The DOI matches its Crossref record; 56 of the 56 references it cites were found in a registry or an index; 4 of the 9 sources its claims cite were checked for support.
Stress-induced cognitive dysfunction: hormone-neurotransmitter interactions in the prefrontal cortex
Open accessAbstract
The mechanisms and neural circuits that drive emotion and cognition are inextricably linked. Activation of the hypothalamic-pituitary-adrenal (HPA) axis as a result of stress or other causes of arousal initiates a flood of hormone and neurotransmitter release throughout the brain, affecting the way we think, decide, and behave. This review will focus on factors that influence the function of the prefrontal cortex (PFC), a brain region that governs higher-level cognitive processes and executive function. The PFC becomes markedly impaired by stress, producing measurable deficits in working memory. These deficits arise from the interaction of multiple neuromodulators, including glucocorticoids, catecholamines, and gonadal hormones; here we will discuss the non-human primate and rodent literature that has furthered our understanding of the circuitry, receptors, and signaling cascades responsible for stress-induced prefrontal dysfunction.
Overview
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Written from the paper’s full text.
TL;DR
This review synthesizes non-human primate and rodent literature showing that stress impairs prefrontal cortex (PFC)-dependent working memory through interacting neuromodulators, principally catecholamines (dopamine and norepinephrine) acting via D1, alpha-1, and alpha-2 receptors, with glucocorticoids and estrogen modulating these effects. It proposes that stress pushes catecholamine signaling to the impairing end of inverted-U curves and that high estrogen may place females "ahead of the curve," increasing stress sensitivity.
Key findings
- Working memory depends on a balanced neurochemical milieu in the PFC; both insufficient and excessive D1 stimulation impair performance, producing the classic "inverted-U" relationship. Stress-induced HPA activation stimulates the VTA, causing excess DA release into the PFC, and these impairments can be reversed by intra-PFC D1 antagonist infusion or by cAMP and PKA inhibitors.
- Under stress, excess NE binds the lower-affinity alpha-1 receptor (rather than the high-affinity alpha-2 receptor active under non-stress conditions), impairing working memory and silencing PFC network activity; alpha-1 antagonists restore PFC function during stress, and PKC inhibition also reverses stress-related working memory impairments.
- Mechanistically, elevated D1 signaling opens HCN channels (via cAMP) on dendritic spines, shunting incoming excitation and suppressing both "noise" and "signal" neurons; alpha-2 receptor activation (Gi-coupled, lowering cAMP) slows HCN conductance and strengthens signal. Pharmacological HCN blockade restores working memory performance and PFC network tuning during stress.
- Glucocorticoids impair PFC working memory directly via GRs (systemic corticosterone reduces Delayed Alternation accuracy; intra-PFC RU 28362 impairs working memory; intra-PFC RU 38486 reverses stress-induced DSWS impairments) and indirectly by blocking extraneuronal catecholamine transporters and by locally driving stress-induced DA efflux in the PFC.
- In female rats, stress sensitivity is driven by high-estrogen phases: females became impaired after lower doses of FG7142 than males, driven by proestrus females; OVX + estrogen rats show impairments similar to proestrus females while OVX + blank-capsule rats perform more like males. A guanfacine dose that rescues stress-induced impairments in males and OVX females has no effect in OVX + estrogen rats.
Methods
- Narrative review of non-human primate and rodent literature on stress-induced PFC dysfunction, covering electrophysiology, pharmacology (receptor agonists/antagonists, cAMP/PKA/PKC inhibitors), microdialysis, lesion, and behavioral studies.
- Behavioral paradigms discussed: Delayed Response task (monkeys), Delayed Alternation and delayed spatial win-shift (DSWS) tasks (rodents); stressors include loud white noise, brief restraint stress, and the anxiogenic drug FG-7142.
- Sex-difference evidence drawn from dose-response studies with FG7142 and restraint stress in male and female rats, including ovariectomized rats with and without estrogen replacement.
Limitations
- The paper states that the vast majority of behavioral neuroscience research is conducted in male animals, so general understanding of stress effects in the PFC is within the context of the male brain, which is problematic from a translational standpoint given that stress-related illnesses like PTSD and major depressive disorder are twice as prevalent in women.
- The paper states that the mechanisms by which estrogen modulates stress-induced impairments are not known, and that estrogen-glucocorticoid interactions have not been investigated in the context of stress-induced working memory impairments.
- Evident from the text: the review is based entirely on animal (non-human primate and rodent) literature, and the estrogen "ahead of the curve" hypothesis is presented as a model (Figure 2) rather than a directly tested mechanism.
Model-written summary. Check it against the paper before relying on it.
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Claims the paper makes
3 No full text of the sources · 2 Partly supported · 2 Own interpretation · 1 Supported · accuracy not yet measured
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 deficits arise from the interaction of multiple neuromodulators, including glucocorticoids, catecholamines, and gonadal hormones; here we will discuss the non-human primate and rodent literature that has furthered our understanding of the circuitry, receptors, and signaling cascades responsible for stress-induced prefrontal dysfunction.”
§ Stress-induced cognitive dysfunction: hormone-neurotransmitter interactions in the prefrontal cortex > Abstract
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.
- Rests on an assumption: Findings from non-human primate and rodent studies of stress-induced prefrontal dysfunction generalize to humans.
In the paper
“When the authors divided the females based on estrus cycle phase, they found that this stress sensitivity was driven by females in proestrus, when estrogen levels are highest.”
§ Stress-induced cognitive dysfunction: hormone-neurotransmitter interactions in the prefrontal cortex > Sex differences and estrogen effects
What the sources say
- Not checked — no full text of the sourcecites Shansky et al., 2004 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. 6
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“While a lack of D1 activity can impair working memory performance, high levels of D1 stimulation also produce cognitive deficits—the classic “inverted-U” relationship.”
- Also stated in: § Dopamine and norepinephrine · plain
“During stress, HPA axis activation leads to stimulation of the VTA, causing excess DA release into the PFC (Murphy et al., 1996). When this DA binds to the D1 receptor, its downstream signaling cascades lead to working memory impairment (Taylor et al., 1999).”
§ Stress-induced cognitive dysfunction: hormone-neurotransmitter interactions in the prefrontal cortex > Dopamine and norepinephrine
What the sources say
- Not checked — no full text of the sourcecites Murphy et al., 1996 source
- Partly supportedcites Taylor et al., 1999 sourceExperimental — accuracy not yet measured
The section “Possible relevance of PKA activation to stress-induced PFC dysfunction” reports that high D1 stimulation impairs working memory and contributes to stress-induced deficits. It does not establish that D1 blockade impairs working-memory performance, so it does not support both sides of the claimed inverted-U relationship. The section also does not explicitly say that stress causes excess dopamine release. (LLM, conf=0.84)
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.
- Also stated in: § Dopamine and norepinephrine · plain
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“stress-related mental illnesses like post-traumatic stress disorder (PTSD) and major depressive disorder are twice as prevalent in women (Becker et al., 2007), suggesting a distinct neurobiology may underlie the stress response in female brains.”
§ Stress-induced cognitive dysfunction: hormone-neurotransmitter interactions in the prefrontal cortex > Sex differences and estrogen effects
What the sources say
- Partly supportedcites Becker et al., 2007 sourceExperimental — accuracy not yet measured
The “Stress and affective disorders” section says women experience depression at approximately twice the rate of men. The “Sex differences in clinical studies” section discusses sex differences in PTSD risk but does not give a twofold prevalence figure for PTSD. The citation therefore supports the depression figure, not its extension to both disorders. (LLM, conf=0.88)
hedgedconditional- 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.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Exposure to stress, however, can disrupt PFC function, markedly impairing working memory (Arnsten, 2009; Arnsten et al., 2012).”
- Also stated in: § Abstract · plain
“The PFC becomes markedly impaired by stress, producing measurable deficits in working memory.”
§ Stress-induced cognitive dysfunction: hormone-neurotransmitter interactions in the prefrontal cortex > Introduction
What the sources say
- Supportedcites Arnsten, 2009 source
The review states that stress rapidly disrupts PFC function and focuses on PFC working memory (passage 1). In its discussion of acute stress and PFC function, it reports that mild stress impaired spatial working-memory performance in rats and monkeys (passage 5). Page numbers are not supplied in our copy. (LLM, conf=0.94)
- Supportedcites Arnsten et al., 2012 source
In “Working memory vs. classic neuroplasticity” (page not provided), the paper says working-memory abilities are greatly impaired during stress. In “Relationship of neuromodulation in dlPFC to arousal states” (page not provided), it describes stress-related weakening of prefrontal network activity and reports that a mild stressor impairs working memory. (LLM, conf=0.94)
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.
- Rests on an assumption: Findings from non-human primate and rodent studies of stress-induced prefrontal dysfunction generalize to humans.
- Also stated in: § Abstract · plain
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
“Pharmacological stimulation of the alpha-2 receptor can increase firing in PFC neurons that code for relevant information, enhancing working memory in monkeys and rodents (Wang et al., 2007).”
- Also stated in: § Dopamine and norepinephrine · plain
“Stimulation of this receptor—either pharmacologically or because of stress-induced NE release—leads to working memory impairment and a silencing of PFC network activity (Arnsten et al., 1999).”
§ Stress-induced cognitive dysfunction: hormone-neurotransmitter interactions in the prefrontal cortex > Dopamine and norepinephrine
What the sources say
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.
- Also stated in: § Dopamine and norepinephrine · plain
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
“Research in non-human primates and rodents has shown that this impairment is driven by increased catecholamine signaling, which may be further modulated or exacerbated by changes in steroid hormone levels.”
§ Stress-induced cognitive dysfunction: hormone-neurotransmitter interactions in the prefrontal cortex > Conclusions
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.
It may state two separate claims as one.
- Rests on an assumption: Findings from non-human primate and rodent studies of stress-induced prefrontal dysfunction generalize to humans.
In the paper
“While this release is critical to the enhancement of long term memories associated with the event (Rodrigues et al., 2009), glucocorticoid actions in the PFC impair working memory.”
- Also stated in: § Glucocorticoids · hedged
“These findings suggest that glucocorticoids can impair PFC function through direct actions at GRs, but glucocorticoids may also indirectly exacerbate working memory impairments through interactions with the catecholamine systems described above.”
§ Stress-induced cognitive dysfunction: hormone-neurotransmitter interactions in the prefrontal cortex > Glucocorticoids
What the sources say
- Not checked — no full text of the sourcecites Rodrigues et al., 2009 source
plainconditional- 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.
- Also stated in: § Glucocorticoids · hedged
The paper relies on this without support.
Findings from non-human primate and rodent studies of stress-induced prefrontal dysfunction generalize to humans.
“here we will discuss the non-human primate and rodent literature that has furthered our understanding of the circuitry, receptors, and signaling cascades responsible for stress-induced prefrontal dysfunction.”
The paper relies on this without support.
Working memory tasks in animals measure the same executive function as human working memory.
“Working memory in animals is assessed using delay-based tasks, which require an animal to keep a piece of information in mind over the course of a delay period, in order to make an accurate choice when the delay ends.”
The paper relies on this without support.
The prefrontal cortex helps to shut down the stress response.
“Because the PFC also helps to shut down the stress response, this loss of PFC function can lead to prolonged glucocorticoid release, which can exacerbate working memory impairments.”
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Stress-induced cognitive dysfunction: hormone-neurotransmitter interactions in the prefrontal cortex > Dopamine and norepinephrine
“Traditionally, HCN channels serve to normalize neuronal membrane potential, opening to allow positive ions into the cell to combat post-firing hyperpolarization (Wahl-Schott and Biel, 2009).”
§ Stress-induced cognitive dysfunction: hormone-neurotransmitter interactions in the prefrontal cortex > Dopamine and norepinephrine
“when cAMP increases (as happens when D1 receptors are over-activated), HCN channels open, letting Na+ and K+ flow out of the cell (Chen et al., 2007).”
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“Interestingly, similar to what we have shown with cocaine exposure, stress seems to modulate prefrontal cortex mechanisms and dorsolateral striatum processes in a way that biases towards model-free strategies (Shansky and Lipps, 2013).”
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“Stress is generally thought to impair executive functioning (Diamond, 2013; Shansky & Lipps, 2013).”
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“Therefore, connecting this evidence, it has been suggested that chronic stress affects the accurate functioning of the PFC [33, 34], which is expressed as the maladaptive generation of behavioral responses observed in neuropsychiatric disorders.”
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Glucocorticoids and cognitive function: a walkthrough in endogenous and exogenous alterations
Alcubierre, D. D., Ferrari, D., Mauro, G. C. D., Isidori, A. M., Tomlinson, J., & Pofi, R. (2023) · Journal of Endocrinological Investigation · doi:10.1007/s40618-023-02091-7 · Cited by 73
“This has to be taken into account both from a functional and structural point of view [129, 130], as degeneration of hippocampal neurons [131], and related impaired performance on declarative memory tasks [132] have been described in AI patients.”
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Corrêa, M. S., Vedovelli, K., Giacobbo, B. L., de Souza, C. E. B., Ferrari, P., Argimon, I. I. D. L., Walz, J. C., Kapczinski, F. P., & Bromberg, E. (2014) · Neuroscience · doi:10.1016/j.neuroscience.2014.11.052 · Cited by 73
Alcohol Effects on Stress Pathways
Blaine, S. K., Milivojevic, V., Fox, H. C., & Sinha, R. (2016) · The Canadian Journal of Psychiatry · doi:10.1177/0706743716632512 · Cited by 68
Solianik, R., Sujeta, A., Terentjevienė, A., & Skurvydas, A. (2016) · BioMed Research International · doi:10.1155/2016/1503956 · Cited by 58
“It is well established that the brain is a target of stress and that the prefrontal cortex is the brain area that is most sensitive to its effects [14, 15]; the prefrontal complex is responsible for highest-order cognitive abilities, such as executive functions [14, 16].”
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“Stressful events can lead to immediate and marked impairments in working memory, which is an executive function [57].”
BackgroundAcute Stress Attenuates Cognitive Flexibility in Males Only: An fNIRS Examination
Kalia, V., Vishwanath, K., Knauft, K. M., Vellen, B. V. D., Luebbe, A. M., & Williams, A. L. (2018) · Frontiers in Psychology · doi:10.3389/fpsyg.2018.02084 · Cited by 56
Role of epigenetic factors in the development of mental illness throughout life
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Chauhan, N. R., Kumar, R., Gupta, A., Meena, R. C., Nanda, S., Mishra, K. P., & Singh, S. B. (2020) · Behavioural Brain Research · doi:10.1016/j.bbr.2020.112895 · Cited by 55
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Valros, A., Palander, P., Heinonen, M., Munsterhjelm, C., Brunberg, E., Keeling, L. J., & Piepponen, P. T. (2015) · Physiology & Behavior · doi:10.1016/j.physbeh.2015.02.049 · Cited by 47
“The function of the prefrontal cortex, which governs higher-level cognitive processes, can be negatively altered by stress, causing changes in behavior [40].”
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“…anti-depressant-like effect in UCMS animals, we first analyzed the serum corticosterone level as a biomarker of excess activation of the HPA axis (Shansky and Lipps, 2013) since it plays an important role not only in therapeutic mechanisms of antidepressant drugs (Kim et al., 2013) but also in…”
BackgroundRole of neuroinflammation and sex hormones in war-related PTSD.
Mendoza, C., Barreto, G., Avila-Rodriguez, M. F., & Echeverría, V. (2016) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2016.05.016 · Cited by 43
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Geissler, C. F., Friehs, M. A., Frings, C., & Domes, G. (2022) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2022.105998 · Cited by 44
Sex-related differences in attention and memory
Solianik, R., Brazaitis, M., & Skurvydas, A. (2016) · Medicina · doi:10.1016/j.medici.2016.11.007 · Cited by 44
“Furthermore, it is known that sex hormones can affect neurotransmitter levels responsible for cognition [2,18,21], thus women were tested during the early follicular phase when estradiol and progesterone levels are low.”
Backgroundd-serine prevents cognitive deficits induced by acute stress
Guercio, G. D., Bevictori, L. E., Vargas-Lopes, C., Madeira, C., Oliveira, A. F., Carvalho, V. F., d’Avila, J. C., & Panizzutti, R. (2014) · Neuropharmacology · doi:10.1016/j.neuropharm.2014.06.021 · Cited by 41
“In fact, stress is a known regulator of many other pathways in the brain, including the dopaminergic and the endocannabinoid systems (Hill and McEwen 2010; Shansky and Lipps, 2013).”
Plieger, T., Felten, A., Splittgerber, H., Duke, É., & Reuter, M. (2017) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2017.10.020 · Cited by 40
Acute stress and working memory in older people
Pulopulos, M. M., Hidalgo, V., Almela, M., Puig‐Pérez, S., Villada, C., & Salvador, A. (2015) · Stress · doi:10.3109/10253890.2015.1004538 · Cited by 44
Chanana, P., & Kumar, A. (2016) · Frontiers in Neuroscience · doi:10.3389/fnins.2016.00084 · Cited by 39
Effect of Cold Stress on Neurobehavioral and Physiological Parameters in Rats
Elmarzouki, H., Aboussaleh, Y., Najimi, M., Chigr, F., & Ahami, A. O. T. (2021) · Frontiers in Physiology · doi:10.3389/fphys.2021.660124 · Cited by 38
Successful voluntary recruitment of cognitive control under acute stress
Plessow, F., Schade, S., Kirschbaum, C., & Fischer, R. (2017) · Cognition · doi:10.1016/j.cognition.2017.06.016 · Cited by 36
“Currently, the most common view on how stress affects cognitive control converges on the assumption that acute uncontrollable stress impairs prefrontal cortex (PFC)-dependent cognitive functions, including cognitive control (Arnsten, 2009; Shansky & Lipps, 2013; Shields, Sazma, & Yonelinas, 2016).”
Corrêa, M. S., de Lima, D. B., Giacobbo, B. L., Vedovelli, K., Argimon, I. I. D. L., & Bromberg, E. (2018) · Stress · doi:10.1080/10253890.2018.1510485 · Cited by 40
“…and BDNF levels seem to play a key role on prefrontal and hippocampal dysfunctions, leading to the impairment of cognitive components such as attention, executive function and different memory types (Kim, Pellman, & Kim, 2015; Lu, Nagappan, & Lu, 2014; Pluchino et al., 2015; Shansky & Lipps, 2013).”
BackgroundSleep, cognition and cortisol in addison’s disease: a mechanistic relationship
Henry, M., Thomas, K. G. F., & Ross, I. L. (2021) · Frontiers in Endocrinology · doi:10.3389/fendo.2021.694046 · Cited by 34
Cognitive emotion regulation and stress: a multiple mediation approach
Miklósi, M., Martos, T., Szabó, M., Kocsis-Bogár, K., & Forintos, D. P. (2014) · Translational Neuroscience · doi:10.2478/s13380-014-0207-9 · Cited by 44
“Executive functions depend on the structural and functional integrity of the prefrontal cortex (PFC) [19], which guides emotions and behaviour through projections to subcortical regions like the hypothalamus and the amygdala [20].”
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“High environmental temperature impairs neuromuscular [1–4], aerobic [5], and cognitive performance [1,6,7,8–10] and the ability to activate skeletal muscles [1,11].”
BackgroundA paradoxical switch: the implications of excitatory GABAergic signaling in neurological disorders
McArdle, C. J., Arnone, A. A., Heaney, C. F., & Raab‐Graham, K. F. (2024) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2023.1296527 · Cited by 33
“For example, stress is associated with anxiety and substance use disorders (172, 173), cognitive dysfunction is present in both stress-related disorders and AD (174, 175), and epileptogenesis occurs in both autism spectrum disorders (ASD) and Alzheimer’s disease patients (176–178).”
BackgroundMualem, R., Morales-Quezada, L., Farraj, R. H., Shance, S., Bernshtein, D. H., Cohen, S., Mualem, L., Salem, N., Yehuda, R. R., Zbedat, Y., et al. (2024) · Frontiers in Public Health · doi:10.3389/fpubh.2024.1376075 · Cited by 59
Solianik, R., Skurvydas, A., Mickevičienė, D., & Brazaitis, M. (2014) · Cryobiology · doi:10.1016/j.cryobiol.2014.08.007 · Cited by 28
Episodic memory impairment in Addison’s disease: results from a telephonic cognitive assessment
Henry, M., & Thomas, K. G. F. (2014) · Metabolic Brain Disease · doi:10.1007/s11011-014-9511-x · Cited by 32
“The effects of cortisol on the hippocampus and PFC can affect memory processes because both of those regions play integral roles in memory processing, and both have dense concentrations of glucocorticoid receptors (Schacter and Wagner 1999; Alderson and Novack 2002; Kim and Diamond 2002; Shansky and Lipps 2013).”
Gargus, M., Ben‐Azu, B., Landwehr, A., Dunn, J., Errico, J. P., & Tremblay, M. (2025) · Frontiers in Neuroscience · doi:10.3389/fnins.2024.1527842 · Cited by 32
Solianik, R., Sujeta, A., & Čekanauskaitė, A. (2018) · Experimental Brain Research · doi:10.1007/s00221-018-5305-4 · Cited by 28
Empathy in pregnant women and new mothers: a systematic literature review
Boorman, R. J., Creedy, D. K., Fenwick, J., & Muurlink, O. T. (2018) · Journal of Reproductive and Infant Psychology · doi:10.1080/02646838.2018.1525695 · Cited by 29
“Cognitive deficits are apparent during periods of stress (Shansky & Lipps, 2013) as well as pregnancy and postpartum (Davies, Lum, Skouteris, Byrne, & Hayden, 2018).”
BackgroundPsychoneuroendocrinology of Stress
Gunnar, M. R., Doom, J. R., & Esposito, E. A. (2015) · Wiley eBooks · doi:10.1002/9781118963418.childpsy304 · Cited by 29
Missing expectations: Windlass tourniquet use without formal training yields poor results
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Albertini, G., Walrave, L., Demuyser, T., Massie, A., Bundel, D. D., & Smolders, I. J. (2017) · Epilepsia · doi:10.1111/epi.13943 · Cited by 28
Kim, B., Samuel, L. J., Thorpe, R. J., Crews, D. C., & Szanton, S. L. (2023) · JAMA Network Open · doi:10.1001/jamanetworkopen.2023.4674 · Cited by 27
Dopamine effects on stress-induced working memory deficits
Bahari, Z., Meftahi, G. H., & Meftahi, M. A. (2018) · Behavioural Pharmacology · doi:10.1097/fbp.0000000000000429 · Cited by 29
“Additional complexity is added by the fact that a subset of midbrain DA neurons may also corelease the excitatory neurotransmitter glutamate (Stuber et al., 2010; Hnasko et al., 2010, 2012) or GABA (Stamatakis et al., 2013).”
BackgroundRinwa, P., & Kumar, A. (2013) · Naunyn-Schmiedeberg s Archives of Pharmacology · doi:10.1007/s00210-013-0925-5 · Cited by 26
“Stress exposure induces several changes in the body, among which the most important is activation of the hypothalamo-pituitary-adrenal (HPA) axis (Shansky and Lipps 2013).”
BackgroundKromrey, S. A., Czoty, P. W., & Nader, M. A. (2015) · Hormones and Behavior · doi:10.1016/j.yhbeh.2015.04.017 · Cited by 27
“With regard to E2 concentrations and task specificity, one possibility is that E2 influences cognitive function involving tasks reliant on the PFC, through the DA system (Shansky and Lipps, 2013).”
BackgroundThe impact of stress on social behavior in adult zebrafish (Danio rerio)
Saszik, S. M., & Smith, C. M. (2017) · Behavioural Pharmacology · doi:10.1097/fbp.0000000000000338 · Cited by 26
“Dopamine and 5-HT transmitter systems interact in the brain (de Deurwaerdere and di Giovanni, 2017) and social behavior has been shown to alter 5-HT levels in the brain (Saif et al., 2013; Teles et al., 2013; Shams et al., 2015).”
BackgroundMethodNakamura, Y., Kato, H., Nojiri, K., Takahata, T., Yoshihara, H., Honda-Takahashi, K., Honda, T., Kubo, S., Sakatsume, K., & Maruta, T. (2014) · Journal of Orthopaedic Science · doi:10.1007/s00776-014-0534-2 · Cited by 25
“levels of mental activity, such as executive function, emotional control, and initiation of behavior, and it dysfunctions when facing the overwhelming stress [14].”
BackgroundThe discrepant effect of acute stress on cognitive inhibition and response inhibition
Kan, Y., Xue, W., Zhao, H., Wang, X., Guo, X., & Duan, H. (2021) · Consciousness and Cognition · doi:10.1016/j.concog.2021.103131 · Cited by 25
Mikneviciute, G., Ballhausen, N., Rimmele, U., & Kliegel, M. (2021) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2021.12.009 · Cited by 31
Complex Dynamics in the Basal Ganglia: Health and Disease Beyond the Motor System
Andrés, D. S., & Darbin, O. (2017) · Journal of Neuropsychiatry · doi:10.1176/appi.neuropsych.17020039 · Cited by 27
Cheng, L., Sit, J. W. H., Leung, D. Y. P., & Li, X. (2016) · Worldviews on Evidence-Based Nursing · doi:10.1111/wvn.12159 · Cited by 25
“Such impairments debilitate individuals’ capability to acknowledge and overcome barriers (McEwen & Gianaros 2011; Shansky & Lipps 2013).”
BackgroundNeural underpinnings of fine motor skills under stress and anxiety: A review
Martins, L. A., Schiavo, A., Paz, L. V., Xavier, L. L., & Mestriner, R. G. (2024) · Physiology & Behavior · doi:10.1016/j.physbeh.2024.114593 · Cited by 30
Stress- and trauma-related blockade of episodic-autobiographical memory processing
Staniloiu, A., Kordon, A., & Markowitsch, H. J. (2020) · Neuropsychologia · doi:10.1016/j.neuropsychologia.2020.107364 · Cited by 22
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A multiscale inflammatory map: linking individual stress to societal dysfunction
Yoram Vodovotz, B., Arciero, J. C., Verschure, P. F. M. J., & Katz, D. L. (2024) · Frontiers in Science · doi:10.3389/fsci.2023.1239462 · Cited by 22
Podvin, S., Bundey, R. A., Toneff, T., Ziegler, M. G., & HOOK, V. Y. H. (2015) · Molecular and Cellular Neuroscience · doi:10.1016/j.mcn.2015.06.008 · Cited by 22
“Epinephrine is a key stress neurotransmitter released from the adrenal medulla for the regulation of metabolic, cardiac, lung, and related physiological functions, as well as emotions, memory, and related behaviors (Joëls et al., 2011; Shansky and Lipps, 2013).”
BackgroundValderrama, J., Hansen, S. K., Pato, C. N., Phillips, K. A., Knowles, J. W., & Pato, M. T. (2020) · Psychiatry Research · doi:10.1016/j.psychres.2020.112962 · Cited by 24
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High prolactin levels are associated with more delirium in septic patients
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“It has been reported that excessive cortisol or catecholamine release is involved in the development of delirium in severe sepsis, Cushing’s disease, psychosis and schizophrenia [6, 8, 23].”
Backgroundd-Arginine as a neuroprotective amino acid: promising outcomes for neurological diseases
Canteros, M. G. (2013) · Drug Discovery Today · doi:10.1016/j.drudis.2013.11.010 · Cited by 19
Behavioral Neuroadaptation to Alcohol: From Glucocorticoids to Histone Acetylation
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Kato, T. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10143122 · Cited by 18
Examining the contribution of histone modification to sex differences in learning and memoryPreprint
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Food Insecurity across the Life-Course and Cognitive Function among Older Mexican Adults
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Metadata
- Authors
- Shansky, R. M., & Lipps, J.
- Affiliations
- Northeastern University (US)
- Corresponding author
- Shansky, Rebecca M.
- ORCID
- Shansky, Rebecca M.
- Venue
- Frontiers in Human Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2013
- Volume
- 7
- Pages
- 123-123
- ISSN
- 1662-5161 (ISSN-L)
- PMC
- PMC3617365
- OpenAlex
- W1977773662
- Semantic Scholar
- c29a390e82744bcb70b04e0c370134134cc8802f
- Cited by
- 205
- References
- 55
- Citations by year
- 2026: 12 · 2025: 18 · 2024: 12 · 2023: 25 · 2022: 14 · 2021: 17 · 2020: 11 · 2019: 8 · 2018: 13 · 2017: 17 · 2016: 20 · 2015: 17 · 2014: 14 · 2013: 7
- FWCI
- 8.72
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Human Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Keywords
- stress, cognitive impairment, prefrontal cortex, hypothalamic-pituitary-adrenal axis, glucocorticoids, catecholamines, gonadal hormones, working memory, executive function, neuromodulation, stress-induced neuroplasticity, receptor signaling
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