• Evolution
• Function
• MiR-34 family

• MicroRNAs/genetics
• MicroRNAs/metabolism
• Humans
• Animals
• Gene Expression Regulation
• Evolution, Molecular
• Multigene Family

• Anxiety
• Meta-Analysis
• Mice
• Open Field
• Rat
• Stress

• GLT1/EAAT2 transporter
• OCD
• PTSD
• WZ-5HT rats
• amygdala and hippocampus
• ceftriaxone
• contextual fear conditioning
• marble-burying test

• Humans
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Biomarkers
• Adolescent
• Mental Disorders/genetics

• R01 DA037911 NIDA NIH HHS

• cancer
• circadian
• cry1
• electromagnetic
• neural
• phthalates

• MicroRNAs/genetics
• MicroRNAs/metabolism
• Humans
• Stress, Psychological/genetics
• Stress, Psychological/metabolism
• Mental Disorders/genetics
• Animals
• Brain/metabolism
• Epigenesis, Genetic/genetics

• 2015HRE757 Ministero dell'Istruzione, dell'Università e della Ricerca (Ministry of Education, University and Research)
• 2017-0620 Fondazione Cariplo (Cariplo Foundation)
• 2014-1133 Fondazione Cariplo (Cariplo Foundation)
• 2019-3357 Fondazione Cariplo (Cariplo Foundation)

• Anxiety Disorders
• DNA methylation
• Epigenetic
• Histone modifications

• Humans
• DNA Methylation
• Epigenesis, Genetic/genetics
• Anxiety Disorders/drug therapy
• Anxiety Disorders/genetics
• Epigenomics
• Histone Deacetylase Inhibitors/pharmacology
• Histone Deacetylase Inhibitors/therapeutic use

• Dorsal Raphè
• GABA
• microRNA
• stress

• Humans
• Animals
• Dorsal Raphe Nucleus/metabolism
• GABAergic Neurons/metabolism
• MicroRNAs/metabolism
• Mammals

• Ministero della Salute (Italy Ministry of Health)
• Sapienza Università di Roma (Sapienza University of Rome)

• Humans
• Anti-Anxiety Agents/pharmacology
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Anxiety/genetics
• RNA, Messenger
• Respiratory Distress Syndrome
• Transcriptional Elongation Factors/metabolism
• E2F5 Transcription Factor/metabolism
• RNA-Binding Proteins

• Corticotropin-releasing factor receptors type 1 and 2
• GABA
• Hippocampus
• Posttraumatic stress disorder
• Resistance

• Animal model of depression-like state
• Early adversities
• Passive coping behavior
• Sex differences
• microRNA-34a

• Chronic unpredictable mild stress
• Corticosterone
• Fluoxetine
• Neurotransmitters
• Serotonin
• miRNAs

Bipolar disorder (BD) is a severe, chronic, and disabling neuropsychiatric disorder characterized by recurrent mood disturbances (mania/hypomania and depression, with or without mixed features) and a constellation of cognitive, psychomotor, autonomic, and endocrine abnormalities. The etiology of BD is multifactorial, including both biological and epigenetic factors. Recently, microRNAs (miRNAs), a class of epigenetic regulators of gene expression playing a central role in brain development and plasticity, have been related to several neuropsychiatric disorders, including BD. Moreover, an alteration in the number/distribution and differentiation potential of neural stem cells has also been described, significantly affecting brain homeostasis and neuroplasticity. This review aimed to evaluate the most reliable scientific evidence on miRNAs as biomarkers for the diagnosis of BD and assess their implications in response to mood stabilizers, such as lithium. Neural stem cell distribution, regulation, and dysfunction in the etiology of BD are also dissected.

• bipolar disorder (BD)
• lithium
• microRNA
• molecular mechanisms
• neural stem cells
• stem cells

• Antimanic Agents/therapeutic use
• Bipolar Disorder/diagnosis
• Bipolar Disorder/drug therapy
• Bipolar Disorder/genetics
• Humans
• Lithium/pharmacology
• Lithium/therapeutic use
• MicroRNAs/genetics
• MicroRNAs/therapeutic use
• Stem Cells/metabolism

• anxiety
• depression
• microRNA
• microbiota
• psychiatric disorders

• CORT
• Dendrite morphology
• Ketamine
• REST
• Stress
• miR-9-5p

Depression is an effect of complex interactions between genetic, epigenetic and environmental factors. It is well established that stress responses are associated with multiple modest and often dynamic molecular changes in the homeostatic balance, rather than with a single genetic factor that has a strong phenotypic penetration. As depression is a multifaceted phenotype, it is important to study biochemical pathways that can regulate the overall allostasis of the brain. One such biological system that has the potential to fine-tune a multitude of diverse molecular processes is RNA interference (RNAi). RNAi is an epigenetic process showing a very low level of evolutionary diversity, and relies on the posttranscriptional regulation of gene expression using, in the case of mammals, primarily short (17–23 nucleotides) noncoding RNA transcripts called microRNAs (miRNA). In this review, our objective was to examine, summarize and discuss recent advances in the field of biomedical and clinical research on the role of miRNA-mediated regulation of gene expression in the development of depression. We focused on studies investigating post-mortem brain tissue of individuals with depression, as well as research aiming to elucidate the biomarker potential of miRNAs in depression and antidepressant response.

• antidepressant treatment
• biomarker
• depression
• human brain
• miRNome
• microRNA

• Caenorhabditis elegans
• Drosophila melanogaster
• Environmental stress
• Epigenetics
• Invertebrate models
• Transgenerational inheritance

• arrhythmias
• cardiac disease
• epigenetic
• miR-34a
• stress

• Animals
• Heart
• Male
• MicroRNAs/genetics
• Rats
• Stress, Psychological/genetics

• molecular neuroscience
• depression

• Animals
• Gene Regulatory Networks
• Humans
• MicroRNAs/genetics
• Mood Disorders/genetics
• Neuronal Plasticity
• RNA, Messenger

• 310030E_179651 Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation)
• 32NE30_189486 Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation)

• 5-HT2C
• Dorsal Raphe
• Fluoxetine
• RDoC
• Target Site Blocker
• miR-34

Although the function of microRNAs (miRNAs) during embryonic development has been intensively studied in recent years, their postnatal physiological functions remain largely unexplored due to inherent difficulties with the presence of redundant paralogs of the same seed. Thus, it is particularly challenging to uncover miRNA functions at neural circuit level since animal behaviors would need to be assessed upon complete loss of miRNA family functions. Here, we focused on the neural functions of MiR34/449 that manifests a dynamic expression pattern in the spinal cord from embryonic to postnatal stages. Our behavioral assays reveal that the loss of MiR34/449 miRNAs perturb thermally induced pain response thresholds and compromised delicate motor output in mice. Mechanistically, MiR34/449 directly target Satb1 and Satb2 to fine-tune the precise number of a sub-population of motor synergy encoder (MSE) neurons. Thus, MiR34/449 fine-tunes optimal development of Satb1/2^on interneurons in the spinal cord, thereby refining explicit sensory-to-motor circuit outputs.

The spinal cord is an information superhighway that connects the body with the brain. There, circuits of neurons process information from the brain before sending commands to muscles to generate movement. Each spinal cord circuit contains many types of neurons, whose identity is defined by the set of genes that are active or ‘expressed’ in each cell.

When a gene is turned on, its DNA sequence is copied to produce a messenger RNA (mRNA), a type of molecule that the cell then uses as a template to produce a protein. MicroRNAs (or miRNAs), on the other hand, are tiny RNA molecules that help to regulate gene expression by binding to and ‘deactivating’ specific mRNAs, stopping them from being used to make proteins.

Mammalian cells contain thousands of types of microRNAs, many of which have unknown roles: this includes MiR34/449, a group of six microRNAs found mainly within the nervous system. By using genetic technology to delete this family from the mouse genome, Chang et al. now show that MiR34/449 has a key role in regulating spinal cord circuits.

The first clue came from discovering that mice without the MiR34/449 family had unusual posture and a tendency to walk on tiptoe. The animals were also more sensitive to heat, flicking their tails away from a heat source more readily than control mice.

At a finer level, the spinal cords of the mutants contained greater numbers of cells in which two genes, Satb1 and Satb2, were turned on. Compared to their counterparts in control mice, the Satb1/2-positive neurons also showed differences in the rest of the genes they expressed. In essence, these neurons had a different genetic profile in MiR34/449 mutant mice, therefore disrupting the neural circuit they belong to.

Based on these findings, Chang et al. propose that in wild-type mice, the MiR34/449 family fine-tunes the expression of Satb1/2 in the spinal cord during development. In doing so, it regulates the formation of the spinal cord circuits that help to control movement. More generally, these results provide clues about how miRNAs help to determine cell identities; further studies could then examine whether other miRNAs contribute to the development and maintenance of neuronal circuits.

• MiR34
• MiR449
• Satb1/2
• developmental biology
• miRNA
• microRNAs
• mouse
• neuroscience
• spinal cord

• Drug development
• Major depressive disorder
• Micro RNA
• Neuroimaging
• Neuroplasticity
• Stress

Cannabidiol (CBD) is the most abundant non-psychoactive component of cannabis; it displays a very low affinity for cannabinoid receptors, facilitates endocannabinoid signaling by inhibiting the hydrolysis of anandamide, and stimulates both transient receptor potential vanilloid 1 and 2 and serotonin type 1A receptors. Since CBD interacts with a wide variety of molecular targets in the brain, its therapeutic potential has been investigated in a number of neuropsychiatric diseases, including anxiety and mood disorders. Specifically, CBD has received growing attention due to its anxiolytic and antidepressant properties. As a consequence, and given its safety profile, CBD is considered a promising new agent in the treatment of anxiety and mood disorders. However, the exact molecular mechanism of action of CBD still remains unknown. In the present preclinical review, we provide a summary of animal-based studies that support the use of CBD as an anxiolytic- and antidepressant-like compound. Next, we describe neuropharmacological evidence that links the molecular pharmacology of CBD to its behavioral effects. Finally, by taking into consideration the effects of CBD on DNA methylation, histone modifications, and microRNAs, we elaborate on the putative role of epigenetic mechanisms in mediating CBD’s therapeutic outcomes.

• 5-HT1A receptors
• CB1 receptors
• DNA methylation
• TRPV1 receptors
• anxiety
• cannabidiol
• depression
• epigenetics
• histone modifications
• miRNA

• Anxiety
• Behaviour
• Sociability
• miRNA

• Animals
• Anxiety/genetics
• Anxiety Disorders/genetics
• Autism Spectrum Disorder/genetics
• Gene Expression Regulation
• Gene Regulatory Networks
• Humans
• MicroRNAs/genetics
• RNA, Messenger/genetics

• DI 1501/5-2, FI 2157/2-1 Deutsche Forschungsgemeinschaft
• 310030E_179651 Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung

Healthy persons hold a very complex system for controlling energy homeostasis. The system functions on the interconnected way between the nutritional, endocrine, neural, and epigenetic regulation, which includes the microRNAs (miRNAs). Currently, it is well accepted that experiences of early life stress (ELS) carry modification of the central control of feeding behavior, one of the factors controlling energy homeostasis. Recently, studies give us a clue on the modulation of eating behavior, which is one of the main factors associated with the development of obesity. This clue connected the neural control through the serotonin (5HT) and dopamine (DA) systems with the fine regulation of miRNAs. The first pieces of evidence highlight the presence of the miR-16 in the regulation of the serotonin transporter (SERT) as well as the receptors 1a (5HT1A) and 2a (5HT2A). On the other hand, miR-504 is related to the dopamine receptor D2 (DRD2). As our knowledge advance, we expected to discover other important pathways for the regulation of the energy homeostasis. As both neurotransmission systems and miRNAs seem to be sensible to ELS, the aim of this review is to bring new insight about the involvement of miRNAs with a central role in the control of eating behavior focusing on the influences of ELS and regulation of neurotransmission systems.

• dopamine
• early life stress
• miRNA
• obesity
• serotonin

Pain and stress are both phenomena that challenge an individual’s homeostasis and have significant overlap in conceptual and physiological processes. Allostasis is the ability to adapt to pain and stress and maintain homeostasis; however, if either process becomes chronic, it may result in negative long-term outcomes. The negative effects of stress on health outcomes on physiology and behavior, including pain, have been well documented; however, the specific mechanisms of how stress and what quantity of stress contributes to the maintenance and exacerbation of pain have not been identified, and thus pharmacological interventions are lacking. The objective of this brief review is to: 1. identify the gaps in the literature on the impact of acute and chronic stress on chronic pain, 2. highlight future directions for stress and chronic pain research; and 3. introduce the Pain-Stress Model in the context of the current literature on stress and chronic pain. A better understanding of the connection between stress and chronic pain could provide greater insight into the neurobiology of these processes and contribute to individualized treatment for pain rehabilitation and drug development for these often comorbid conditions.

• allostatic load
• behavior
• chronic pain
• chronic stress
• physiology
• reactivity

• Wnt signaling
• amygdala
• depression
• epigenetics
• miRNA
• stress

• Candidate gene
• Cocaine effects
• Early stress
• Nucleus accumbens
• Vulnerability

• Anxiety disorders
• Anxiolytic
• Epigenetics
• RDoc
• microRNA

MicroRNAs (miRNAs) are a family of short, non-coding RNAs that have been linked to critical cellular activities, most notably regulation of gene expression. The identification of miRNA is a cross-disciplinary approach that requires both computational identification methods and wet-lab validation experiments, making it a resource-intensive procedure. While numerous machine learning methods have been developed to increase classification accuracy and thus reduce validation costs, most methods use supervised learning and thus require large labeled training data sets, often not feasible for less-sequenced species. On the other hand, there is now an abundance of unlabeled RNA sequence data due to the emergence of high-throughput wet-lab experimental procedures, such as next-generation sequencing.

This paper explores the application of semi-supervised machine learning for miRNA classification in order to maximize the utility of both labeled and unlabeled data. We here present the novel combination of two semi-supervised approaches: active learning and multi-view co-training. Results across six diverse species show that this multi-stage semi-supervised approach is able to improve classification performance using very small numbers of labeled instances, effectively leveraging the available unlabeled data.

The proposed semi-supervised miRNA classification pipeline holds the potential to identify novel miRNA with high recall and precision while requiring very small numbers of previously known miRNA. Such a method could be highly beneficial when studying miRNA in newly sequenced genomes of niche species with few known examples of miRNA.

• Active learning
• Co-training
• Machine learning
• Next-generation sequencing
• Semi-supervised learning
• miRNA prediction

Stress can be defined as an acute threat to the homeostasis of an organism, and in order to manage stress, and maintain stability, the allostatic systems activate an adaptive response. Stress has been shown to have both short - and long-term effects on the function of the gastrointestinal tract, but long-term exposure to stress is more likely to cause endocrine disorders.

The aim of this study was to investigate the endocrine response to stress, and evaluate the relationship between somatization and gastrointestinal symptoms.

A systematic literature search was conducted on several academic databases, which included, Pubmed, EBSCO and Science Direct. The search was performed using the keywords, “endocrine response to stress”, “somatization” and “gastrointestinal symptoms”.

The hypothalamic-pituitary-adrenal (HPA) axis is essential in controlling physiological stress responses. Dysfunction is related to several mental disorders, including anxiety and depression, or somatization. Symptoms associated with genetic, or other traumatic experiences of individuals under stress, can lead to a maladaptive response to stress. These stressful life events were found to be associated with digestive system-related chronic diseases. Gastrointestinal disorders significantly affect millions of people worldwide.

This study examined how the endocrine system responds to stress, and the effect this has in causing stress-related gastrointestinal distresses. Our findings indicate that stress-related psychological disorders are strongly associated with the severity of gastrointestinal symptoms.

• Stress
• endocrine response
• gastrointestinal symptoms
• somatization

• Endocrine System Diseases/etiology
• Gastrointestinal Diseases/etiology
• Humans
• Hypothalamo-Hypophyseal System/physiopathology
• Pituitary-Adrenal System/physiopathology
• Psychophysiologic Disorders/etiology
• Receptors, Corticotropin-Releasing Hormone/metabolism
• Receptors, Serotonin, 5-HT3/metabolism
• Stress, Psychological/complications

MicroRNA (miRNA) are short, non-coding RNAs involved in cell regulation at post-transcriptional and translational levels. Numerous computational predictors of miRNA been developed that generally classify miRNA based on either sequence- or expression-based features. While these methods are highly effective, they require large labelled training data sets, which are often not available for many species. Simultaneously, emerging high-throughput wet-lab experimental procedures are producing large unlabelled data sets of genomic sequence and RNA expression profiles. Existing methods use supervised machine learning and are therefore unable to leverage these unlabelled data. In this paper, we design and develop a multi-view co-training approach for the classification of miRNA to maximize the utility of unlabelled training data by taking advantage of multiple views of the problem. Starting with only 10 labelled training data, co-training is shown to significantly (p < 0.01) increase classification accuracy of both sequence- and expression-based classifiers, without requiring any new labelled training data. After 11 iterations of co-training, the expression-based view of miRNA classification experiences an average increase in AUPRC of 15.81% over six species, compared to 11.90% for self-training and 4.84% for passive learning. Similar results are observed for sequence-based classifiers with increases of 46.47%, 39.53% and 29.43%, for co-training, self-training, and passive learning, respectively. The final co-trained sequence and expression-based classifiers are integrated into a final confidence-based classifier which shows improved performance compared to both the expression (1.5%, p = 0.021) and sequence (3.7%, p = 0.006) views. This study represents the first application of multi-view co-training to miRNA prediction and shows great promise, particularly for understudied species with few available training data.

• Amphetamine binge
• Chronic restraint stress
• Epigenetics
• Individual differences
• Mesolimbic dopaminergic system
• miRNAs

• depression
• glioblastoma
• health-related quality of life
• miR-34a expression
• prognosis
• survival

• Amygdala
• Anxiety
• Hippocampus
• Pten
• Sirt1
• miR-132
• miR-212

• Acute Disease
• Amygdala/metabolism
• Animals
• Anxiety/etiology
• Anxiety/metabolism
• Chronic Disease
• Disease Models, Animal
• Female
• Hippocampus/metabolism
• Male
• Mice, Transgenic
• MicroRNAs/metabolism
• PTEN Phosphohydrolase/metabolism
• Sirtuin 1/metabolism
• Stress, Psychological/complications
• Stress, Psychological/metabolism
• Up-Regulation

• R21 AI127582 NIAID NIH HHS
• R01 MH103361 NIMH NIH HHS
• R01 NS066345 NINDS NIH HHS
• R01 NS091302 NINDS NIH HHS
• T32 GM086252 NIGMS NIH HHS
• R01 MH062335 NIMH NIH HHS
• F32 MH011857 NIMH NIH HHS

• Endocrinology
• Neuroendocrine regulation
• growth factors

• Adrenal Insufficiency/etiology
• Adrenal Insufficiency/physiopathology
• Adrenocorticotropic Hormone/metabolism
• Animals
• Cell Line, Tumor
• Corticosterone/metabolism
• Corticotrophs/metabolism
• Disease Models, Animal
• Down-Regulation
• Female
• Humans
• Hypothalamo-Hypophyseal System/cytology
• Hypothalamo-Hypophyseal System/physiology
• Male
• Mice
• Mice, Transgenic
• MicroRNAs/metabolism
• Pituitary-Adrenal System/cytology
• Pituitary-Adrenal System/physiology
• Receptors, Corticotropin-Releasing Hormone/genetics
• Receptors, Corticotropin-Releasing Hormone/metabolism
• Receptors, Somatostatin/genetics
• Receptors, Somatostatin/metabolism
• Stress, Psychological/complications
• Stress, Psychological/physiopathology

• R01 DK113998 NIDDK NIH HHS
• R21 DK103198 NIDDK NIH HHS
• T32 DK007770 NIDDK NIH HHS
• National Institutes of Health

Parents’ stressful experiences can influence an offspring’s vulnerability to many pathological conditions, including psychopathologies, and their effects may even endure for several generations. Nevertheless, the cause of this phenomenon has not been determined, and only recently have scientists turned to epigenetics to answer this question. There is extensive literature on epigenetics, but no consensus exists with regard to how and what can (and must) be considered to study and define epigenetics processes and their inheritance. In this work, we aimed to clarify and systematize these concepts. To this end, we analyzed the dynamics of epigenetic changes over time in detail and defined three types of epigenetics: a direct form of epigenetics (DE) and two indirect epigenetic processes—within (WIE) and across (AIE). DE refers to changes that occur in the lifespan of an individual, due to direct experiences with his environment. WIE concerns changes that occur inside of the womb, due to events during gestation. Finally, AIE defines changes that affect the individual’s predecessors (parents, grandparents, etc.), due to events that occur even long before conception and that are somehow (e.g., through gametes, the intrauterine environment setting) transmitted across generations. This distinction allows us to organize the main body of epigenetic evidence according to these categories and then focus on the latter (AIE), referring to it as a faster route of informational transmission across generations—compared with genetic inheritance—that guides human evolution in a Lamarckian (i.e., experience-dependent) manner. Of the molecular processes that are implicated in this phenomenon, well-known (methylation) and novel (non-coding RNA, ncRNA) regulatory mechanisms are converging. Our discussion of the chief methods that are used to study epigenetic inheritance highlights the most compelling technical and theoretical problems of this discipline. Experimental suggestions to expand this field are provided, and their practical and ethical implications are discussed extensively.

• epigenetic
• inheritance
• methylation
• microRNA
• psychopathology
• stress
• transgenerational
• transmission

• Animals
• Base Pairing
• Evolution, Molecular
• Gene Expression Regulation
• Gene Silencing
• Genomics
• Humans
• MicroRNAs/antagonists & inhibitors
• MicroRNAs/chemistry
• MicroRNAs/metabolism
• Nucleic Acid Conformation
• RNA Isoforms/genetics
• RNA Isoforms/metabolism

• R35 GM118135 NIGMS NIH HHS
• Howard Hughes Medical Institute

• Amygdala
• Corticotropin-releasing factor receptor type 1
• Dorsal raphe nuclei
• Prefrontal cortex
• Stress
• microRNA-34

PM_2.5 (particulate matter ≤ 2.5 μm) is one of the leading environmental risk factors for the global burden of disease. Whereas increasing evidence has linked the adverse roles of PM_2.5 with cardiovascular and respiratory diseases, limited but growing emerging evidence suggests that PM_2.5 exposure can affect the nervous system, causing neuroinflammation, synaptic dysfunction and cognitive deterioration. However, the molecular mechanisms underlying the synaptic and cognitive deficits elicited by PM_2.5 exposure are largely unknown.

C57BL/6 mice received oropharyngeal aspiration of PM_2.5 (1 and 5 mg/kg bw) every other day for 4 weeks. The mice were also stereotaxically injected with β-site amyloid precursor protein cleaving enzyme 1 (β-secretase, BACE1) shRNA or LV-miR-574-5p lentiviral constructs in the absence or presence of PM_2.5 aspiration at 5 mg/kg bw every other day for 4 weeks. Spatial learning and memory were assessed with the Morris water maze test, and synaptic function integrity was evaluated with electrophysiological recordings of long-term potentiation (LTP) and immunoblot analyses of glutamate receptor subunit expression. The expression of α-secretase (ADAM10), BACE1, and γ-secretase (nicastrin) and the synthesis and accumulation of amyloid β (Aβ) were measured by immunoblot and enzyme-linked immunosorbent assay (ELISA). MicroRNA (miRNA) expression was screened with a microRNA microarray analysis and confirmed by real-time quantitative reverse transcription PCR (qRT-PCR) analysis. Dual-luciferase reporter gene and chromatin immunoprecipitation (ChIP) analyses were used to detect the binding of miR-574-5p in the 3’UTR of BACE1 and NF-κB p65 in the promoter of miR-574-5p, respectively.

PM_2.5 aspiration caused neuroinflammation and deteriorated synaptic function integrity and spatial learning and memory, and the effects were associated with the induction of BACE1. The action was mediated by NF-κB p65-regulated downregulation of miR-574-5p, which targets BACE1. Overexpression of miR-574-5p in the hippocampal region decreased BACE1 expression, restored synaptic function, and improved spatial memory and learning following PM_2.5 exposure.

Taken together, our findings reveal a novel molecular mechanism underlying impaired synaptic and cognitive function following exposure to PM_2.5, suggesting that miR-574-5p is a potential intervention target for the prevention and treatment of PM_2.5-induced neurological disorders.

The online version of this article (10.1186/s12989-017-0215-3) contains supplementary material, which is available to authorized users.

• MicroRNA-574-5p (miR-574-5p)
• NF-κB
• PM2.5
• Spatial memory and learning
• Synaptic dysfunction
• β-site amyloid precursor protein cleaving enzyme 1 (β-secretase, BACE1)

• amygdala
• high responder
• low responder
• polycomb repressive complex 2

• Amygdala
• Dorsal raphe
• High responder/low responder
• Stress coping
• c-Fos
• microRNA

• Adaptation, Psychological/physiology
• Amygdala/metabolism
• Animals
• Disease Models, Animal
• Dorsal Raphe Nucleus/metabolism
• Electroshock/adverse effects
• Exploratory Behavior
• Gene Expression Regulation/physiology
• Gene Ontology
• Gene Regulatory Networks/physiology
• Immobility Response, Tonic/physiology
• Male
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Nociception/physiology
• Proto-Oncogene Proteins c-fos/metabolism
• RNA, Messenger/genetics
• RNA, Messenger/metabolism
• Rats
• Rats, Sprague-Dawley
• Stress, Psychological/metabolism
• Stress, Psychological/pathology
• Tryptophan Hydroxylase/metabolism

• T32 NS061788 NINDS NIH HHS
• R00 MH081927 NIMH NIH HHS
• R01 NR012686 NINR NIH HHS
• R01 MH105447 NIMH NIH HHS
• T32 GM008361 NIGMS NIH HHS