The dopaminergic response to acute stress in health and psychopathology: A systematic review

Vaessen, Thomas; Hernaus, Dennis; Myin-Germeys, Inez; Amelsvoort, Thérèse van

doi:10.1016/j.neubiorev.2015.07.008

Cited by 67 publications

(52 citation statements)

References 125 publications

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“…67 This treatment mimics to some extent dopamine release induced by environmental stress. 68 Such GBR treatment did not have any significant effects however in WT mice. 39 These findings indicate that an exogenous stress during development induces long-lasting oxidative stress along with PVI/PNN deficits in GRIN2A KO mice.…”

Section: Oxidative Stress and Pvi Integrity In Preclinical Models Of mentioning

confidence: 89%

Oxidative stress-driven parvalbumin interneuron impairment as a common mechanism in models of schizophrenia

et al. 2017

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Parvalbumin inhibitory interneurons (PVIs) are crucial for maintaining proper excitatory/inhibitory balance and high-frequency neuronal synchronization. Their activity supports critical developmental trajectories, sensory and cognitive processing, and social behavior. Despite heterogeneity in the etiology across schizophrenia and autism spectrum disorder, PVI circuits are altered in these psychiatric disorders. Identifying mechanism(s) underlying PVI deficits is essential to establish treatments targeting in particular cognition. On the basis of published and new data, we propose oxidative stress as a common pathological mechanism leading to PVI impairment in schizophrenia and some forms of autism. A series of animal models carrying genetic and/or environmental risks relevant to diverse etiological aspects of these disorders show PVI deficits to be all accompanied by oxidative stress in the anterior cingulate cortex. Specifically, oxidative stress is negatively correlated with the integrity of PVIs and the extracellular perineuronal net enwrapping these interneurons. Oxidative stress may result from dysregulation of systems typically affected in schizophrenia, including glutamatergic, dopaminergic, immune and antioxidant signaling. As convergent end point, redox dysregulation has successfully been targeted to protect PVIs with antioxidants/redox regulators across several animal models. This opens up new perspectives for the use of antioxidant treatments to be applied to at-risk individuals, in close temporal proximity to environmental impacts known to induce oxidative stress.

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Section: Oxidative Stress and Pvi Integrity In Preclinical Models Of mentioning

confidence: 89%

Oxidative stress-driven parvalbumin interneuron impairment as a common mechanism in models of schizophrenia

et al. 2017

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“…For example, the fact that serotonin depletion appears to increase sensitive to both negative feedback (Evers et al, 2005) and threats (Hariri and Holmes, 2006, Fisher and Hariri, 2013) could have the effect of either increasing impulsive shifting in the face of misleading punishments (Harrison et al, 1997, Chamberlain et al, 2006) or indirectly driving compulsive behavior by increasing anxiety (Deakin, 1998, Stein and Stahl, 2000, Maron et al, 2012) and/or interacting with other neuromodulatory pathways, such as dopamine systems (Perani et al, 2008). By contrast, SSRIs may reduce compulsivity by reducing threat sensitivity (Fisher and Hariri, 2013, Williams et al, 2015) and/or stress-related dopamine release (Vaessen et al, 2015). Theorists (Daw et al, 2002, Boureau and Dayan, 2011) have proposed that dopaminergic and serotoninergic systems interact in systematic and possibly oppositional ways.…”

Section: Reversal Learning As a Paradigm Case – Difference Neural mentioning

confidence: 99%

The neural underpinnings of cognitive flexibility and their disruption in psychotic illness

Waltz

2017

Neuroscience

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Schizophrenia has long been associated with a variety of cognitive deficits, including reduced cognitive flexibility. More recent findings, however, point to tremendous inter-individual variability among patients on measures of cognitive flexibility/set-shifting. With an eye toward shedding light on potential sources of variability in set-shifting abilities among schizophrenia patients, I examine the neural substrates of underlying probabilistic reversal learning (PRL) – a paradigmatic measure of cognitive flexibility – as well as neuromodulatory influences upon these systems. Finally, I report on behavioral and neuroimaging studies of PRL in schizophrenia patients, discussing the potentially influences of illness profile and antipsychotic medications on cognitive flexibility in schizophrenia.

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“…The neuroendocrine effects of the HPA axis are initiated with the secretion of corticotropin-releasing hormone (CRH) from the paraventricular nucleus of the hypothalamus, which in turn promotes the concatenated release of adrenocorticotropic hormone (ACTH) from the pituitary gland, and cortisol from the adrenal cortex. The rapid surge of these hormones is essential for stress coping; one of the mechanisms that mediate this action may be the increase in dopamine release following acute release of CRH and cortisol (Lemos et al, 2012; Vaessen et al, 2015). This increased dopamine efflux has been primarily documented in key regions of the mesocorticolimbic system, including the prefrontal cortex, nucleus accumbens and dorsal striatum (Abercrombie et al, 1989; Lavicky and Dunn, 1993; Hermans et al, 2014), and appears to be essential for stress resilience and coping (Cabib and Puglisi-Allegra, 2012; Pfau and Russo, 2015).…”

Section: Conclusion: Neurobiological Mechanisms and Therapeutic Pmentioning

confidence: 99%

What makes you tic? Translational approaches to study the role of stress and contextual triggers in Tourette syndrome

Godar¹,

Bortolato

2017

Neuroscience & Biobehavioral Reviews

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Tourette syndrome (TS) is a neurodevelopmental condition characterized by multiple, recurring motor and phonic tics. Rich empirical evidence shows that the severity of tics and associated manifestations is increased by several stressors and contextual triggers; however, the neurobiological mechanisms responsible for symptom exacerbation in TS remain poorly understood. This conceptual gap partially reflects the high phenotypic variability in tics, as well as the existing difficulties in operationalizing and standardizing stress and its effects in a clinical setting. Animal models of TS may be highly informative tools to overcome some of these limitations; these experimental preparations have already provided critical insights on key aspects of TS pathophysiology, and may prove useful to identify the neurochemical alterations induced by different stressful contingencies. In particular, emerging knowledge on the role of contextual triggers in animal models of TS may inform the development of novel pharmacological interventions to reduce tic fluctuations in this disorder.

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The dopaminergic response to acute stress in health and psychopathology: A systematic review

Cited by 67 publications

References 125 publications

Oxidative stress-driven parvalbumin interneuron impairment as a common mechanism in models of schizophrenia

Oxidative stress-driven parvalbumin interneuron impairment as a common mechanism in models of schizophrenia

The neural underpinnings of cognitive flexibility and their disruption in psychotic illness

What makes you tic? Translational approaches to study the role of stress and contextual triggers in Tourette syndrome

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