Can stress cause depression?

Praag, H. M. van

doi:10.1016/j.pnpbp.2004.05.031

Cited by 334 publications

(229 citation statements)

References 136 publications

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“…The clinical anxiety disorders recognized in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V) include the following: generalized anxiety disorder, obsessive compulsive disorder, panic disorder, acute and chronic posttraumatic stress disorder, and various phobias, including agoraphobia, social phobia, and specific phobia (eg, fear of flying) [2] . Anxiety disorders, commonly occurring with depression and drug abuse, can be triggered or promoted by stress [3,4] . The most widely used therapeutic agents for the treatment of anxiety disorders include selective serotonin reuptake inhibitors, serotonin and norepinephrine reuptake inhibitors, benzodiazepine anxiolytic and NMDA receptor modulators [5] .…”

Section: Introductionmentioning

confidence: 99%

The role of the dynorphin/κ opioid receptor system in anxiety

Hang

Wang

et al. 2015

Acta Pharmacol Sin

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Anxiety disorders are the most common and prevalent forms of psychiatric disease, although the biological basis of anxiety is not well understood. The dynorphin/κ opioid receptor system is widely distributed in the central nervous system and has been shown to play a critical role in modulating mood and emotional behaviors. In the present review, we summarize current literature relating to the role played by the dynorphin/κ opioid receptor system in anxiety and κ opioid receptor antagonists as potential therapeutic agents for the treatment of anxiety disorders.

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Section: Introductionmentioning

confidence: 99%

The role of the dynorphin/κ opioid receptor system in anxiety

Hang

Wang

et al. 2015

Acta Pharmacol Sin

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“…This idea is supported by numerous observations. Exposure to stressful events is a primary causal factor in the development of mood disorders including depression (Kendler et al, 1999, van Praag, 2005, and the hippocampus is particularly sensitive to stress. For example, stressor exposure inhibits dentate gyrus (DG) neurogenesis (Gould et al, 1998, Gould andTanapat, 1999) and causes hippocampal neuronal atrophy (McEwen, 1999).…”

Section: Introductionmentioning

confidence: 99%

Learned helplessness is independent of levels of brain-derived neurotrophic factor in the hippocampus

et al. 2007

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Reduced levels of brain-derived neurotrophic factor (BDNF) in the hippocampus have been implicated in human affective disorders and behavioral stress responses. The current studies examined the role of BDNF in the behavioral consequences of inescapable stress, or learned helplessness. Inescapable stress decreased BDNF mRNA and protein in the hippocampus of sedentary rats. Rats allowed voluntary access to running wheels for either 3 or 6 weeks prior to exposure to stress were protected against stress-induced reductions of hippocampal BDNF protein.The observed prevention of stress-induced deceases in BDNF, however, occurred in a time course inconsistent with the prevention of learned helplessness by wheel running, which is evident following 6 weeks, but not 3 weeks, of wheel running. BDNF suppression in physically active rats was produced by administering a single injection of the selective serotonin reuptake inhibitor fluoxetine (10 mg/ kg) just prior to stress. Despite reduced levels of hippocampal BDNF mRNA following stress, physically active rats given the combination of fluoxetine and stress remained resistant against learned helplessness. Sedentary rats given both fluoxetine and stress still demonstrated typical learned helplessness behaviors. Fluoxetine by itself reduced BDNF mRNA in sedentary rats only, but did not affect freezing or escape learning 24 hours later. Finally, bilateral injections of BDNF (1 μg) into the dentate gyrus prior to stress prevented stress-induced reductions of hippocampal BDNF but did not prevent learned helplessness in sedentary rats.These data indicate that learned helplessness behaviors are independent of the presence or absence of hippocampal BDNF because blocking inescapable stress-induced BDNF suppression does not always prevent learned helplessness, and learned helplessness does not always occur in the presence of reduced BDNF. Results also suggest that the prevention of stress-induced hippocampal BDNF suppression is not necessary for the protective effect of wheel running against learned helplessness.

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“…The inappropriate regulation of stress responses is associated with the development of anxiety disorders, depression, and schizophrenia (Gispen-de Wied and Jansen, 2002;Kathol et al, 1989;Rasmusson et al, 2001;van Praag, 2004). Investigating the CNS mechanisms that regulate responses to stressful stimuli and anxiety-related responses may lead to advanced neuropsychiatric therapies.…”

Section: Introductionmentioning

confidence: 99%

Melanin-Concentrating Hormone-1 Receptor Modulates Neuroendocrine, Behavioral, and Corticolimbic Neurochemical Stress Responses in Mice

Smith

Davis

Rorick-Kehn

et al. 2005

Neuropsychopharmacol

100

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Repeated exposure to stressful conditions is linked to the etiology of affective disorders. The melanin-concentrating hormone-1 receptor (MCHR1) may be a novel mechanism that is involved in the modulation of stress responses and affective states. The role of MCHR1 in neuroendocrine, behavioral, and neurochemical stress, and anxiety-related responses was examined by monitoring the effects of melanin-concentrating hormone (MCH) and the selective MCHR1 antagonist, GW3430, in inbred C57Bl/6NTac and MCHR1-knockout (KO) and wild-type (WT) mice. Intracerebroventricular injection of MCH increased plasma corticosterone, and produced anxiety-related responses in the elevated plus maze. The selective MCHR1 antagonist, GW3430, blocked the neuroendocrine and behavioral effects of MCH and produced anxiolytic-like effects by itself in animal models of anxiety. Moreover, KO mice had an anxiolytic-like phenotype in behavioral models of anxiety, and GW3430 had anxiolytic-like effects in WT, but not KO mice. Lastly, stressor-evoked acetylcholine release within the prefrontal cortex of inbred and WT mice, but not KO mice, was blocked by GW3430. We show that MCH elicits anxiety-like responses and that the effects of a selective MCHR1 antagonist and the phenotype of KO mice are consistent with anxiolyticlike action. Distinct behavioral, physiological, and neurochemical stress, and anxiety-related responses were selectively modulated by the MCHR1, and these actions may involve corticolimbic regulation of stress responsivity and anxiety.

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Can stress cause depression?

Cited by 334 publications

References 136 publications

The role of the dynorphin/κ opioid receptor system in anxiety

The role of the dynorphin/κ opioid receptor system in anxiety

Learned helplessness is independent of levels of brain-derived neurotrophic factor in the hippocampus

Melanin-Concentrating Hormone-1 Receptor Modulates Neuroendocrine, Behavioral, and Corticolimbic Neurochemical Stress Responses in Mice

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