Dataset Information

Oxytocin and Stress-related Disorders: Neurobiological Mechanisms and Treatment Opportunities.

ABSTRACT: Novel pharmacotherapies that improve outcomes for individuals with stress-related psychiatric disorders are needed. The neurohormone oxytocin (OT) is a promising candidate given its influence on the social-emotional brain. In this review, we present an overview of evidence supporting OT's utility for treating major depressive disorder and posttraumatic stress disorder. We first discuss endogenous OT, which research suggests is not yet a reliable biomarker of stress-related disorders. Second, we review effects of intranasal (IN) OT on processes relevant to stress-related disorders in healthy populations (anhedonia, reward processing, psychosocial stress reactivity, fear/anxiety, and social behavior) and their neurobiological mechanisms (e.g., the salience network and hypothalamic-pituitary-adrenal axis). Third, we present the sparse but promising findings from clinical populations, followed by discussion of critical moderating variables to consider in the service of maximizing the therapeutic potential of OT (e.g., patient sex and child maltreatment). We also identify heterogeneous findings and limitations of existing research, including reliance on single-dose studies in psychiatrically healthy samples and unanswered questions regarding the effectiveness of IN drug delivery and dosing schedules. Well-controlled multidose studies including women and measures of potentially moderating variables are sorely needed and would inform our understanding of the utility of OT for preventing and treating stress-related psychiatric disorders.

SUBMITTER: Sippel LM

PROVIDER: S-EPMC5482285 | biostudies-other | 2017 Feb

REPOSITORIES: biostudies-other

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Oxytocin and Stress-related Disorders: Neurobiological Mechanisms and Treatment Opportunities.

Sippel Lauren M LM Allington Casey E CE Pietrzak Robert H RH Harpaz-Rotem Ilan I Mayes Linda C LC Olff Miranda M

Chronic stress (Thousand Oaks, Calif.) 20170217

Novel pharmacotherapies that improve outcomes for individuals with stress-related psychiatric disorders are needed. The neurohormone oxytocin (OT) is a promising candidate given its influence on the social-emotional brain. In this review, we present an overview of evidence supporting OT's utility for treating major depressive disorder and posttraumatic stress disorder. We first discuss endogenous OT, which research suggests is not yet a reliable biomarker of stress-related disorders. Second, we ...[more]

PMID: 28649672

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Project description:BackgroundVehicle exhaust emissions are known to be significant contributors to physical and psychological stress. Vehicle exhaust-induced stress and associated respiratory and cardiovascular complications are well-known, but the impact of this stress on the brain is unclear. Simulated vehicle exhaust exposure (SVEE) in rats causes behavioral and cognitive deficits. In the present study, the underlying mechanisms were examined. Our postulation is that SVEE, a simulation of physiologically relevant concentrations of pro-oxidants (0.04% carbon dioxide, 0.9 ppm nitrogen dioxide, 3 ppm carbon monoxide) creates a toxic stress environment in the brain that results in an imbalance between production of reactive oxygen species and the counteracting antioxidant mechanisms. This impairs mitochondrial function in the high bioenergetic demand areas of the brain including the hippocampus (HIP), amygdala (AMY) and the prefrontal cortex (PFC), disrupting neuronal network, and causing behavioral deficits. Mitochondria-targeted antioxidant Mito-Q protects against these impairments.MethodsSprague Dawley rats were provided with Mito-Q (250 μM) in drinking water for 4 weeks followed by SVEE 5 h/day for 2 weeks, followed by behavioral and biochemical assessments.ResultsSVEE resulted in anxiety- and depression-like behavior, accompanied with increased oxidative stress, diminished antioxidant response and mitochondrial impairment reflected from electron transport chain (ETC) disruption, reduced oxygen consumption, low adenosine tri-phosphate (ATP) synthesis and an alteration in the mitochondrial biochemical dynamics assessed via protein expression profiles of mitochondrial fission marker, dynamin-related protein-1 and fusion markers, mitofusin-1/2 in the HIP, AMY and the PFC. Mito-Q treatment prevented SVEE-induced behavioral deficits, attenuated rise in oxidative stress and also prevented SVEE-induced mitochondrial impairment.ConclusionThis study demonstrates a causal mechanism mediating SVEE-induced behavioral deficits in rats. We further established that SVEE is a toxicological stressor that induces oxidative stress and results in mitochondrial impairment, which by disrupting neural circuitry impairs cognitive and behavioral functions.

Dataset Information

Oxytocin and Stress-related Disorders: Neurobiological Mechanisms and Treatment Opportunities.

Publications

Oxytocin and Stress-related Disorders: Neurobiological Mechanisms and Treatment Opportunities.

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