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Article ; Online: Psilocybin induces acute anxiety and changes in amygdalar phosphopeptides independently from the 5-HT2A receptor.

Harari, Ram / Chatterjee, Ipsita / Getselter, Dmitriy / Elliott, Evan

iScience

2024 Volume 27, Issue 5, Page(s) 109686

Abstract: Psilocybin, and its metabolite psilocin, induces psychedelic effects through activation of the 5-HT2A receptor. Psilocybin has been proposed as a treatment for depression and anxiety but sometimes induces anxiety in humans. An understanding of mechanisms ...

Abstract	Psilocybin, and its metabolite psilocin, induces psychedelic effects through activation of the 5-HT2A receptor. Psilocybin has been proposed as a treatment for depression and anxiety but sometimes induces anxiety in humans. An understanding of mechanisms underlying the anxiety response will help to better develop therapeutic prospects of psychedelics. In the current study, psilocybin induced an acute increase in anxiety in behavioral paradigms in mice. Importantly, pharmacological blocking of the 5-HT2A receptor attenuates psilocybin-induced head twitch response, a behavioral proxy for the psychedelic response, but does not rescue psilocybin's effect on anxiety-related behavior. Phosphopeptide analysis in the amygdala uncovered signal transduction pathways that are dependent or independent of the 5-HT2A receptor. Furthermore, presynaptic proteins are specifically involved in psilocybin-induced acute anxiety. These insights into how psilocybin may induce short-term anxiety are important for understanding how psilocybin may best be used in the clinical framework.
Language	English
Publishing date	2024-04-09
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2024.109686
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The Mechanisms of CHD8 in Neurodevelopment and Autism Spectrum Disorders.

Weissberg, Orly / Elliott, Evan

Genes

2021 Volume 12, Issue 8

Abstract: Chromodomain-helicase-DNA-binding protein 8 (CHD8) has been identified as one of the genes with the strongest association with autism. The CHD8 protein is a transcriptional regulator that is expressed in nearly all cell types and has been implicated in ... ...

Abstract	Chromodomain-helicase-DNA-binding protein 8 (CHD8) has been identified as one of the genes with the strongest association with autism. The CHD8 protein is a transcriptional regulator that is expressed in nearly all cell types and has been implicated in multiple cellular processes, including cell cycle, cell adhesion, neuronal development, myelination, and synaptogenesis. Considering the central role of CHD8 in the genetics of autism, a deeper understanding of the physiological functions of CHD8 is important to understand the development of the autism phenotype and potential therapeutic targets. Different CHD8 mutant mouse models were developed to determine autism-like phenotypes and to fully understand their mechanisms. Here, we review the current knowledge on CHD8, with an emphasis on mechanistic lessons gained from animal models that have been studied.
MeSH term(s)	Animals ; Autism Spectrum Disorder/physiopathology ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/physiology ; Disease Models, Animal ; Humans ; Mice ; Neurodevelopmental Disorders/physiopathology ; Phenotype ; Transcription Factors/genetics ; Transcription Factors/physiology
Chemical Substances	CHD8 protein, human ; DNA-Binding Proteins ; Transcription Factors
Language	English
Publishing date	2021-07-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes12081133
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Article: The Mechanisms of CHD8 in Neurodevelopment and Autism Spectrum Disorders

Weissberg, Orly / Elliott, Evan

Genes. 2021 July 26, v. 12, no. 8

2021

Abstract	Chromodomain-helicase-DNA-binding protein 8 (CHD8) has been identified as one of the genes with the strongest association with autism. The CHD8 protein is a transcriptional regulator that is expressed in nearly all cell types and has been implicated in multiple cellular processes, including cell cycle, cell adhesion, neuronal development, myelination, and synaptogenesis. Considering the central role of CHD8 in the genetics of autism, a deeper understanding of the physiological functions of CHD8 is important to understand the development of the autism phenotype and potential therapeutic targets. Different CHD8 mutant mouse models were developed to determine autism-like phenotypes and to fully understand their mechanisms. Here, we review the current knowledge on CHD8, with an emphasis on mechanistic lessons gained from animal models that have been studied.
Keywords	autism ; cell adhesion ; cell cycle ; mice ; mutants ; myelination ; neurodevelopment ; neurons ; phenotype ; synaptogenesis ; therapeutics ; transcription factors
Language	English
Dates of publication	2021-0726
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes12081133
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: CHD8 regulates gut epithelial cell function and affects autism-related behaviors through the gut-brain axis.

Chatterjee, Ipsita / Getselter, Dmitriy / Ghanayem, Nasreen / Harari, Ram / Davis, Liron / Bel, Shai / Elliott, Evan

Translational psychiatry

2023 Volume 13, Issue 1, Page(s) 305

Abstract: Autism is a neurodevelopmental disorder characterized by early-onset social behavioral deficits and repetitive behaviors. Chromodomain helicase DNA-binding protein (CHD8) is among the genes most strongly associated with autism. In addition to the core ... ...

Abstract	Autism is a neurodevelopmental disorder characterized by early-onset social behavioral deficits and repetitive behaviors. Chromodomain helicase DNA-binding protein (CHD8) is among the genes most strongly associated with autism. In addition to the core behavioral symptoms of autism, affected individuals frequently present with gastrointestinal symptoms that are also common among individuals harboring mutations in the gene encoding CHD8. However, little is known regarding the mechanisms whereby CHD8 affects gut function. In addition, it remains unknown whether gastrointestinal manifestations contribute to the behavioral phenotypes of autism. The current study found that mice haploinsufficient for the large isoform of Chd8 (Chd8L) exhibited increased intestinal permeability, transcriptomic dysregulation in gut epithelial cells, reduced tuft cell and goblet cell counts in the gut, and an overall increase in microbial load. Gut epithelial cell-specific Chd8 haploinsufficiency was associated with increased anxiety-related behaviors together with a decrease in tuft cell numbers. Antibiotic treatment of Chd8L haploinsufficient mice attenuated social behavioral deficits. Together, these results suggest Chd8 as a key determinant of autism-related gastrointestinal deficits, while also laying the ground for future studies on the link between GI deficits and autism-related behaviors.
MeSH term(s)	Mice ; Animals ; Autistic Disorder/genetics ; Brain-Gut Axis ; Gene Expression Regulation, Developmental ; DNA-Binding Proteins/genetics ; Autism Spectrum Disorder/genetics ; Epithelial Cells
Chemical Substances	DNA-Binding Proteins
Language	English
Publishing date	2023-10-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2609311-X
ISSN	2158-3188 ; 2158-3188
ISSN (online)	2158-3188
ISSN	2158-3188
DOI	10.1038/s41398-023-02611-2
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Article ; Online: Microbes, metabolites and (synaptic) malleability, oh my! The effect of the microbiome on synaptic plasticity.

Glinert, Ayala / Turjeman, Sondra / Elliott, Evan / Koren, Omry

Biological reviews of the Cambridge Philosophical Society

2021 Volume 97, Issue 2, Page(s) 582–599

Abstract: The microbiome influences the emotional and cognitive phenotype of its host, as well as the neurodevelopment and pathophysiology of various brain processes and disorders, via the well-established microbiome-gut-brain axis. Rapidly accumulating data link ... ...

Abstract	The microbiome influences the emotional and cognitive phenotype of its host, as well as the neurodevelopment and pathophysiology of various brain processes and disorders, via the well-established microbiome-gut-brain axis. Rapidly accumulating data link the microbiome to severe neuropsychiatric disorders in humans, including schizophrenia, Alzheimer's and Parkinson's. Moreover, preclinical work has shown that perturbation of the microbiome is closely associated with social, cognitive and behavioural deficits. The potential of the microbiome as a diagnostic and therapeutic tool is currently undercut by a lack of clear mechanistic understanding of the microbiome-gut-brain axis. This review establishes the hypothesis that the mechanism by which this influence is carried out is synaptic plasticity - long-term changes to the physical and functional neuronal structures that enable the brain to undertake learning, memory formation, emotional regulation and more. By examining the different constituents of the microbiome-gut-brain axis through the lens of synaptic plasticity, this review explores the diverse aspects by which the microbiome shapes the behaviour and mental wellbeing of the host. Key elements of this complex bi-directional relationship include neurotransmitters, neuronal electrophysiology, immune mediators that engage with both the central and enteric nervous systems and signalling cascades that trigger long-term potentiation of synapses. The importance of establishing mechanistic correlations along the microbiome-gut-brain axis cannot be overstated as they hold the potential for furthering current understanding regarding the vast fields of neuroscience and neuropsychiatry. This review strives to elucidate the promising theory of microbiome-driven synaptic plasticity in the hope of enlightening current researchers and inspiring future ones.
MeSH term(s)	Brain/metabolism ; Gastrointestinal Microbiome/physiology ; Microbiota ; Neuronal Plasticity ; Neurons/physiology
Language	English
Publishing date	2021-11-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1423558-4
ISSN	1469-185X ; 0006-3231 ; 1464-7931
ISSN (online)	1469-185X
ISSN	0006-3231 ; 1464-7931
DOI	10.1111/brv.12812
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Article ; Online: The microbiota and the hypothalamus-pituitary-adrenocortical (HPA) axis, implications for anxiety and stress disorders.

Frankiensztajn, Linoy Mia / Elliott, Evan / Koren, Omry

Current opinion in neurobiology

2020 Volume 62, Page(s) 76–82

Abstract: There is growing evidence for the involvement of the gut-microbiota in the regulation of emotions, behavior, and higher cognitive functions through the 'microbiome-gut-brain axis'. This relationship between the gut microbiota and the brain is pivotal for ...

Abstract	There is growing evidence for the involvement of the gut-microbiota in the regulation of emotions, behavior, and higher cognitive functions through the 'microbiome-gut-brain axis'. This relationship between the gut microbiota and the brain is pivotal for the development of the newborn, which receives its commensal microbiota at birth; dysbiosis may result in altered neurodevelopment. The hypothalamus-pituitary-adrenocortical (HPA) axis is actively involved in the stress response but is undeveloped in the newborn. Here, we describe how changes in the commensal microbiota influence the normal development of the HPA axis and review recent findings describing the essential crosstalk between the gut microbiota and the HPA axis and suggesting a role for the maternal and commensal microbiota in the development of the HPA axis and of the stress response.
MeSH term(s)	Anxiety ; Brain ; Humans ; Hypothalamo-Hypophyseal System ; Microbiota ; Pituitary-Adrenal System ; Stress, Psychological
Language	English
Publishing date	2020-01-20
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1078046-4
ISSN	1873-6882 ; 0959-4388
ISSN (online)	1873-6882
ISSN	0959-4388
DOI	10.1016/j.conb.2019.12.003
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Article ; Online: CTCF in parvalbumin-expressing neurons regulates motor, anxiety and social behavior and neuronal identity.

Davis, Liron / Rayi, Prudhvi Raj / Getselter, Dmitriy / Kaphzan, Hanoch / Elliott, Evan

Molecular brain

2022 Volume 15, Issue 1, Page(s) 30

Abstract: CCCTC-binding factor (CTCF) is a regulator of chromatin organization and has direct effects on gene transcription. Mutations in CTCF have been identified in individuals with neurodevelopmental conditions. There are wide range of behaviors associated with ...

Abstract	CCCTC-binding factor (CTCF) is a regulator of chromatin organization and has direct effects on gene transcription. Mutations in CTCF have been identified in individuals with neurodevelopmental conditions. There are wide range of behaviors associated with these mutations, including intellectual disabilities, changes in temperament, and autism. Previous mice-model studies have identified roles for CTCF in excitatory neurons in specific behaviors, particularly in regards to learning and memory. However, the role of CTCF in inhibitory neurons is less well defined. In the current study, specific knockout of CTCF in parvalbumin-expressing neurons, a subset of inhibitory neurons, induced a specific behavioral phenotype, including locomotor abnormalities, anxiolytic behavior, and a decrease in social behavior. The anxiolytic and social abnormalities are detected before the onset of locomotor abnormalities. Immunohistochemical analysis revealed a disbalance in parvalbumin-expressing and somatostatin-expressing cells in these mice. Single nuclei RNA sequencing identified changes in gene expression in parvalbumin-expressing neurons that are specific to inhibitory neuronal identity and function. Electrophysiology analysis revealed an enhanced inhibitory tone in the hippocampal pyramidal neurons in knockout mice. These findings indicate that CTCF in parvalbumin-expressing neurons has a significant role in the overall phenotype of CTCF-associated neurodevelopmental deficits.
MeSH term(s)	Animals ; Anxiety ; CCCTC-Binding Factor ; Mice ; Mice, Knockout ; Neurons/metabolism ; Parvalbumins/metabolism ; Social Behavior
Chemical Substances	CCCTC-Binding Factor ; Ctcf protein, mouse ; Parvalbumins
Language	English
Publishing date	2022-04-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2436057-0
ISSN	1756-6606 ; 1756-6606
ISSN (online)	1756-6606
ISSN	1756-6606
DOI	10.1186/s13041-022-00916-9
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Article ; Online: Delineating the Common Biological Pathways Perturbed by ASD's Genetic Etiology: Lessons from Network-Based Studies.

Oron, Oded / Elliott, Evan

International journal of molecular sciences

2017 Volume 18, Issue 4

Abstract: In recent decades it has become clear that Autism Spectrum Disorder (ASD) possesses a diverse and heterogeneous genetic etiology. Aberrations in hundreds of genes have been associated with ASD so far, which include both rare and common variations. While ... ...

Abstract	In recent decades it has become clear that Autism Spectrum Disorder (ASD) possesses a diverse and heterogeneous genetic etiology. Aberrations in hundreds of genes have been associated with ASD so far, which include both rare and common variations. While one may expect that these genes converge on specific common molecular pathways, which drive the development of the core ASD characteristics, the task of elucidating these common molecular pathways has been proven to be challenging. Several studies have combined genetic analysis with bioinformatical techniques to uncover molecular mechanisms that are specifically targeted by autism-associated genetic aberrations. Recently, several analysis have suggested that particular signaling mechanisms, including the Wnt and Ca
MeSH term(s)	Animals ; Autism Spectrum Disorder/genetics ; Autism Spectrum Disorder/metabolism ; Calcium Signaling ; Calmodulin/metabolism ; Computational Biology/methods ; Gene Expression Profiling ; Genetic Predisposition to Disease ; Humans ; Mutation ; Protein Binding ; Protein Interaction Mapping ; Signal Transduction ; Wnt Signaling Pathway
Chemical Substances	Calmodulin
Language	English
Publishing date	2017-04-14
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms18040828
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Article: Role of Tryptophan in Microbiota-Induced Depressive-Like Behavior: Evidence From Tryptophan Depletion Study.

Lukić, Iva / Getselter, Dmitriy / Koren, Omry / Elliott, Evan

Frontiers in behavioral neuroscience

2019 Volume 13, Page(s) 123

Abstract: During the past decade, there has been a substantial rise in the knowledge about the effects of gut microbiota on host physiology and behavior, including depressive behavior. Initial studies determined that gut microbiota can regulate host tryptophan ... ...

Abstract	During the past decade, there has been a substantial rise in the knowledge about the effects of gut microbiota on host physiology and behavior, including depressive behavior. Initial studies determined that gut microbiota can regulate host tryptophan levels, which is a main serotonin precursor. A dysfunctional serotonergic system is considered to be one of the main factors contributing to the development of depression. Therefore, we hypothesized that regulation of brain tryptophan and serotonin can explain, at least partly, the effects of microbiota on depressive behavior. To test this hypothesis, we examined depressive-like behavior and brain levels of serotonin and tryptophan, of germ free (GF) and specific-pathogen free (SPF) mice under basal conditions, or after acute tryptophan depletion (ATD) procedure, which is a method to decrease tryptophan and serotonin levels in the brain. In basal conditions, GF mice exhibited less depressive-like behavior in sucrose preference, tail-suspension and forced swim tests, compared to SPF mice. In addition, in mice that were not subjected to ATD, GF mice displayed higher levels of tryptophan, serotonin and 5-hydroxyindoleacetic acid (the main degradation product of serotonin) in medial prefrontal cortex (mPFC) and hippocampus (HIPPO), compared to SPF mice. Interestingly, ATD increased depressive-like behavior of GF, but not of SPF mice. These behavioral changes were accompanied by a stronger reduction of tryptophan, serotonin and 5-hydroxyindoleacetic acid in mPFC and HIPPO in GF mice after ATD, when compared to SPF mice. Therefore, the serotonergic system of GF mice is more vulnerable to the acute challenge of tryptophan reduction, and GF mice after tryptophan reduction behave more similarly to SPF mice. These data provide functional evidence that microbiota affects depression-like behavior through influencing brain tryptophan accessibility and the serotonergic system.
Language	English
Publishing date	2019-06-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452960-6
ISSN	1662-5153
ISSN	1662-5153
DOI	10.3389/fnbeh.2019.00123
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Article: The Interaction between the Immune System and Epigenetics in the Etiology of Autism Spectrum Disorders.

Nardone, Stefano / Elliott, Evan

Frontiers in neuroscience

2016 Volume 10, Page(s) 329

Abstract: Recent studies have firmly established that the etiology of autism includes both genetic and environmental components. However, we are only just beginning to elucidate the environmental factors that might be involved in the development of autism, as well ...

Abstract	Recent studies have firmly established that the etiology of autism includes both genetic and environmental components. However, we are only just beginning to elucidate the environmental factors that might be involved in the development of autism, as well as the molecular mechanisms through which they function. Mounting epidemiological and biological evidence suggest that prenatal factors that induce a more activated immune state in the mother are involved in the development of autism. In parallel, molecular studies have highlighted the role of epigenetics in brain development as a process susceptible to environmental influences and potentially causative of autism spectrum disorders (ASD). In this review, we will discuss converging evidence for a multidirectional interaction between immune system activation in the mother during pregnancy and epigenetic regulation in the brain of the fetus that may cooperate to produce an autistic phenotype. This interaction includes immune factor-induced changes in epigenetic signatures in the brain, dysregulation of epigenetic modifications specifically in genomic regions that encode immune functions, and aberrant epigenetic regulation of microglia. Overall, the interaction between immune system activation in the mother and the subsequent epigenetic dysregulation in the developing fetal brain may be a main consideration for the environmental factors that cause autism.
Language	English
Publishing date	2016-07-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2016.00329
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