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Editorial of the Special Issue “Neurobiological Mechanisms Implicated in Stress-Related Psychiatric Disorders”

by Zoya Marinova

Int. J. Mol. Sci. 2023, 24(9), 7856; https://doi.org/10.3390/ijms24097856 - 26 Apr 2023

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Abstract

Mental disorders may seriously impair the quality of life of affected individuals and cause a significant public health burden [...] Full article

(This article belongs to the Special Issue Neurobiological Mechanisms Implicated in Stress-Related Psychiatric Disorders)

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21 pages, 4706 KiB

Open AccessArticle

Alterations in Metabolome and Microbiome Associated with an Early Stress Stage in Male Wistar Rats: A Multi-Omics Approach

by Julia Hernandez-Baixauli, Pere Puigbò, Nerea Abasolo, Hector Palacios-Jordan, Elisabet Foguet-Romero, David Suñol, Mar Galofré, Antoni Caimari, Laura Baselga-Escudero, Josep M. Del Bas and Miquel Mulero

Int. J. Mol. Sci. 2021, 22(23), 12931; https://doi.org/10.3390/ijms222312931 - 29 Nov 2021

Cited by 6 | Viewed by 2861

Abstract

Stress disorders have dramatically increased in recent decades becoming the most prevalent psychiatric disorder in the United States and Europe. However, the diagnosis of stress disorders is currently based on symptom checklist and psychological questionnaires, thus making the identification of candidate biomarkers necessary [...] Read more.

Stress disorders have dramatically increased in recent decades becoming the most prevalent psychiatric disorder in the United States and Europe. However, the diagnosis of stress disorders is currently based on symptom checklist and psychological questionnaires, thus making the identification of candidate biomarkers necessary to gain better insights into this pathology and its related metabolic alterations. Regarding the identification of potential biomarkers, omic profiling and metabolic footprint arise as promising approaches to recognize early biochemical changes in such disease and provide opportunities for the development of integrative candidate biomarkers. Here, we studied plasma and urine metabolites together with metagenomics in a 3 days Chronic Unpredictable Mild Stress (3d CUMS) animal approach that aims to focus on the early stress period of a well-established depression model. The multi-omics integration showed a profile composed by a signature of eight plasma metabolites, six urine metabolites and five microbes. Specifically, threonic acid, malic acid, alpha-ketoglutarate, succinic acid and cholesterol were proposed as key metabolites that could serve as key potential biomarkers in plasma metabolome of early stages of stress. Such findings targeted the threonic acid metabolism and the tricarboxylic acid (TCA) cycle as important pathways in early stress. Additionally, an increase in opportunistic microbes as virus of the Herpesvirales was observed in the microbiota as an effect of the primary stress stages. Our results provide an experimental biochemical characterization of the early stage of CUMS accompanied by a subsequent omic profiling and a metabolic footprinting that provide potential candidate biomarkers. Full article

(This article belongs to the Special Issue Neurobiological Mechanisms Implicated in Stress-Related Psychiatric Disorders)

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13 pages, 2409 KiB

Open AccessArticle

Crabp1 Modulates HPA Axis Homeostasis and Anxiety-like Behaviors by Altering FKBP5 Expression

by Yu-Lung Lin, Chin-Wen Wei, Thomas A. Lerdall, Jennifer Nhieu and Li-Na Wei

Int. J. Mol. Sci. 2021, 22(22), 12240; https://doi.org/10.3390/ijms222212240 - 12 Nov 2021

Cited by 8 | Viewed by 2544

Abstract

Retinoic acid (RA), the principal active metabolite of vitamin A, is known to be involved in stress-related disorders. However, its mechanism of action in this regard remains unclear. This study reports that, in mice, endogenous cellular RA binding protein 1 (Crabp1) is highly [...] Read more.

Retinoic acid (RA), the principal active metabolite of vitamin A, is known to be involved in stress-related disorders. However, its mechanism of action in this regard remains unclear. This study reports that, in mice, endogenous cellular RA binding protein 1 (Crabp1) is highly expressed in the hypothalamus and pituitary glands. Crabp1 knockout (CKO) mice exhibit reduced anxiety-like behaviors accompanied by a lowered stress induced-corticosterone level. Furthermore, CRH/DEX tests show an increased sensitivity (hypersensitivity) of their feedback inhibition in the hypothalamic–pituitary–adrenal (HPA) axis. Gene expression studies show reduced FKBP5 expression in CKO mice; this would decrease the suppression of glucocorticoid receptor (GR) signaling thereby enhancing their feedback inhibition, consistent with their dampened corticosterone level and anxiety-like behaviors upon stress induction. In AtT20, a pituitary gland adenoma cell line elevating or reducing Crabp1 level correspondingly increases or decreases FKBP5 expression, and its endogenous Crabp1 level is elevated by GR agonist dexamethasone or RA treatment. This study shows, for the first time, that Crabp1 regulates feedback inhibition of the the HPA axis by modulating FKBP5 expression. Furthermore, RA and stress can increase Crabp1 level, which would up-regulate FKBP5 thereby de-sensitizing feedback inhibition of HPA axis (by decreasing GR signaling) and increasing the risk of stress-related disorders. Full article

(This article belongs to the Special Issue Neurobiological Mechanisms Implicated in Stress-Related Psychiatric Disorders)

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16 pages, 2633 KiB

Open AccessArticle

Loss of mGluR5 in D1 Receptor-Expressing Neurons Improves Stress Coping

by Luca Zangrandi, Claudia Schmuckermair, Hussein Ghareh, Federico Castaldi, Regine Heilbronn, Gerald Zernig, Francesco Ferraguti and Arnau Ramos-Prats

Int. J. Mol. Sci. 2021, 22(15), 7826; https://doi.org/10.3390/ijms22157826 - 22 Jul 2021

Cited by 4 | Viewed by 3262

Abstract

The metabotropic glutamate receptor type 5 (mGluR5) has been proposed to play a crucial role in the selection and regulation of cognitive, affective, and emotional behaviors. However, the mechanisms by which these receptors mediate these effects remain largely unexplored. Here, we studied the [...] Read more.

The metabotropic glutamate receptor type 5 (mGluR5) has been proposed to play a crucial role in the selection and regulation of cognitive, affective, and emotional behaviors. However, the mechanisms by which these receptors mediate these effects remain largely unexplored. Here, we studied the role of mGluR5 located in D1 receptor-expressing (D1) neurons in the manifestation of different behavioral expressions. Mice with conditional knockout (cKO) of mGluR5 in D1 neurons (mGluR5^D1 cKO) and littermate controls displayed similar phenotypical profiles in relation to memory expression, anxiety, and social behaviors. However, mGluR5^D1 cKO mice presented different coping mechanisms in response to acute escapable or inescapable stress. mGluR5^D1 cKO mice adopted an enhanced active stress coping strategy upon exposure to escapable stress in the two-way active avoidance (TWA) task and a greater passive strategy upon exposure to inescapable stress in the forced swim test (FST). In summary, this work provides evidence for a functional integration of the dopaminergic and glutamatergic system to mediate control over internal states upon stress exposure and directly implicates D1 neurons and mGluR5 as crucial mediators of behavioral stress responses. Full article

(This article belongs to the Special Issue Neurobiological Mechanisms Implicated in Stress-Related Psychiatric Disorders)

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17 pages, 7161 KiB

Open AccessArticle

Cobalt Regulates Activation of Camk2α in Neurons by Influencing Fructose 1,6-Bisphosphatase 2 Quaternary Structure and Subcellular Localization

by Przemysław Duda, Bartosz Budziak and Dariusz Rakus

Int. J. Mol. Sci. 2021, 22(9), 4800; https://doi.org/10.3390/ijms22094800 - 30 Apr 2021

Cited by 3 | Viewed by 2266

Abstract

Fructose 1,6-bisphosphatase 2 (Fbp2) is a gluconeogenic enzyme and multifunctional protein modulating mitochondrial function and synaptic plasticity via protein-protein interactions. The ability of Fbp2 to bind to its cellular partners depends on a quaternary arrangement of the protein. NAD⁺ and AMP stabilize [...] Read more.

Fructose 1,6-bisphosphatase 2 (Fbp2) is a gluconeogenic enzyme and multifunctional protein modulating mitochondrial function and synaptic plasticity via protein-protein interactions. The ability of Fbp2 to bind to its cellular partners depends on a quaternary arrangement of the protein. NAD⁺ and AMP stabilize an inactive T-state of Fbp2 and thus, affect these interactions. However, more subtle structural changes evoked by the binding of catalytic cations may also change the affinity of Fbp2 to its cellular partners. In this report, we demonstrate that Fbp2 interacts with Co²⁺, a cation which in excessive concentrations, causes pathologies of the central nervous system and which has been shown to provoke the octal-like events in hippocampal slices. We describe for the first time the kinetics of Fbp2 in the presence of Co²⁺, and we provide a line of evidence that Co²⁺ blocks the AMP-induced transition of Fbp2 to the canonical T-state triggering instead of a new, non-canonical T-state. In such a state, Fbp2 is still partially active and may interact with its binding partners e.g., Ca²⁺/calmodulin-dependent protein kinase 2α (Camk2α). The Fbp2-Camk2α complex seems to be restricted to mitochondria membrane and it facilitates the Camk2α autoactivation and thus, synaptic plasticity. Full article

(This article belongs to the Special Issue Neurobiological Mechanisms Implicated in Stress-Related Psychiatric Disorders)

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11 pages, 5619 KiB

Open AccessArticle

Serotonin/5-HT1A Signaling in the Neurovascular Unit Regulates Endothelial CLDN5 Expression

by Kotaro Sugimoto, Naoki Ichikawa-Tomikawa, Keisuke Nishiura, Yasuto Kunii, Yasuteru Sano, Fumitaka Shimizu, Akiyoshi Kakita, Takashi Kanda, Tetsuya Imura and Hideki Chiba

Int. J. Mol. Sci. 2021, 22(1), 254; https://doi.org/10.3390/ijms22010254 - 29 Dec 2020

Cited by 11 | Viewed by 3387

Abstract

We previously reported that site-selective claudin-5 (CLDN5) breakdown and protein kinase A (PKA) activation are observed in brain microvessels of schizophrenia, but the underlying molecular basis remains unknown. The 5-HT1 receptors decline the intracellular cAMP levels and inactivate the major downstream PKA, and [...] Read more.

We previously reported that site-selective claudin-5 (CLDN5) breakdown and protein kinase A (PKA) activation are observed in brain microvessels of schizophrenia, but the underlying molecular basis remains unknown. The 5-HT1 receptors decline the intracellular cAMP levels and inactivate the major downstream PKA, and the 5-HT1A receptor is a promising target for schizophrenia. Therefore, we elucidated the involvement of serotonin/5-HT1A signaling in the endothelial CLDN5 expression. We demonstrate, by immunohistochemistry using post-mortem human brain tissue, that the 5-HT1A receptor is expressed in brain microvascular endothelial cells (BMVECs) and mural cells of the normal prefrontal cortex (PFC) gray matter. We also show that PKA is aberrantly activated not only in BMVECs but also in mural cells of the schizophrenic PFC. We subsequently revealed that the endothelial cell–pericyte tube-like structure was formed in a novel two-dimensional co-culture of human primary BMVECs and a human brain-derived pericyte cell line, in both of which the 5-HT1A receptor was expressed. Furthermore, we disclose that the serotonin/5-HT1A signaling enhances endothelial CLDN5 expression in BMVECs under two-dimensional co-culture conditions. Our findings provide novel insights into the physiological and pathological significance of serotonin/5-HT1A signaling in the region-specific regulation of the blood-brain barrier. Full article

(This article belongs to the Special Issue Neurobiological Mechanisms Implicated in Stress-Related Psychiatric Disorders)

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20 pages, 1629 KiB

Open AccessArticle

HIV-1 Tat Dysregulates the Hypothalamic-Pituitary-Adrenal Stress Axis and Potentiates Oxycodone-Mediated Psychomotor and Anxiety-Like Behavior of Male Mice

by Mohammed F. Salahuddin, Fakhri Mahdi and Jason J. Paris

Int. J. Mol. Sci. 2020, 21(21), 8212; https://doi.org/10.3390/ijms21218212 - 3 Nov 2020

Cited by 19 | Viewed by 3455

Abstract

Human immunodeficiency virus (HIV) is associated with co-morbid affective and stress-sensitive neuropsychiatric disorders that may be related to dysfunction of the hypothalamic-pituitary-adrenal (HPA) stress axis. The HPA axis is perturbed in up to 46% of HIV patients, but the mechanisms are not known. [...] Read more.

Human immunodeficiency virus (HIV) is associated with co-morbid affective and stress-sensitive neuropsychiatric disorders that may be related to dysfunction of the hypothalamic-pituitary-adrenal (HPA) stress axis. The HPA axis is perturbed in up to 46% of HIV patients, but the mechanisms are not known. The neurotoxic HIV-1 regulatory protein, trans-activator of transcription (Tat), may contribute. We hypothesized that HPA dysregulation may contribute to Tat-mediated interactions with oxycodone, a clinically-used opioid often prescribed to HIV patients. In transgenic male mice, Tat expression produced significantly higher basal corticosterone levels with adrenal insufficiency in response to a natural stressor or pharmacological blockade of HPA feedback, recapitulating the clinical phenotype. On acute exposure, HIV-1 Tat interacted with oxycodone to potentiate psychomotor and anxiety like-behavior in an open field and light-dark transition tasks, whereas repeated exposure sensitized stress-related psychomotor behavior and the HPA stress response. Pharmacological blockade of glucocorticoid receptors (GR) partially-restored the stress response and decreased oxycodone-mediated psychomotor behavior in Tat-expressing mice, implicating GR in these effects. Blocking corticotrophin-releasing factor (CRF) receptors reduced anxiety-like behavior in mice that were exposed to oxycodone. Together, these effects support the notion that Tat exposure can dysregulate the HPA axis, potentially raising vulnerability to stress-related substance use and affective disorders. Full article

(This article belongs to the Special Issue Neurobiological Mechanisms Implicated in Stress-Related Psychiatric Disorders)

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25 pages, 3033 KiB

Open AccessArticle

Effects of Early Life Stress on Bone Homeostasis in Mice and Humans

by Karin Wuertz-Kozak, Martin Roszkowski, Elena Cambria, Andrea Block, Gisela A. Kuhn, Thea Abele, Wolfgang Hitzl, David Drießlein, Ralph Müller, Michael A. Rapp, Isabelle M. Mansuy, Eva M. J. Peters and Pia M. Wippert

Int. J. Mol. Sci. 2020, 21(18), 6634; https://doi.org/10.3390/ijms21186634 - 10 Sep 2020

Cited by 8 | Viewed by 5274

Abstract

Bone pathology is frequent in stressed individuals. A comprehensive examination of mechanisms linking life stress, depression and disturbed bone homeostasis is missing. In this translational study, mice exposed to early life stress (MSUS) were examined for bone microarchitecture (μCT), metabolism (qPCR/ELISA), and neuronal [...] Read more.

Bone pathology is frequent in stressed individuals. A comprehensive examination of mechanisms linking life stress, depression and disturbed bone homeostasis is missing. In this translational study, mice exposed to early life stress (MSUS) were examined for bone microarchitecture (μCT), metabolism (qPCR/ELISA), and neuronal stress mediator expression (qPCR) and compared with a sample of depressive patients with or without early life stress by analyzing bone mineral density (BMD) (DXA) and metabolic changes in serum (osteocalcin, PINP, CTX-I). MSUS mice showed a significant decrease in NGF, NPYR1, VIPR1 and TACR1 expression, higher innervation density in bone, and increased serum levels of CTX-I, suggesting a milieu in favor of catabolic bone turnover. MSUS mice had a significantly lower body weight compared to control mice, and this caused minor effects on bone microarchitecture. Depressive patients with experiences of childhood neglect also showed a catabolic pattern. A significant reduction in BMD was observed in depressive patients with childhood abuse and stressful life events during childhood. Therefore, future studies on prevention and treatment strategies for both mental and bone disease should consider early life stress as a risk factor for bone pathologies. Full article

(This article belongs to the Special Issue Neurobiological Mechanisms Implicated in Stress-Related Psychiatric Disorders)

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Review

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53 pages, 662 KiB

Open AccessReview

Neurobiological Highlights of Cognitive Impairment in Psychiatric Disorders

by Anna Morozova, Yana Zorkina, Olga Abramova, Olga Pavlova, Konstantin Pavlov, Kristina Soloveva, Maria Volkova, Polina Alekseeva, Alisa Andryshchenko, Georgiy Kostyuk, Olga Gurina and Vladimir Chekhonin

Int. J. Mol. Sci. 2022, 23(3), 1217; https://doi.org/10.3390/ijms23031217 - 22 Jan 2022

Cited by 41 | Viewed by 8021

Abstract

This review is focused on several psychiatric disorders in which cognitive impairment is a major component of the disease, influencing life quality. There are plenty of data proving that cognitive impairment accompanies and even underlies some psychiatric disorders. In addition, sources provide information [...] Read more.

This review is focused on several psychiatric disorders in which cognitive impairment is a major component of the disease, influencing life quality. There are plenty of data proving that cognitive impairment accompanies and even underlies some psychiatric disorders. In addition, sources provide information on the biological background of cognitive problems associated with mental illness. This scientific review aims to summarize the current knowledge about neurobiological mechanisms of cognitive impairment in people with schizophrenia, depression, mild cognitive impairment and dementia (including Alzheimer’s disease).The review provides data about the prevalence of cognitive impairment in people with mental illness and associated biological markers. Full article

(This article belongs to the Special Issue Neurobiological Mechanisms Implicated in Stress-Related Psychiatric Disorders)

22 pages, 779 KiB

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Associations between Melatonin, Neuroinflammation, and Brain Alterations in Depression

by Eunsoo Won, Kyoung-Sae Na and Yong-Ku Kim

Int. J. Mol. Sci. 2022, 23(1), 305; https://doi.org/10.3390/ijms23010305 - 28 Dec 2021

Cited by 56 | Viewed by 10455

Abstract

Pro-inflammatory systemic conditions that can cause neuroinflammation and subsequent alterations in brain regions involved in emotional regulation have been suggested as an underlying mechanism for the pathophysiology of major depressive disorder (MDD). A prominent feature of MDD is disruption of circadian rhythms, of [...] Read more.

Pro-inflammatory systemic conditions that can cause neuroinflammation and subsequent alterations in brain regions involved in emotional regulation have been suggested as an underlying mechanism for the pathophysiology of major depressive disorder (MDD). A prominent feature of MDD is disruption of circadian rhythms, of which melatonin is considered a key moderator, and alterations in the melatonin system have been implicated in MDD. Melatonin is involved in immune system regulation and has been shown to possess anti-inflammatory properties in inflammatory conditions, through both immunological and non-immunological actions. Melatonin has been suggested as a highly cytoprotective and neuroprotective substance and shown to stimulate all stages of neuroplasticity in animal models. The ability of melatonin to suppress inflammatory responses through immunological and non-immunological actions, thus influencing neuroinflammation and neurotoxicity, along with subsequent alterations in brain regions that are implicated in depression, can be demonstrated by the antidepressant-like effects of melatonin. Further studies that investigate the associations between melatonin, immune markers, and alterations in the brain structure and function in patients with depression could identify potential MDD biomarkers. Full article

(This article belongs to the Special Issue Neurobiological Mechanisms Implicated in Stress-Related Psychiatric Disorders)

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12 pages, 857 KiB

Open AccessReview

The Role of HPA Axis and Allopregnanolone on the Neurobiology of Major Depressive Disorders and PTSD

by Felipe Borges Almeida, Graziano Pinna and Helena Maria Tannhauser Barros

Int. J. Mol. Sci. 2021, 22(11), 5495; https://doi.org/10.3390/ijms22115495 - 23 May 2021

Cited by 59 | Viewed by 7896

Abstract

Under stressful conditions, the hypothalamic-pituitary-adrenal (HPA) axis acts to promote transitory physiological adaptations that are often resolved after the stressful stimulus is no longer present. In addition to corticosteroids (e.g., cortisol), the neurosteroid allopregnanolone (3α,5α-tetrahydroprogesterone, 3α-hydroxy-5α-pregnan-20-one) participates in negative feedback mechanisms that restore [...] Read more.

Under stressful conditions, the hypothalamic-pituitary-adrenal (HPA) axis acts to promote transitory physiological adaptations that are often resolved after the stressful stimulus is no longer present. In addition to corticosteroids (e.g., cortisol), the neurosteroid allopregnanolone (3α,5α-tetrahydroprogesterone, 3α-hydroxy-5α-pregnan-20-one) participates in negative feedback mechanisms that restore homeostasis. Chronic, repeated exposure to stress impairs the responsivity of the HPA axis and dampens allopregnanolone levels, participating in the etiopathology of psychiatric disorders, such as major depressive disorder (MDD) and post-traumatic stress disorder (PTSD). MDD and PTSD patients present abnormalities in the HPA axis regulation, such as altered cortisol levels or failure to suppress cortisol release in the dexamethasone suppression test. Herein, we review the neurophysiological role of allopregnanolone both as a potent and positive GABAergic neuromodulator but also in its capacity of inhibiting the HPA axis. The allopregnanolone function in the mechanisms that recapitulate stress-induced pathophysiology, including MDD and PTSD, and its potential as both a treatment target and as a biomarker for these disorders is discussed. Full article

(This article belongs to the Special Issue Neurobiological Mechanisms Implicated in Stress-Related Psychiatric Disorders)

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11 pages, 559 KiB

Open AccessReview

Altered Task-Evoked Corticolimbic Responsivity in Generalized Anxiety Disorder

by Nayoung Kim and M. Justin Kim

Int. J. Mol. Sci. 2021, 22(7), 3630; https://doi.org/10.3390/ijms22073630 - 31 Mar 2021

Cited by 7 | Viewed by 6644

Abstract

Generalized anxiety disorder (GAD) is marked by uncontrollable, persistent worry and exaggerated response to uncertainty. Here, we review and summarize the findings from the GAD literature that employs functional neuroimaging methods. In particular, the present review focuses on task-based blood oxygen level-dependent (BOLD) [...] Read more.

Generalized anxiety disorder (GAD) is marked by uncontrollable, persistent worry and exaggerated response to uncertainty. Here, we review and summarize the findings from the GAD literature that employs functional neuroimaging methods. In particular, the present review focuses on task-based blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI) studies. We find that select brain regions often regarded as a part of a corticolimbic circuit (e.g., amygdala, anterior cingulate cortex, prefrontal cortex) are consistently targeted for a priori hypothesis-driven analyses, which, in turn, shows varying degrees of abnormal BOLD responsivity in GAD. Data-driven whole-brain analyses show the insula and the hippocampus, among other regions, to be affected by GAD, depending on the task used in each individual study. Overall, while the heterogeneity of the tasks and sample size limits the generalizability of the findings thus far, some promising convergence can be observed in the form of the altered BOLD responsivity of the corticolimbic circuitry in GAD. Full article

(This article belongs to the Special Issue Neurobiological Mechanisms Implicated in Stress-Related Psychiatric Disorders)

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20 pages, 1662 KiB

Open AccessReview

Inflammatory Depression—Mechanisms and Non-Pharmacological Interventions

by Klara Suneson, Jesper Lindahl, Simon Chamli Hårsmar, Gustav Söderberg and Daniel Lindqvist

Int. J. Mol. Sci. 2021, 22(4), 1640; https://doi.org/10.3390/ijms22041640 - 6 Feb 2021

Cited by 57 | Viewed by 13031

Abstract

Treatment of depression is hampered by the failure to identify distinct symptom profiles with distinct pathophysiologies that differentially respond to distinct treatments. We posit that inflammatory depression is a meaningful depression subtype associated with specific symptoms and biological abnormalities. We review several upstream, [...] Read more.

Treatment of depression is hampered by the failure to identify distinct symptom profiles with distinct pathophysiologies that differentially respond to distinct treatments. We posit that inflammatory depression is a meaningful depression subtype associated with specific symptoms and biological abnormalities. We review several upstream, potentially causative, mechanisms driving low-grade inflammation in this subtype of depression. We also discuss downstream mechanisms mediating the link between inflammation and symptoms of depression, including alterations in dopaminergic neurotransmission and tryptophan metabolism. Finally, we review evidence for several non-pharmacological interventions for inflammatory depression, including probiotics, omega-3 fatty acids, and physical exercise interventions. While some evidence suggests that these interventions may be efficacious in inflammatory depression, future clinical trials should consider enriching patient populations for inflammatory markers, or stratify patients by inflammatory status, to confirm or refute this hypothesis. Full article

(This article belongs to the Special Issue Neurobiological Mechanisms Implicated in Stress-Related Psychiatric Disorders)

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