [58] Birnbaum, 2004, Protein kinase C overactivity impairs prefrontal cortical regulation of working memory, Science source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Stimulation of α2A receptors strengthens firing for the neuron’s preferred direction by inhibiting cAMP production, which, in turn, reduces cAMP opening of potassium channels, increasing the efficacy of nearby synaptic inputs (Figure 2E).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > The Underappreciated Role of Norepinephrine
What the sources say
- Not checked — no full text of the sourcecites [57] Wang, 2007, Alpha2A-adrenoceptors strengthen working memory networks by inhibiting cAMP-HCN channel signaling in prefrontal cortex, Cell source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“The dorsolateral PFC is especially sensitive to levels of norepinephrine and dopamine, whereby either too little or too much markedly impairs PFC function.”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > Abstract
What the sources say
- Not checked — no full text of the sourcecites [4] Brozoski, 1979, Cognitive deficit caused by regional depletion of dopamine in prefrontal cortex of rhesus monkey, Science source
- Not checked — no full text of the sourcecites [5] Arnsten, 1985, Stress produces opioid-like effects on investigatory behavior, Pharmacol Biochem Behav source
- Not checked — no full text of the sourcecites [6] Roberts, 1994, 6-Hydroxydopamine lesions of the prefrontal cortex in monkeys enhance performance on an analog of the Wisconsin Card Sort Test: Possible interactions with subcortical dopamine, J Neurosci source
- Not checked — no full text of the sourcecites [7] Robbins, 2007, Differential regulation of fronto-executive function by the monoamines and acetylcholine, Cereb Cortex source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Either depletion of NE (35) or blockade of α2A receptors in PFC (36) impairs working memory performance in monkeys, suggesting that endogenous NE plays a large role in strengthening working memory performance.”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > The Underappreciated Role of Norepinephrine
What the sources say
- Not checked — no full text of the sourcecites [35] Arnsten, 1985, Alpha 2-adrenergic mechanisms in prefrontal cortex associated with cognitive decline in aged nonhuman primates, Science source
- Not checked — no full text of the sourcecites [36] Li, 1994, Delayed-response deficit induced by local injection of the alpha 2-adrenergic antagonist yohimbine into the dorsolateral prefrontal cortex in young adult monkeys, Behav Neural Biol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Norepinephrine neurons in the locus coeruleus are silent during rapid eye movement sleep and have low tonic firing during slow wave sleep, moderate tonic firing and pronounced phasic firing to relevant stimuli during nonstressed waking, and high tonic firing with dysregulated phasic firing during stress (27).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > The Strength of Network Connections Is Rapidly Altered by the Neurochemical Environment: Integrating Arousal and Cognition
What the sources say
- Not checked — no full text of the sourcecites [27] Aston-Jones, 1999, Role of locus coeruleus in attention and behavioral flexibility, Biol Psychiatry source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These studies have revealed that NE and DA have complementary effects on the strength of PFC network connections, with NE strengthening connectivity via α2A receptor stimulation and DA sculpting network inputs via D1 receptors.”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
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A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Iontophoresis of an α2A agonist such as guanfacine onto PFC neurons enhances neuronal firing during the delay period for the neurons’ preferred direction (Figure 3A), while blockade of α2A receptors markedly reduces PFC neuronal firing during the delay period (indeed, high doses can silence a neuron) (57,61).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > The Underappreciated Role of Norepinephrine
What the sources say
- Not checked — no full text of the sourcecites [57] Wang, 2007, Alpha2A-adrenoceptors strengthen working memory networks by inhibiting cAMP-HCN channel signaling in prefrontal cortex, Cell source
- Not checked — no full text of the sourcecites [61] Li, 1999, Alpha-2 adrenergic modulation of prefrontal cortical neuronal activity related to spatial working memory in monkeys, Neuropsychopharmacology source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“All medications currently approved for the treatment of ADHD influence NE transmission (Figure 2E), and all can improve at least some aspects of PFC function (82).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > NE Mechanisms and ADHD Medications
What the sources say
- Not checked — no full text of the sourcecites [82] Chamberlain, 2011, Translational approaches to frontostriatal dysfunction in attention-deficit/hyperactivity disorder using a computerized neuropsychological battery, Biol Psychiatry source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Animal studies have also shown that the enhancing effects of methylphenidate and atomoxetine on working memory performance involve D1/5 receptor stimulation, as well as the NE α2 receptor actions described above.”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > DA Mechanisms and ADHD Medications
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Studies of catecholamine actions on dorsolateral PFC microcircuitry have revealed intricate and powerful mechanisms to regulate the strength of persistent neuronal firing and the degree of neuronal tuning.”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > Conclusions
boosteddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Iontophoresis of D2 drugs onto PFC neurons has no effect on delay cell firing during the delay period in a working memory task but has marked effects on response cell firing in relationship to the eye movement response (124).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > D2 Receptor Mechanisms
What the sources say
- Not checked — no full text of the sourcecites [124] Wang, 2004, Selective D2 receptor actions on the functional circuitry of working memory, Science source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“On the other hand, stimulants likely enhance motivation and other striatal functions not engaged by NE medications (135).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > DA Mechanisms and ADHD Medications
What the sources say
- Not checked — no full text of the sourcecites [135] Cousins, 1996, Nucleus accumbens dopamine depletions alter relative response allocation in a T-maze cost/benefit task, Behav Brain Res source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Thus, DA and NE have complementary roles: NE α2A receptor stimulation enhances network firing for shared, preferred inputs (i.e., increasing signals [57]), whereas D1 receptor stimulation sculpts neuronal firing by decreasing firing to nonpreferred inputs (i.e., decreasing noise [109]).”
§ Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks > D1/5 Receptor Mechanisms
What the sources say
- Not checked — no full text of the sourcecites [57] Wang, 2007, Alpha2A-adrenoceptors strengthen working memory networks by inhibiting cAMP-HCN channel signaling in prefrontal cortex, Cell source
- Not checked — no full text of the sourcecites [109] Vijayraghavan, 2007, Inverted-U dopamine D1 receptor actions on prefrontal neurons engaged in working memory, Nat Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
Many symptoms of ADHD arise from dysfunction of the prefrontal cortex and its connections with cortical and subcortical brain regions.
“As described in this special issue, many of the symptoms of attention-deficit/hyperactivity disorder (ADHD) are thought to arise from dysfunction of the prefrontal cortex (PFC) and its connections with cortical and subcortical brain regions.”
The paper relies on this without support.
Prefrontal cortex networks are able to represent information in the absence of bottom-up external stimulation, but this fragile process is tremendously dependent on the correct neurochemical environment.
“Prefrontal cortex networks are able to represent information in the absence of bottom-up external stimulation, but this fragile process is tremendously dependent on the correct neurochemical environment, whereby arousal pathways coordinate cognitive state with environmental events.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“microdialysis studies suggest that atomoxetine may selectively increase dopamine levels in the prefrontal cortex, via the norepinephrine transporter or perhaps via a secondary signaling mechanism [23].”
From Atomoxetine Effects on Executive Function as Measured by the BRIEF-A in Young Adults with ADHD: A Randomized, Double-Blind, Placebo-Controlled Study (2014) · cites this paper as [23]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“However, excessive DA stimulation might cause PFC dysfunction leading to impaired inhibition of undesirable behavior, and a deficit in sustaining attention, as these two behaviors are highly regulated by dopaminergic release in the PFC (Russell, 2003; Brennan and Arnsten, 2008; Arnsten, 2011).”
From The Effects of Methylphenidate on Goal-directed Behavior in a Rat Model of ADHD (2015) · cites this paper as Arnsten, 2011
In the citing paper
“Reduced catecholamine transmission has been linked to ADHD, while overamplified noradrenergic transmission is associated with PTSD 46.”
From Mechanisms of synaptic transmission dysregulation in the prefrontal cortex: pathophysiological implications (2022) · cites this paper as [46]
In the citing paper
“Stimulation of D1R produces an inverted-U dose response on PFC neuronal firing and cognitive performance during working memory tasks 46.”
From Mechanisms of synaptic transmission dysregulation in the prefrontal cortex: pathophysiological implications (2022) · cites this paper as [46]
In the citing paper
“Norepinephrine (NE) and dopamine (DA) are believed to modulate attention and other cognitive capabilities105, generally with dose–response following classic inverted-U shaped curves.”
From Paying attention to attention in depression (2019) · cites this paper as [105]
In the citing paper
“both neuromodulators have distinct roles to facilitate information processing in the prefrontal cortex [33, 34].”
In the citing paper
“Although much previous work on cognitive functioning has stressed the importance of intact dopaminergic levels, particularly with respect to functions mediated by prefrontal cortex, such as working memory, it is now being recognized that norepinephrine plays a similarly important role [33]”
Citations
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Cited by
Sorted by citations
Items 201–300 of 494
The computational pharmacology of oculomotion
Parr, T., & Friston, K. J. (2019) · Psychopharmacology · doi:10.1007/s00213-019-05240-0 · Cited by 21
“Despite this, there is evidence for neurophysiological changes in circuits implicated in task performance when prefrontal α 2-adrenoreceptors are modulated (Arnsten 2011; Arnsten and Li 2005; Sawaguchi et al. 1990).”
BackgroundPrediction of sleep side effects following methylphenidate treatment in ADHD youth
Yoo, J. H., Sharma, V., Kim, J. W., McMakin, D. L., Hong, S.-B., Zalesky, A., Kim, B.-N., & Ryan, N. D. (2019) · NeuroImage Clinical · doi:10.1016/j.nicl.2019.102030 · Cited by 23
Acute vagus nerve stimulation enhances reversal learning in rats
Altidor, L., Bruner, M. M., Deslauriers, J. F., Garman, T. S., Ramirez, S., Dirr, E. W., Olczak, K. P., Maurer, A. P., Lamb, D. G., Otto, K. J., et al. (2021) · Neurobiology of Learning and Memory · doi:10.1016/j.nlm.2021.107498 · Cited by 20
Heterogeneous organization of Locus coeruleus: An intrinsic mechanism for functional complexity
Ma, H., Zhang, H.-C., Zuo, Z., & Liu, Y. (2023) · Physiology & Behavior · doi:10.1016/j.physbeh.2023.114231 · Cited by 24
Perez-Palomar, B., Erdozain, A. M., Erkizia-Santamaría, I., Ortega, J. E., & Meana, J. J. (2023) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-023-10070-1 · Cited by 22
“Indeed, extracellular concentrations of dopamine (DA) and noradrenaline (NA) in the area act in concert and may rapidly alter the strength of the PFC network connections to coordinate cognitive status with physiological demands [4, 6, 7].”
BackgroundPillidge, K., Porter, A. J., Dudley, J., Tsai, Y., Heal, D. J., & Stanford, S. C. (2014) · British Journal of Pharmacology · doi:10.1111/bph.12860 · Cited by 23
“Noradrenergic signalling strongly influences frontal cortical regions that mediate attention and working memory (see Arnsten and Li, 2005; Robbins and Roberts, 2007) and the classical bell-shaped treatment/response curve applies (Aston-Jones and Cohen, 2005; Arnsten, 2011).”
Ott, T., Stein, A. M., & Nieder, A. (2023) · Nature Communications · doi:10.1038/s41467-023-43271-6 · Cited by 26
van Amelsvoort, T., & Hernaus, D. (2016) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2016.00082 · Cited by 21
“While preliminary, the combination of atypical antipsychotics and atomoxetine may have led to overstimulation of frontal cortex dopamine and noradrenaline release, thereby missing the narrow window in which frontal cortex dopamine and noradrenaline levels optimally mediate cognitive performance (163, 167).”
Foote, S. L., & Berridge, C. W. (2018) · Brain Research · doi:10.1016/j.brainres.2018.09.033 · Cited by 20
“Nonetheless, Arnsten and colleagues have largely observed comparable actions of NE on prefrontal cortex-dependent cognitive function across rat, monkey, and in the context of the pharmacology of ADHD, humans (Arnsten, 2011).”
BackgroundWillmott, C., Ponsford, J. L., McAllister, T. W., & Burke, R. (2013) · Brain Injury · doi:10.3109/02699052.2013.809553 · Cited by 21
“The authors interpreted the findings in the context of the inverted-U hypothesis of prefrontal dopaminergic function [26].”
BackgroundBraz, B. Y., Galiñanes, G. L., Taravini, I. R. E., Belforte, J. E., & Murer, M. G. (2015) · Neuropsychopharmacology · doi:10.1038/npp.2015.104 · Cited by 21
The Effects of Methylphenidate on Goal-directed Behavior in a Rat Model of ADHD
Natsheh, J. Y., & Shiflett, M. W. (2015) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2015.00326 · Cited by 21
“The therapeutic dose of MPH works primarily via (1) increasing DA signaling through multiple actions, including DAT blockade in the PFC, and significantly enhancing extracellular DA release in the striatum (Volkow et al., 2002; Wilens, 2008) and (2) indirectly increasing NE actions through blockade of its transporters…”
BackgroundInfluentialSandiego, C. M., Matuskey, D., Lavery, M. E., McGovern, E. M., Huang, Y. H., Nabulsi, N., Ropchan, J. R., Picciotto, M. R., Morris, E. D., McKee, S. A., et al. (2017) · Neuropsychopharmacology · doi:10.1038/npp.2017.223 · Cited by 21
“The dlPFC is particularly sensitive to catecholamine levels (Arnsten, 2011), and aberrant norepinephrine and dopamine levels, such as are found in cognitive and stressrelated disorders, can compromise the ability to manage arousal and executive function.”
BackgroundInfluentialHeinrichs‐Graham, E., Franzen, J. D., Knott, N. L., White, M. L., Wetzel, M. W., & Wilson, T. W. (2014) · Psychiatry Research Neuroimaging · doi:10.1016/j.pscychresns.2014.01.002 · Cited by 21
“Multiple brain imaging studies have shown volumetric structural deficits, functional aberrations, and abnormal structural and functional connectivity involving prefrontal regions in both children and adults with ADHD (Konrad and Eickhoff, 2010; Arnsten, 2011; Liston et al., 2011).”
BackgroundResultInfluentialRamasubbu, R., Singh, H., Zhu, H., & Dunn, J. F. (2012) · Human Psychopharmacology: Clinical and Experimental · doi:10.1002/hup.2258 · Cited by 20
Atomoxetine treatment in adults with attention-deficit/hyperactivity disorder
Walker, D. J., Mason, O., Clemow, D. B., & Day, K. A. (2015) · Postgraduate Medicine · doi:10.1080/00325481.2015.1081046 · Cited by 20
“Selective a2-adrenergic receptor agonists (including guanfacine and clonidine) directly mimic the effects of NE at postsynaptic a2A-adrenergic receptors [20,21], but guanfacine and clonidine do not have indications for treatment of adult ADHD.”
BackgroundMotor impulsivity in Parkinson disease: Associations with COMT and DRD 2 polymorphisms
Ziegler, D. A., Ashourian, P., Wonderlick, J. S., Sarokhan, A. K., Prelec, D., Scherzer, C. R., & Corkin, S. (2014) · Scandinavian Journal of Psychology · doi:10.1111/sjop.12113 · Cited by 20
“Further, too much dopamine in the PFC results in a general reduction in neuronal activity (Arnsten, 2011; Kroener, Chandler, Phillips & Seamans, 2009; Wang, Vijayraghavan & Goldman-Rakic, 2004).”
BackgroundBhardwaj, S. K., Tse, Y. C., Ryan, R., Wong, T. P., & Srivastava, L. K. (2014) · Neuropsychopharmacology · doi:10.1038/npp.2014.142 · Cited by 21
“NE is increasingly being recognized as an important modulator of prefrontal cognitive functions, impairments in which is a hallmark of schizophrenia and other psychiatric disorders (Arnsten, 2011).”
InfluentialTian, X., Richard, A. D., El-Saadi, M. W., Bhandari, A., Latimer, B., Savage, I. V., Holmes, K., Klein, R. L., Dwyer, D. S., Goeders, N. E., et al. (2019) · Molecular Psychiatry · doi:10.1038/s41380-019-0492-3 · Cited by 20
Biomarkers for ADHD: the Present and Future Directions
Mehta, T., Mannem, N., Yarasi, N., & Bollu, P. C. (2020) · Current Developmental Disorders Reports · doi:10.1007/s40474-020-00196-9 · Cited by 20
Wanner, P., Müller, T., Cristini, J., Pfeifer, K., & Steib, S. (2019) · Neuroscience · doi:10.1016/j.neuroscience.2019.11.027 · Cited by 24
Khandekar, P., Shenoy, S., & Sathe, A. (2022) · The Journal of General Psychology · doi:10.1080/00221309.2022.2048785 · Cited by 20
“Noradrenaline is responsible for activation of dorsolateral prefrontal cortex, anterior cingulate cortx and hippocampus which are involved in cognitive processing, resulting in a more efficient allocation of resources (Arnsten, 2011).”
BackgroundAvery, M. C., Dutt, N. D., & Krichmar, J. L. (2013) · Frontiers in Computational Neuroscience · doi:10.3389/fncom.2013.00133 · Cited by 22
“When keeping the DA concentration optimal and varying the NE concentration (Figure 5A), we also find a similar invertedU dose-response function as was shown in Arnsten (2011).”
BackgroundResultInfluentialBenn, A., & Robinson, E. S. J. (2016) · Psychopharmacology · doi:10.1007/s00213-016-4458-8 · Cited by 19
“In removing the noradrenergic input to the PFC, we may have created an imbalance in noradrenergic versus dopaminergic modulation meaning that the effects of amphetamine were potentiated (Arnsten 2011).”
BackgroundByun, K., Hyodo, K., Suwabe, K., Fukuie, T., & Soya, H. (2016) · The Journal of Physical Fitness and Sports Medicine · doi:10.7600/jpfsm.5.361 · Cited by 21
Learning Experience Reverses Catecholaminergic Effects on Adaptive Behavior
Mückschel, M., Eggert, E., Prochnow, A., & Beste, C. (2019) · The International Journal of Neuropsychopharmacology · doi:10.1093/ijnp/pyz058 · Cited by 19
“The catecholaminergic system, including norepinephrine (NE) and dopamine (DA), is central for many cognitive processes, including cognitive control mechanisms (Robbins and Arnsten, 2009; Arnsten, 2011).”
BackgroundSchrantee, A., Mutsaerts, H. J. M. M., Bouziane, C., Tamminga, H. G. H., Bottelier, & Reneman, L. (2016) · NeuroImage Clinical · doi:10.1016/j.nicl.2016.11.021 · Cited by 19
“Its therapeutic ef fi cacy has largely been ascribed to its ability to prevent reuptake of catecholamines, such as dopamine (DA) and noradrenalin (NA), thereby enhancing DAergic and noradrenergic neurotransmission (Arnsten, 2011).”
Perceptual salience does not influence emotional arousal’s impairing effects on top-down attention.
Sutherland, M. R., McQuiggan, D. A., Ryan, J. D., & Mather, M. (2017) · Emotion · doi:10.1037/emo0000245 · Cited by 20
Cieślak, P. E., Llamosas, N., Kos, T., Ugedo, L., Jastrzębska, K., Torrecilla, M., & Parkitna, J. M. R. (2017) · Genes Brain & Behavior · doi:10.1111/gbb.12383 · Cited by 19
“α1) thus shifting control of behavior toward the amygdala and striatum (Arnsten 2011; Berridge et al. 2012).”
BackgroundZhi, J., Zhang, S., Huang, M., Qin, H., He, X., Chang, Q., & Wang, Y. (2024) · Frontiers in Neuroscience · doi:10.3389/fnins.2024.1494272 · Cited by 19
Tong, J., McKinley, L., Cummins, T. D. R., Johnson, B. P., Matthews, N. L., Vance, A. L. A., Heussler, H., Gill, M., Kent, L., Bellgrove, M. A., et al. (2015) · The World Journal of Biological Psychiatry · doi:10.3109/15622975.2015.1036771 · Cited by 18
“Convergent evidence from pharmacology, animal models, neuropsychology and brain imaging, suggests that dysregulated catecholamine signalling is a key pathophysiological substrate for ADHD (Pliszka 2005; Arnsten 2011).”
BackgroundHeterogeneous organization and function of the central noradrenergic system
Waterhouse, B. D., & Chandler, D. J. (2015) · Brain Research · doi:10.1016/j.brainres.2015.12.050 · Cited by 22
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“Often examined neurobiological factors on set shifting performance are catecholamines (Arnsten, 2011) and the brain-derived neurotrophic factor (BDNF) (Nakazato et al.”
BackgroundThe Unique Properties of the Prefrontal Cortex and Mental Illness
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“[145] Levy, F. and M. Farrow, Working memory in ADHD: prefrontal/parietal connections.”
BackgroundInfluentialBraun, U., Harneit, A., Pergola, G., Menara, T., Schaefer, A., Betzel, R. F., Zang, Z., Schweiger, J. I., Schwarz, K., Chen, J., et al. (2019) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/679670 · Cited by 20
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“These nuclei are structurally and functionally connected to the hippocampus and prefrontal cortex (Arnsten, 2011).”
BackgroundMcMorris, T., Hale, B. J., Pine, B. S., & Williams, T. B. (2024) · Behavioural Brain Research · doi:10.1016/j.bbr.2024.114982 · Cited by 19
“However, this hypothesis is primarily the result of studies with rodents, which have used far greater stressors than are used in human studies [7, 8].”
Effects of DSP4 and methylphenidate on spatial memory performance in rats
Sontag, T. A., Hauser, J., Tucha, O. M., & Lange, K. W. (2011) · ADHD Attention Deficit and Hyperactivity Disorders · doi:10.1007/s12402-011-0067-x · Cited by 17
“The prevailing theory regarding the neurobiology of ADHD suggests an imbalance of dopamine and noradrenaline in the prefrontal cortex (Arnsten 2009, 2011; Himelstein et al. 2000).”
BackgroundMethylphenidate alleviates manganese-induced impulsivity but not distractibility
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Normalization of increased retinal background noise after ADHD treatment: A neuronal correlate
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“The relationship has been conceptualized as an inverted U-shaped curve (Arnsten, 2011) whereby either too low or too high levels of either dopamine (Dreher et al.”
BackgroundMartínez-Torres, N. I., Vázquez-Hernández, N., Martín-Amaya-Barajas, F. L., Flores-Soto, M. E., & González‐Burgos, I. (2021) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2021.173883 · Cited by 16
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“Although we did not assess adrenaline and noradrenaline level directly in the brain, excess noradrenaline appears to impair prefrontal cortex function including cognitive function in the brain (Arnsten, 2011).”
BackgroundWatt, M. L., Rorick‐Kehn, L. M., Shaw, D. B., et al. (2013) · Neuropsychopharmacology · doi:10.1038/npp.2013.186 · Cited by 16
“As D1 receptors reside on dendritic spines in key frontal cortical structures and modulate the integrity of cortical networks (Arnsten, 2011), the close neuroanatomical and functional relationship between M4 and D1 receptors would be predicted to affect both cortical and striatal functioning, key substrates that are d…”
Mückschel, M., Roessner, V., & Beste, C. (2020) · European Neuropsychopharmacology · doi:10.1016/j.euroneuro.2020.03.013 · Cited by 16
Psychopharmacological characterisation of the successive negative contrast effect in rats
Phelps, C. E., Mitchell, E. N., Nutt, D., Marston, H. M., & Robinson, E. S. J. (2015) · Psychopharmacology · doi:10.1007/s00213-015-3905-2 · Cited by 15
“This increase in premature responding may involve a specific effect on impulse control and the proposal that α2-adrencoceptors play an important role in regulating this behaviour (Franowicz et al. 2002; Arnsten 2011).”
BackgroundOwens, J. A., Spitz, G., Ponsford, J., Dymowski, A. R., Ferris, N., & Willmott, C. (2016) · Brain and Behavior · doi:10.1002/brb3.608 · Cited by 12
“Dysfunction of DA circuitry has previously been found in other clinical groups demonstrating attentional deficits, particularly Attention Deficit/ Hyperactivity Disorder (see del Campo, Chamberlain, Sahakian, & Robbins, 2011 for review), with administration of DA agonists found to ameliorate attentional impairments (A…”
BackgroundFridman, E. A., & Schiff, N. D. (2021) · Journal of Clinical Neurophysiology · doi:10.1097/wnp.0000000000000729 · Cited by 16
Robust encoding of stimulus–response mapping by neurons in visual cortex
Jonikaitis, D., Xia, R., & Moore, T. (2025) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2408079122 · Cited by 17
Kennett, A., Heal, D. J., & Wonnacott, S. (2012) · Nicotine & Tobacco Research · doi:10.1093/ntr/nts128 · Cited by 15
Improvement of attention with amphetamine in low- and high-performing rats
Turner, K. M., & Burne, T. H. J. (2016) · Psychopharmacology · doi:10.1007/s00213-016-4376-9 · Cited by 15
Furlong, T. M., Pan, M. J., & Corbit, L. H. (2015) · Translational Psychiatry · doi:10.1038/tp.2015.130 · Cited by 17
Rubio, G., Lopez-Munoz, F. J., Barba, R. J., Martínez‐Gras, I., Rodríguez–Jiménez, R., Espinosa, R., Nieto, M. Á. P., Moratti, S., Jiménez‐Arriero, M. Á., & Leza, J. C. (2015) · Psychiatry Research · doi:10.1016/j.psychres.2015.05.097 · Cited by 16
“On the other hand, the chronic stress would produce a loss of neuronal spines in these same areas (Arnsten, 2011).”
BackgroundLane, T. A., Boerner, T., Bannerman, D. M., Kew, J. N. C., Tunbridge, E. M., Sharp, T., & Harrison, P. J. (2013) · BMC Neuroscience · doi:10.1186/1471-2202-14-102 · Cited by 14
Sun, Z., Ma, Y., Li, W., He, J., Li, J., Yang, X., Mao, P., Cubells, J. F., & Tang, Y. (2017) · Schizophrenia Research · doi:10.1016/j.schres.2017.06.028 · Cited by 15
“Such a change could alter the balance between dopaminergic and noradrenergic systems in the brain, which may in turn alter cognitive performance (Arnsten, 2011; Cubells and Zabetian, 2004).”
Effects of reward on spatial working memory in schizophrenia.
Cho, Y., Lam, N. H., Starc, M., Santamauro, N. P., Savić, A., Diehl, C., Schleifer, C. H., Moujaes, F., Srihari, V. H., Repovš, G., et al. (2018) · Journal of Abnormal Psychology · doi:10.1037/abn0000369 · Cited by 15
“This model simulated a local cortical microcircuit containing thousands of spiking excitatory (E) pyramidal cells, individually tuned to angular location (Arnsten, 2011), and untuned inhibitory (I) interneurons.”
Eggert, E., Bluschke, A., Takács, Á., Kleimaker, M., Münchau, A. M., Roessner, V., Mückschel, M., & Beste, C. (2021) · The International Journal of Neuropsychopharmacology · doi:10.1093/ijnp/pyab012 · Cited by 14
“…catecholaminergic system plays a central role in the stability of information in working memory (Seamans and Yang, 2004; Robbins and Arnsten, 2009; Arnsten, 2011; Cools and D’Esposito, 2011), and studies indicate that increased levels of catecholamines enhance the strength of working memory…”
BackgroundMethodInfluentialEggert, E., Prochnow, A., Roessner, V., Frings, C., Münchau, A. M., Mückschel, M., & Beste, C. (2022) · Communications Biology · doi:10.1038/s42003-022-03864-1 · Cited by 18
The effects of the neurotoxin DSP4 on spatial learning and memory in Wistar rats
Hauser, J., Sontag, T. A., Tucha, O. M., & Lange, K. W. (2012) · ADHD Attention Deficit and Hyperactivity Disorders · doi:10.1007/s12402-012-0076-4 · Cited by 14
“dopamine and noradrenaline is as yet unclear, recent findings indicate a dysbalance between these neurotransmitters (Arnsten 2011; Heal et al. 2008).”
BackgroundResultInfluentialHoward, S. L., Beaudin, S. A., Strupp, B. J., & Smith, D. R. (2024) · Neurotoxicology and Teratology · doi:10.1016/j.ntt.2024.107337 · Cited by 13
Maran, T. K., Sachse, P., & Furtner, M. R. (2015) · Frontiers in Psychology · doi:10.3389/fpsyg.2015.01297 · Cited by 13
“…in Psychology | www.frontiersin.org 11 August 2015 | Volume 6 | Article 1297 1994; Berridge, 2008; Arnsten, 2011) and thereby disrupts phasic signaling (Valentino andWehby, 1988; Berridge andWaterhouse, 2003; Arnsten, 2011), resulting in a state of indiscriminate cognitive processing.”
BackgroundStress-Induced Executive Dysfunction in GDNF-Deficient Mice, A Mouse Model of Parkinsonism
Buhusi, M. C., Olsen, K. A., Yang, B. Z., & Buhusi, C. V. (2016) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2016.00114 · Cited by 13
“Stress alters dopaminergic tone and DA processing in key areas of the brain (Ahmad et al., 2010; Wanat et al., 2013; Belujon and Grace, 2015) and stress-level catecholamines (including norepinephrine) impair executive function and workingmemory (Thierry et al., 1976; Arnsten, 2011).”
Prefrontal Cortical Organization and Function: Implications for Externalizing Disorders
Arnsten, A. F. T., & Casey, B. J. (2011) · Biological Psychiatry · doi:10.1016/j.biopsych.2011.03.010 · Cited by 13
“Arnsten AFT (2011): Catecholamine influences on dorsolateral prefrontal cortical networks.”
BackgroundSelf-citationEffect of sustained high-intensity exercise on executive function
Konishi, K., Kimura, T., Yuhaku, A., Kurihara, T., Fujimoto, M., Hamaoka, T., & Sanada, K. (2017) · The Journal of Physical Fitness and Sports Medicine · doi:10.7600/jpfsm.6.111 · Cited by 14
Bodensohn, L., Maurer, A., Daamen, M., Upadhyay, N., Werkhausen, J., Lohaus, M., Manunzio, U., Manunzio, C., Radbruch, A., Attenberger, U. I., et al. (2024) · Brain and Cognition · doi:10.1016/j.bandc.2024.106156 · Cited by 12
“…low neuromodulation by light exercise, and an excessive increase in catecholamines by high-intensity exercise seem to weaken the signal-to-noise ratio and to impair cognitive performance ( “ catecholamine hypothesis ” ) (Arnsten, 2011; Cooper, 1973; McMorris et al., 2016; Sudo et al., 2022).”
Miguel, P. M., Deniz, B. F., Confortim, H. D., de Almeida, W., Bronauth, L., Vieira, M. C., Bertoldi, K., Siqueira, I. R., Silveira, P. P., & Pereira, L. O. (2020) · Journal of Psychopharmacology · doi:10.1177/0269881120913153 · Cited by 12
“In our previous study, we also observed that MPH disturbed learning acquisition in a task involving food reward, corroborating data reporting cognitive impairments related to excessive PFC DA stimulation (as by the MPH administration) (Arnsten, 2011; Floresco, 2013).”
BackgroundResultVolnova, A. B., Kurzina, N. P., Belskaya, A. D., Gromova, A. A., Pelevin, A., Ptukha, M. A., Fesenko, Z. S., Ignashchenkova, A., & Gainetdinov, R. R. (2023) · Biomedicines · doi:10.3390/biomedicines11010222 · Cited by 13
Mathai, D. S., Holst, M., Rodgman, C., Haile, C. N., Keller, J., Hussain, M. Z., Kosten, T. R., Newton, T. F., & Verrico, C. D. (2018) · The Journal of Neuropsychiatry and Clinical Neurosciences · doi:10.1176/appi.neuropsych.16120328 · Cited by 12
Reduced distractor interference during vagus nerve stimulation
van Bochove, M. E., Taeye, L. D., Raedt, R., Vonck, K. E. J., Meurs, A., Boon, P., Dauwe, I., Notebaert, W., & Verguts, T. (2018) · International Journal of Psychophysiology · doi:10.1016/j.ijpsycho.2018.03.015 · Cited by 13
PT-31, a putative α2-adrenoceptor agonist, is effective in schizophrenia cognitive symptoms in mice
Betti, A. H., Antonio, C. B., Herzfeldt, V., Pitta, M. G. D. R., Pitta, I. D. R., do Rego, J. L., do-Rego, J.-C., Vaudry, D., & Rates, S. M. K. (2019) · Behavioural Pharmacology · doi:10.1097/fbp.0000000000000494 · Cited by 12
“…networks regulate various aspects of attention, cognition, and emotion and require optimal catecholamine signaling, including stimulation of postsynaptic α 2 -adrenoceptors (Arnsten, 2010, 2011), agonists of these receptors, such as PT-31, seem to have beneficial effects on memory and cognition.”
BackgroundSalatino‐Oliveira, A., Wagner, F., Akutagava‐Martins, G. C., Bruxel, E. M., Genro, J. P., Zeni, C., Kieling, C., Polanczyk, G. V., Rohde, L. A., & Hutz, M. H. (2015) · European Archives of Psychiatry and Clinical Neuroscience · doi:10.1007/s00406-015-0626-9 · Cited by 12
Prefrontal norepinephrine represents a threat prediction error under uncertaintyPreprint
Basu, A., Yang, J.-H., Yu, A. L., Glaeser-Khan, S., Feng, J., Krystal, J. H., Li, Y., & Kaye, A. P. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.10.13.511463 · Cited by 12
“…behaviors, and contributes to trace conditioning of fear (Uematsu et al., 2017)(Gilmartin et al., 2014; Giustino & Maren, 2015)(Agster et al., 2013; Arnsten, 2011; Chandler et al., 2014), Neuromodulators have have computational roles in the prediction of outcomes, although the precise role of…”
BackgroundZhang, Y., Lai, S., Zhang, J., Wang, Y., Zhao, H., He, J., Huang, D., Chen, G., Qi, Z., Chen, P., et al. (2024) · Journal of Affective Disorders · doi:10.1016/j.jad.2024.01.272 · Cited by 11
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The acute effects of continuous and intermittent cycling on executive function in children
Martins, R., Duncan, M. J., Clark, C. C. T., & Eyre, E. L. J. (2021) · Acta Psychologica · doi:10.1016/j.actpsy.2021.103363 · Cited by 12
Aydın, A. G., & Adıgüzel, E. (2023) · Laboratory Animal Research · doi:10.1186/s42826-023-00172-5 · Cited by 11
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Barceló, P., Nicolau, C., Gamundı́, A., Fiol-deRoque, M. A., Tresguerres, J. A. F., Akaârir, M., & Rial, R. V. (2016) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2016/5863402 · Cited by 11
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“The reduced cortical thickness observed in the infra-normal subtype suggests disruptions in the top-down regulations between numerous cortices and basal ganglia (57).”
BackgroundLeikauf, J. E., Griffiths, K. R., Saggar, M., Hong, D. S., Clarke, S., Efron, D., Tsang, T. W., Hermens, D. F., Kohn, M. R., & Williams, L. M. (2017) · Personalized Medicine in Psychiatry · doi:10.1016/j.pmip.2017.02.001 · Cited by 14
“Theories have also implicated the physiologic construct of arousal, which involves the coordination of both central and peripheral response via norepinephrine release including effects on cognitive performance [9,10,8,11].”
BackgroundOláh, V., Knakker, B., Trunk, A., Lendvai, B., & Hernádi, I. (2020) · European Journal of Neuroscience · doi:10.1111/ejn.14852 · Cited by 9
Potentiation of prefrontal cortex dopamine function by the novel cognitive enhancer d-govadine
Nesbit, M. O., Ahn, S., Zou, H., Floresco, S., & Phillips, A. G. (2024) · Neuropharmacology · doi:10.1016/j.neuropharm.2024.109849 · Cited by 11
Wu, J., Toporek, A., Lin, Q., Goldstein, F. C., Loring, D. W., Kelberman, M. A., Weinshenker, D., Levey, A. I., Lah, J. J., & Qiu, D. (2025) · Alzheimer s Research & Therapy · doi:10.1186/s13195-025-01701-1 · Cited by 10
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Prochnow, A., Mückschel, M., Eggert, E., Senftleben, J., Frings, C., Münchau, A. M., Roessner, V., Bluschke, A., & Beste, C. (2024) · The International Journal of Neuropsychopharmacology · doi:10.1093/ijnp/pyae003 · Cited by 10
“The catecholaminergic system is related to the stability of mental representations (Durstewitz and Seamans, 2008; Hamilton et al., 2010; Arnsten, 2011; Cools and D’Esposito, 2011), which should be particularly evident at the neurophysiological level.”
BackgroundMueller, A. L., Shepard, S. B., & Moore, T. (2018) · Frontiers in Neural Circuits · doi:10.3389/fncir.2018.00012 · Cited by 12
“This is particularly relevant given the known role of dopamine in attention (Arnsten, 2011; Del Campo et al., 2011; Noudoost and Moore, 2011b; Ranganath and Jacob, 2016).”
BackgroundValero-Aracama, M. J., Reboreda, A., Arboit, A., Sauvage, M. M., & Yoshida, M. (2021) · eNeuro · doi:10.1523/eneuro.0440-20.2020 · Cited by 10
Cristini, J., Kraft, V. S., Heras, B. D. L., Rodrigues, L., Parwanta, Z., Hermsdörfer, J., Steib, S., & Roig, M. (2023) · Neurobiology of Learning and Memory · doi:10.1016/j.nlm.2023.107846 · Cited by 10
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Effects of Catecholaminergic and Transcranial Direct Current Stimulation on Response Inhibition
Koyun, A. H., Wendiggensen, P., Roessner, V., Beste, C., & Stock, A. (2024) · The International Journal of Neuropsychopharmacology · doi:10.1093/ijnp/pyae023 · Cited by 9
“Given the importance of catecholaminergic signaling in SNR regulation (Arnsten, 2011) as well as response control and inhibitory performance (Bensmann et al., 2018), we used methylphenidate (MPH) as an experimental modulator in the current study.”
MethodUnraveling the peripheral nervous System's role in tumor: A Double-edged Sword
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Carucci, S., Zuddas, A., Lampis, A., Man, K. K. C., Balia, C., Buitelaar, J. K., Danckaerts, M., Dittmann, R., Donno, F., Falissard, B., et al. (2024) · Journal of Attention Disorders · doi:10.1177/10870547241226726 · Cited by 11
“The therapeutic effects on attention and behavior also appear to be related to the enhanced neurotransmission of these catecholamines, especially in the pre-frontal cortex (Arnsten, 2011).”
BackgroundBrocos‐Mosquera, I., Gabilondo, A. M., Dı́ez-Alarcia, R., Muguruza, C., Erdozain, A. M., Meana, J. J., & Callado, L. F. (2021) · European Neuropsychopharmacology · doi:10.1016/j.euroneuro.2021.05.012 · Cited by 9
Metadata
- Authors
- Arnsten, A. F. T.
- Affiliations
- Yale University (US)
- Corresponding author
- Arnsten, Amy F.T.
- ORCID
- Arnsten, Amy F.T.
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2011-06
- Volume
- 69
- Issue
- 12
- Pages
- e89-e99
- ISSN
- 0006-3223 (ISSN-L)
- PMC
- PMC3145207
- OpenAlex
- W2091646494
- Cited by
- 493
- References
- 139
- Citations by year
- 2026: 40 · 2025: 40 · 2024: 33 · 2023: 30 · 2022: 14 · 2021: 24 · 2020: 26 · 2019: 32 · 2018: 30 · 2017: 34 · 2016: 36 · 2015: 49 · 2014: 36 · 2013: 26 · 2012: 33
- FWCI
- 4.36
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Alcohol Abuse and Alcoholism (RL1AA017536)
- National Institute on Aging (R37AG006036, P01AG030004, R01AG006036, AG06036)
- National Institute of Mental Health (P50MH068789)
- National Center for Research Resources (U54RR024350)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Keywords
- attention deficit hyperactivity disorder, dorsolateral prefrontal cortex, catecholamines, norepinephrine, dopamine, alpha2A-adrenoceptor, dopamine D1 receptor, network connectivity, working memory, atomoxetine, guanfacine, stimulant medication, norepinephrine transporter, dopamine transporter
- MeSH terms
- Atomoxetine Hydrochloride, Adrenergic alpha-Agonists, Animals, Arousal, Attention Deficit Disorder with Hyperactivity, Catecholamines, Cognition, Humans, Memory, Short-Term, Methylphenidate, Models, Neurological, Neural Pathways, Synaptic Transmission, Propylamines, Guanfacine, Prefrontal Cortex, Adrenergic Uptake Inhibitors
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