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      The human hypothalamus in mood disorders: The HPA axis in the center

      review-article
      a , * , a , b
      IBRO Reports
      Elsevier
      The hypothalamo-pituitary-adrenal axis, Glutamate, GABA, Neuropeptide, Sex differences

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          Abstract

          There are no specific structural neuropathological hallmarks found in the brain of mood disorders. Instead, there are molecular, functional and structural alterations reported in many brain areas. The neurodevelopmental underpinning indicated the presence of various genetic and developmental risk factors. The effect of genetic polymorphisms and developmental sequalae, some of which may start in the womb, result in functional changes in a network mediated by neurotransmitters and neuropeptides, which make the emotion- and stress-related brain systems more vulnerable to stressful events. This network of stress-related neurocircuits consists of, for instance, brainstem nuclei, the amygdala, habenula, prefrontal cortex and hypothalamus. Various nuclei of the hypothalamus form indeed one of the crucial hubs in this network. This structure concerns not only the hypothalamo-pituitary-adrenal (HPA) axis that integrate the neuro-endocrine-immune responses to stress, but also other hypothalamic nuclei and systems that play a key role in the symptoms of depression, such as disordered day-night rhythm, lack of reward feelings, disturbed eating, sex, and disturbed cognitive functions. The present review will focus on the changes in the human hypothalamus in depression, with the HPA axis in the center. We will discuss the inordinate network of neurotransmitters and neuropeptides involved, with the hope to find the most vulnerable neurobiological systems and the possible development of tailor-made treatments for mood disorders in the future.

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          Most cited references134

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          Mood is indirectly related to serotonin, norepinephrine and dopamine levels in humans: a meta-analysis of monoamine depletion studies.

          Dysfunction in the monoamine systems of serotonin (5-HT), norepinephrine (NE) and dopamine (DA) may causally be related to major depressive disorder (MDD). Monoamine depletion studies investigate the direct effects of monoamines on mood. Acute tryptophan depletion (ATD) or para-chlorophenylalanine (PCPA) deplete 5-HT, acute phenylalanine/tyrosine depletion (APTD) or alpha-methyl-para-tyrosine (AMPT) deplete NE/DA. Available depletion studies found conflicting results in heterogeneous populations: healthy controls, patients with previous MDD in remission and patients suffering from MDD. The decrease in mood after 5-HT and NE/DA depletion in humans is reviewed and quantified. Systematic search of MEDLINE and EMBASE (1966-October 2006) and cross-references was carried out. Randomized studies applying ATD, PCPA, APTD or AMPT vs control depletion were included. Pooling of results by meta-analyses was stratified for studied population and design of the study (within or between subjects). Seventy-three ATD, 2 PCPA, 10 APTD and 8 AMPT studies were identified of which 45 ATD and 8 APTD studies could be meta-analyzed. 5-HT or NE/DA depletion did not decrease mood in healthy controls. 5-HT or NE/DA depletion slightly lowered mood in healthy controls with a family history of MDD. In drug-free patients with MDD in remission, a moderate mood decrease was found for ATD, without an effect of APTD. ATD induced relapse in patients with MDD in remission who used serotonergic antidepressants. In conclusion, monoamine depletion studies demonstrate decreased mood in subjects with a family history of MDD and in drug-free patients with MDD in remission, but do not decrease mood in healthy humans. Although depletion studies usefully investigate the etiological link of 5-HT and NE with MDD, they fail to demonstrate a causal relation. They presumably clarify a vulnerability trait to become depressed. Directions for further investigation of this vulnerability trait are proposed.
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            Cortisol and post-traumatic stress disorder in adults: systematic review and meta-analysis.

            Post-traumatic stress disorder (PTSD) has inconsistently been associated with lower levels of cortisol. To compare basal cortisol levels in adults with current PTSD and in people without psychiatric disorder. Systematic review and meta-analysis. Standardised mean differences (SMD) in basal cortisol levels were calculated and random-effects models using inverse variance weighting were applied. Across 37 studies, 828 people with PTSD and 800 controls did not differ in cortisol levels (pooled SMD=-0.12, 95% CI=-0.32 to 0.080). Subgroup analyses revealed that studies assessing plasma or serum showed significantly lower levels in people with PTSD than in controls not exposed to trauma. Lower levels were also found in people with PTSD when females were included, in studies on physical or sexual abuse, and in afternoon samples. Low cortisol levels in PTSD are only found under certain conditions. Future research should elucidate whether low cortisol is related to gender or abuse and depends on the measurement methods used.
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              Dopamine release in response to a psychological stress in humans and its relationship to early life maternal care: a positron emission tomography study using [11C]raclopride.

              Mesolimbic dopamine is thought to play a role in the processing of rewards. However, animal studies also demonstrate dopamine release in response to aversive stressful stimuli. Also, in animal studies, disruptions of the mother-infant relationship have been shown to have long-lasting effects on the mesolimbic dopamine system and the hypothalamic-pituitary adrenal axis. We therefore investigated dopamine release in response to stress in human subjects, considering the relationship to early life parental care. We screened 120 healthy young college students for parental care in early life using a combination of telephone interviews and questionnaires. Five students from the top end and five students from the bottom end of the parental care distribution were then invited for a positron emission tomography study using [11C]raclopride and a psychosocial stress task. The psychosocial stressor caused a significant release of dopamine in the ventral striatum as indicated by a reduction in [11C]raclopride binding potential in the stress versus resting condition in subjects reporting low parental care. Moreover, the magnitude of the salivary cortisol response to stress was significantly correlated with the reduction in [11C]raclopride binding in the ventral striatum (r = 0.78), consistent with a facilitating effect of cortisol on dopamine neuron firing. These data suggest that aversive stressful events can be associated with mesolimbic dopamine release in humans, and that the method presented here may be useful to study the effects of early life events on neurobiological stress systems.
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                Author and article information

                Contributors
                Journal
                IBRO Rep
                IBRO Rep
                IBRO Reports
                Elsevier
                2451-8301
                14 December 2018
                June 2019
                14 December 2018
                : 6
                : 45-53
                Affiliations
                [a ]Department of Neurobiology and Department of Neurology of the Second Affiliated Hospital, Institute of neuroscience, NHC and CAMS key laboratory of Medical Neurobiology, Zhejiang University School of Medicine, Hangzhou, China
                [b ]Netherlands Institute for Neuroscience, An Institute of the Royal Netherlands Academy of Arts and Sciences, Amsterdam, the Netherlands
                Author notes
                [* ]Corresponding author. baoaimin@ 123456zju.edu.cn
                Article
                S2451-8301(17)30043-2
                10.1016/j.ibror.2018.11.008
                6562194
                31211281
                06d5ee5f-f293-493e-bc6e-139bb24df5c4
                © 2018 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 14 November 2017
                : 28 November 2018
                Categories
                Articles from the Special Issue on Emotion and mood disorders: from molecular mechanisms to neuronal circuits; Edited by Jiang-Ning Zhou

                the hypothalamo-pituitary-adrenal axis,glutamate,gaba,neuropeptide,sex differences

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