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Article ; Online: The pharmacology and neurotoxicology of synthetic cathinones.

Angoa-Perez, Mariana / Kuhn, Donald M

Advances in pharmacology (San Diego, Calif.)

2023 Volume 99, Page(s) 61–82

Abstract: The synthetic cathinones are man-made compounds derived from the naturally occurring drug cathinone, which is found in the khat plant. The drugs in this pharmacological class that will be the focus of this chapter include mephedrone, MDPV, methcathinone ... ...

Abstract	The synthetic cathinones are man-made compounds derived from the naturally occurring drug cathinone, which is found in the khat plant. The drugs in this pharmacological class that will be the focus of this chapter include mephedrone, MDPV, methcathinone and methylone. These drugs are colloquially known as "bath salts". This misnomer suggests that these drugs are used for health improvement or that they have legitimate medical uses. The synthetic cathinones are dangerous drugs with powerful pharmacological effects that include high abuse potential, hyperthermia and hyperlocomotion. These drugs also share many of the pharmacological effects of the amphetamine class of drugs including methamphetamine, amphetamine and MDMA and therefore have high potential to cause damage to the central nervous system. The synthetic cathinones are frequently taken in combination with other psychoactive drugs such as alcohol, marijuana and the amphetamine-like stimulants, creating a situation where heightened pharmacological and neurotoxicological effects are likely to occur. Despite the structural features shared by the synthetic cathinones and amphetamine-like stimulants, including their actions at monoamine transporters and receptors, the effects of the synthetic cathinones do not always match those of the amphetamines. In particular, the synthetic cathinones are far less neurotoxic than their amphetamine counterparts, they produce a weaker hyperthermia, and they cause less glial activation. This chapter will briefly review the pharmacology and neurotoxicology of selected synthetic cathinones with the aim of delineating key areas of agreement and disagreement in the literature particularly as it relates to neurotoxicological outcomes.
MeSH term(s)	Humans ; Synthetic Cathinone ; Methamphetamine/adverse effects ; Amphetamine ; Central Nervous System Stimulants/adverse effects
Chemical Substances	Synthetic Cathinone ; Methamphetamine (44RAL3456C) ; Amphetamine (CK833KGX7E) ; Central Nervous System Stimulants
Language	English
Publishing date	2023-12-26
Publishing country	United States
Document type	Journal Article
ISSN	1557-8925
ISSN (online)	1557-8925
DOI	10.1016/bs.apha.2023.12.001
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Article ; Online: The Role of Brain-Derived Neurotrophic Factor in the Pathophysiology of Psychiatric and Neurological Disorders.

Angoa-Pérez, Mariana / Anneken, John H / Kuhn, Donald M

Journal of psychiatry and psychiatric disorders

2022 Volume 1, Issue 5, Page(s) 252–269

Abstract: Brain-derived neurotrophic factor (BDNF) is a neurotrophin highly expressed in the brain with a potent influence on several aspects of neuronal function. Since its discovery in the early 1980s, BDNF has prompted a great interest in better understanding ... ...

Abstract	Brain-derived neurotrophic factor (BDNF) is a neurotrophin highly expressed in the brain with a potent influence on several aspects of neuronal function. Since its discovery in the early 1980s, BDNF has prompted a great interest in better understanding its physiological role and has been established as the main central neurotrophic factor. BDNF is initially synthesized as a precursor, pro-BDNF, which is then cleaved to form mature BDNF (m-BDNF). A regulated balance between pro-BDNF and m-BDNF is crucial for physiological as well as pathological conditions. The diverse effects of BDNF are mediated through the p75 NT receptor (p75NTR), which binds to its precursor form, and the tropomyosin receptor kinase B (TrkB), which binds to its mature form. Activation of TrkB and p75NTR may produce opposite outcomes in that TrkB receptors have a well-defined trophic role and their activation is proposed to mediate neuronal survival, whereas p75NTR may promote apoptosis. BDNF is highly expressed in limbic structures and cerebral cortex, making it a crucial factor in the regulation of learning and memory, affective behaviors and reward processes. Abnormal BDNF signaling has been proposed to have a crucial role in the course and development of numerous psychiatric and neurological disorders. Moreover, psychotropic drugs used to treat some of these conditions are known to activate BDNF signaling. The present review gives an overview of the involvement of BDNF in the pathology of psychiatric and neurological disorders, compiling what is known from human and animal studies.
Language	English
Publishing date	2022-01-25
Publishing country	United States
Document type	Journal Article
ISSN	2572-519X
ISSN (online)	2572-519X
DOI	10.26502/jppd.2572-519X0024
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Article ; Online: Evidence for Modulation of Substance Use Disorders by the Gut Microbiome: Hidden in Plain Sight.

Angoa-Pérez, Mariana / Kuhn, Donald M

Pharmacological reviews

2021 Volume 73, Issue 2, Page(s) 571–596

Abstract: The gut microbiome modulates neurochemical function and behavior and has been implicated in numerous central nervous system (CNS) diseases, including developmental, neurodegenerative, and psychiatric disorders. Substance use disorders (SUDs) remain a ... ...

Abstract	The gut microbiome modulates neurochemical function and behavior and has been implicated in numerous central nervous system (CNS) diseases, including developmental, neurodegenerative, and psychiatric disorders. Substance use disorders (SUDs) remain a serious threat to the public well-being, yet gut microbiome involvement in drug abuse has received very little attention. Studies of the mechanisms underlying SUDs have naturally focused on CNS reward circuits. However, a significant body of research has accumulated over the past decade that has unwittingly provided strong support for gut microbiome participation in drug reward.
MeSH term(s)	Dysbiosis ; Gastrointestinal Microbiome ; Humans ; Illicit Drugs ; Microbiota ; Substance-Related Disorders
Chemical Substances	Illicit Drugs
Language	English
Publishing date	2021-02-17
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	209898-2
ISSN	1521-0081 ; 0031-6997
ISSN (online)	1521-0081
ISSN	0031-6997
DOI	10.1124/pharmrev.120.000144
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Article ; Online: Cocaine hydrochloride, cocaine methiodide and methylenedioxypyrovalerone (MDPV) cause distinct alterations in the structure and composition of the gut microbiota.

Angoa-Pérez, Mariana / Zagorac, Branislava / Francescutti, Dina M / Shaffer, Zachary D / Theis, Kevin R / Kuhn, Donald M

Scientific reports

2023 Volume 13, Issue 1, Page(s) 13754

Abstract: Cocaine is a highly addictive psychostimulant drug of abuse that constitutes an ongoing public health threat. Emerging research is revealing that numerous peripheral effects of this drug may serve as conditioned stimuli for its central reinforcing ... ...

Abstract	Cocaine is a highly addictive psychostimulant drug of abuse that constitutes an ongoing public health threat. Emerging research is revealing that numerous peripheral effects of this drug may serve as conditioned stimuli for its central reinforcing properties. The gut microbiota is emerging as one of these peripheral sources of input to cocaine reward. The primary objective of the present study was to determine how cocaine HCl and methylenedioxypyrovalerone, both of which powerfully activate central reward pathways, alter the gut microbiota. Cocaine methiodide, a quaternary derivative of cocaine that does not enter the brain, was included to assess peripheral influences on the gut microbiota. Both cocaine congeners caused significant and similar alterations of the gut microbiota after a 10-day course of treatment. Contrary to expectations, the effects of cocaine HCl and MDPV on the gut microbiota were most dissimilar. Functional predictions of metabolic alterations caused by the treatment drugs reaffirmed that the cocaine congeners were similar whereas MDPV was most dissimilar from the other two drugs and controls. It appears that the monoamine transporters in the gut mediate the effects of the treatment drugs. The effects of the cocaine congeners and MDPV on the gut microbiome may form the basis of interoceptive cues that can influence their abuse properties.
MeSH term(s)	Synthetic Cathinone ; Gastrointestinal Microbiome ; Cocaine/pharmacology ; Central Nervous System Stimulants
Chemical Substances	cocaine methiodide (83FKO5XD6J) ; Synthetic Cathinone ; Cocaine (I5Y540LHVR) ; Central Nervous System Stimulants
Language	English
Publishing date	2023-08-23
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-40892-1
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Article ; Online: Effects of gut microbiota remodeling on the dysbiosis induced by high fat diet in a mouse model of Gulf war illness.

Angoa-Pérez, Mariana / Zagorac, Branislava / Francescutti, Dina M / Theis, Kevin R / Kuhn, Donald M

Life sciences

2021 Volume 279, Page(s) 119675

Abstract: Gulf war illness (GWI) is a chronic disorder of unknown etiology characterized by multiple symptoms such as pain, fatigue, gastrointestinal disturbances and neurocognitive problems. Increasing evidence suggests that gut microbiome perturbations play a ... ...

Abstract	Gulf war illness (GWI) is a chronic disorder of unknown etiology characterized by multiple symptoms such as pain, fatigue, gastrointestinal disturbances and neurocognitive problems. Increasing evidence suggests that gut microbiome perturbations play a key role in the pathology of this disorder. GWI courses with gut microbiota alterations and their metabolites (e.g. short chain fatty acids -SCFA-), which can be aggravated by lifestyle risk factors such as a high fat diet (HF). To investigate the causative role of the gut microbiome, non-absorbable antibiotics (Abx) were administered to mice treated with GWI agents and concomitantly fed with a HF. In light of the wide use of Abx as pseudo-germ-free models, we evaluated the effects of Abx exposure on GWI and HF on body weight, food intake, gut microbiota changes and levels of the SCFA acetate. Results show that HF decreased food intake while increasing body weight in both controls and GWI. Exposure to Abx prevented these HF effects by offsetting the body weight gain in GWI. GWI and HF led to decreases in α-diversity, disruptions in the composition and structure of the gut bacterial community and decreases in acetate levels. This Abx-induced remodeling of the gut microbiome was characterized by an expansion of Proteobacteria, decreases in Bacteroidetes and Firmicutes, and overall increases in acetate levels, as well as by the proliferation of potential pathobionts. Therefore, the use of Abx may not represent a dependable approach to deplete the gut microbiome and its advantages as a pseudo germ-free model warrant further investigation.
MeSH term(s)	Animals ; Bacteria/pathogenicity ; Diet, High-Fat/adverse effects ; Disease Models, Animal ; Dysbiosis/etiology ; Dysbiosis/pathology ; Gastrointestinal Microbiome ; Inflammation/etiology ; Inflammation/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Persian Gulf Syndrome/complications
Language	English
Publishing date	2021-05-31
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2021.119675
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Article: Long access heroin self-administration significantly alters gut microbiome composition and structure.

Greenberg, Jonathan M / Winters, Andrew D / Zagorac, Branislava / Kracht, David J / Francescutti, Dina M / Cannella, Nazzareno / Ciccocioppo, Roberto / Woods, Leah C Solberg / Mackle, James / Hardiman, Gary T / Kuhn, Brittany N / Kalivas, Peter W / Kuhn, Donald M / Angoa-Perez, Mariana

Frontiers in psychiatry

2024 Volume 15, Page(s) 1369783

Abstract: Introduction: It is well known that chronic opioid use disorder is associated with alterations in gastrointestinal (GI) function that include constipation, reduced motility, and increased bacterial translocation due to compromised gut barrier function. ... ...

Abstract	Introduction: It is well known that chronic opioid use disorder is associated with alterations in gastrointestinal (GI) function that include constipation, reduced motility, and increased bacterial translocation due to compromised gut barrier function. These signs of disrupted GI function can be associated with alterations in the gut microbiome. However, it is not known if long-access opioid self-administration has effects on the gut microbiome. Methods: We used 16S rRNA gene sequencing to investigate the gut microbiome in three independent cohorts (N=40 for each) of NIH heterogeneous stock rats before onset of long-access heroin self-administration (i.e., naïve status), at the end of a 15-day period of self-administration, and after post-extinction reinstatement. Measures of microbial α- and β-diversity were evaluated for all phases. High-dimensional class comparisons were carried out with MaAsLin2. PICRUSt2 was used for predicting functional pathways impacted by heroin based on marker gene sequences. Results: Community α-diversity was not altered by heroin at any of the three phases by comparison to saline-yoked controls. Analyses of β-diversity showed that the heroin and saline-yoked groups clustered significantly apart from each other using the Bray-Curtis (community structure) index. Heroin caused significant alterations at the ASV level at the self-administration and extinction phases. At the phylum level, the relative abundance of Firmicutes was increased at the self-administration phase. Deferribacteres was decreased in heroin whereas Patescibacteria was increased in heroin at the extinction phase. Potential biomarkers for heroin emerged from the MaAsLin2 analysis. Bacterial metabolomic pathways relating to degradation of carboxylic acids, nucleotides, nucleosides, carbohydrates, and glycogen were increased by heroin while pathways relating to biosynthesis of vitamins, propionic acid, fatty acids, and lipids were decreased. Discussion: These findings support the view that long access heroin self-administration significantly alters the structure of the gut microbiome by comparison to saline-yoked controls. Inferred metabolic pathway alterations suggest the development of a microbial imbalance favoring gut inflammation and energy expenditure. Potential microbial biomarkers and related functional pathways likely invoked by heroin self-administration could be targets for therapeutic intervention.
Language	English
Publishing date	2024-02-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564218-2
ISSN	1664-0640
ISSN	1664-0640
DOI	10.3389/fpsyt.2024.1369783
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Article: Effects of gut microbiota remodeling on the dysbiosis induced by high fat diet in a mouse model of Gulf war illness

Angoa-Pérez, Mariana / Zagorac, Branislava / Francescutti, Dina M / Theis, Kevin R / Kuhn, Donald M

Elsevier Inc. Life sciences. 2021 Aug. 15, v. 279

2021

Abstract	Gulf war illness (GWI) is a chronic disorder of unknown etiology characterized by multiple symptoms such as pain, fatigue, gastrointestinal disturbances and neurocognitive problems. Increasing evidence suggests that gut microbiome perturbations play a key role in the pathology of this disorder. GWI courses with gut microbiota alterations and their metabolites (e.g. short chain fatty acids -SCFA-), which can be aggravated by lifestyle risk factors such as a high fat diet (HF). To investigate the causative role of the gut microbiome, non-absorbable antibiotics (Abx) were administered to mice treated with GWI agents and concomitantly fed with a HF. In light of the wide use of Abx as pseudo-germ-free models, we evaluated the effects of Abx exposure on GWI and HF on body weight, food intake, gut microbiota changes and levels of the SCFA acetate. Results show that HF decreased food intake while increasing body weight in both controls and GWI. Exposure to Abx prevented these HF effects by offsetting the body weight gain in GWI. GWI and HF led to decreases in α-diversity, disruptions in the composition and structure of the gut bacterial community and decreases in acetate levels. This Abx-induced remodeling of the gut microbiome was characterized by an expansion of Proteobacteria, decreases in Bacteroidetes and Firmicutes, and overall increases in acetate levels, as well as by the proliferation of potential pathobionts. Therefore, the use of Abx may not represent a dependable approach to deplete the gut microbiome and its advantages as a pseudo germ-free model warrant further investigation.
Keywords	Bacteroidetes ; Firmicutes ; Proteobacteria ; acetates ; bacterial communities ; body weight changes ; dysbiosis ; etiology ; food intake ; gastrointestinal system ; high fat diet ; intestinal microorganisms ; lifestyle ; metabolites ; mice ; pain
Language	English
Dates of publication	2021-0815
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2021.119675
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Article: Neurotoxicology of Synthetic Cathinone Analogs.

Angoa-Pérez, Mariana / Anneken, John H / Kuhn, Donald M

Current topics in behavioral neurosciences

2017 Volume 32, Page(s) 209–230

Abstract: The present review briefly explores the neurotoxic properties of methcathinone, mephedrone, methylone, and methylenedioxypyrovalerone (MDPV), four synthetic cathinones most commonly found in "bath salts." Cathinones are β-keto analogs of the commonly ... ...

Abstract	The present review briefly explores the neurotoxic properties of methcathinone, mephedrone, methylone, and methylenedioxypyrovalerone (MDPV), four synthetic cathinones most commonly found in "bath salts." Cathinones are β-keto analogs of the commonly abused amphetamines and display pharmacological effects resembling cocaine and amphetamines, but despite their commonalities in chemical structures, synthetic cathinones possess distinct neuropharmacological profiles and produce unique effects. Among the similarities of synthetic cathinones with their non-keto analogs are their targeting of monoamine systems, the release of neurotransmitters, and their stimulant properties. Most of the literature on synthetic cathinones has focused on describing their properties as psychostimulants, their behavioral effects on locomotion, memory, and potential for abuse, whereas descriptions of their neurotoxic properties are not abundant. The biochemical gauges of neurotoxicity induced by non-keto analogs are well studied in humans and experimental animals and include their ability to induce neuroinflammation, oxidative stress, excitotoxicity, temperature alterations as well as dysregulation of neurotransmitter systems and induce changes in monoamine transporters and receptors. These neurotoxicity gauges will serve as parameters to discuss the effects of the four previously mentioned synthetic cathinones alone or in combination with either another cathinone or with some of their non-keto analogs. Bath salts are not a defined combination of drugs and may consist of one synthetic cathinone compound or combinations of more cathinones. Furthermore, this review also presents some of the mechanisms that are thought to underlie this toxicity. A better understanding of the cellular and molecular mechanisms involved in the synthetic cathinones-induced neurotoxicity should contribute to generate modern therapeutic approaches to prevent or attenuate the adverse consequences of use of these drugs in humans.
MeSH term(s)	Alkaloids/adverse effects ; Alkaloids/pharmacology ; Animals ; Benzodioxoles/adverse effects ; Benzodioxoles/pharmacology ; Blood-Brain Barrier/drug effects ; Blood-Brain Barrier/metabolism ; Body Temperature/drug effects ; Body Temperature Regulation/drug effects ; Central Nervous System Stimulants/adverse effects ; Central Nervous System Stimulants/pharmacology ; Dopamine/metabolism ; Dopamine Plasma Membrane Transport Proteins/drug effects ; Dopamine Plasma Membrane Transport Proteins/metabolism ; Fever/chemically induced ; Humans ; Inflammation/chemically induced ; Methamphetamine/adverse effects ; Methamphetamine/analogs & derivatives ; Methamphetamine/pharmacology ; Neurotoxicity Syndromes/etiology ; Oxidative Stress/drug effects ; Propiophenones/adverse effects ; Propiophenones/pharmacology ; Pyrrolidines/adverse effects ; Pyrrolidines/pharmacology ; Serotonin/metabolism ; Serotonin Plasma Membrane Transport Proteins/drug effects ; Serotonin Plasma Membrane Transport Proteins/metabolism ; Synthetic Cathinone
Chemical Substances	Alkaloids ; Benzodioxoles ; Central Nervous System Stimulants ; Dopamine Plasma Membrane Transport Proteins ; Propiophenones ; Pyrrolidines ; Serotonin Plasma Membrane Transport Proteins ; Serotonin (333DO1RDJY) ; monomethylpropion (386QA522QG) ; Methamphetamine (44RAL3456C) ; cathinone (540EI4406J) ; mephedrone (8BA8T27317) ; methylone (L4I4B1R01F) ; Dopamine (VTD58H1Z2X) ; Synthetic Cathinone
Language	English
Publishing date	2017-05-12
Publishing country	Germany
Document type	Journal Article ; Review
ISSN	1866-3370
ISSN	1866-3370
DOI	10.1007/7854_2016_21
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Article ; Online: Blood biomarkers for assessment of mild traumatic brain injury and chronic traumatic encephalopathy.

Hiskens, Matthew I / Schneiders, Anthony G / Angoa-Pérez, Mariana / Vella, Rebecca K / Fenning, Andrew S

Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals

2020 Volume 25, Issue 3, Page(s) 213–227

Abstract: Mild traumatic brain injuries (mTBI) are prevalent and can result in significant debilitation. Current diagnostic methods have implicit limitations, with clinical assessment tools reliant on subjective self-reported symptoms or non-specific clinical ... ...

Abstract	Mild traumatic brain injuries (mTBI) are prevalent and can result in significant debilitation. Current diagnostic methods have implicit limitations, with clinical assessment tools reliant on subjective self-reported symptoms or non-specific clinical observations, and commonly available imaging techniques lacking sufficient sensitivity to detect mTBI. A blood biomarker would provide a readily accessible detector of mTBI to meet the current measurement gap. Suitable options would provide objective and quantifiable information in diagnosing mTBI, in monitoring recovery, and in establishing a prognosis of resultant neurodegenerative disease, such as chronic traumatic encephalopathy (CTE). A biomarker would also assist in progressing research, providing suitable endpoints for testing therapeutic modalities and for further exploring mTBI pathophysiology. This review highlights the most promising blood-based protein candidates that are expressed in the central nervous system (CNS) and released into systemic circulation following mTBI. To date, neurofilament light (NF-L) may be the most suitable candidate for assessing neuronal damage, and glial fibrillary acidic protein (GFAP) for assessing astrocyte activation, although further work is required. Ultimately, the heterogeneity of cells in the brain and each marker's limitations may require a combination of biomarkers, and recent developments in microRNA (miRNA) markers of mTBI show promise and warrant further exploration.
MeSH term(s)	Biomarkers/blood ; Brain Concussion/blood ; Brain Concussion/diagnosis ; Chronic Traumatic Encephalopathy/blood ; Chronic Traumatic Encephalopathy/diagnosis ; Glial Fibrillary Acidic Protein/blood ; Humans ; Interleukins/blood ; Neurofilament Proteins/blood ; S100 Calcium Binding Protein beta Subunit/blood ; Sensitivity and Specificity ; Ubiquitin Thiolesterase/blood
Chemical Substances	Biomarkers ; GFAP protein, human ; Glial Fibrillary Acidic Protein ; Interleukins ; Neurofilament Proteins ; S100 Calcium Binding Protein beta Subunit ; S100B protein, human ; neurofilament protein L ; Ubiquitin Thiolesterase (EC 3.4.19.12)
Language	English
Publishing date	2020-03-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1324372-x
ISSN	1366-5804 ; 1354-750X
ISSN (online)	1366-5804
ISSN	1354-750X
DOI	10.1080/1354750X.2020.1735521
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Article ; Online: Responses to chronic corticosterone on brain glucocorticoid receptors, adrenal gland, and gut microbiota in mice lacking neuronal serotonin.

Angoa-Pérez, Mariana / Zagorac, Branislava / Francescutti, Dina M / Theis, Kevin R / Kuhn, Donald M

Brain research

2020 Volume 1751, Page(s) 147190

Abstract: Dysregulation of the stress-induced activation of the hypothalamic-pituitary-adrenocortical axis can result in disease. Bidirectional communication exists between the brain and the gut, and alterations in these interactions appear to be involved in ... ...

Abstract	Dysregulation of the stress-induced activation of the hypothalamic-pituitary-adrenocortical axis can result in disease. Bidirectional communication exists between the brain and the gut, and alterations in these interactions appear to be involved in stress regulation and in the pathogenesis of neuropsychiatric diseases, such as depression. Serotonin (5HT) plays a crucial role in the functions of these two major organs but its direct influence under stress conditions remains unclear. To investigate the role of neuronal 5HT on chronic stress responses and its influence on the gut microbiome, mice lacking the gene for tryptophan hydroxylase-2 were treated with the stress hormone corticosterone (CORT) for 21 days. The intake of fluid and food, as well as body weights were recorded daily. CORT levels, expression of glucocorticoid receptors (GR) in the brain and the size of the adrenal gland were evaluated. Caecum was used for 16S rRNA gene characterization of the gut microbiota. Results show that 5HT depletion produced an increase in food intake and a paradoxical reduction in body weight that were enhanced by CORT. Neuronal 5HT depletion impaired the feedback regulation of CORT levels but had no putative effect on the CORT-induced decrease in hippocampal GR expression and the reduction of the adrenal cortex size. Finally, the composition and structure of the gut microbiota were significantly impacted by the absence of neuronal 5HT, and these alterations were enhanced by chronic CORT treatment. Therefore, we conclude that neuronal 5HT influences the stress-related responses at different levels involving CORT levels regulation and the gut microbiome.
MeSH term(s)	Adrenal Glands/drug effects ; Adrenal Glands/metabolism ; Animals ; Brain/metabolism ; Corticosterone/metabolism ; Corticosterone/pharmacology ; Gastrointestinal Microbiome/drug effects ; Gastrointestinal Microbiome/physiology ; Hypothalamo-Hypophyseal System/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neurons/metabolism ; Pituitary-Adrenal System/metabolism ; RNA, Ribosomal, 16S/metabolism ; Receptors, Glucocorticoid/drug effects ; Receptors, Glucocorticoid/metabolism ; Serotonin/genetics ; Serotonin/metabolism ; Stress, Psychological/metabolism ; Tryptophan Hydroxylase/genetics
Chemical Substances	RNA, Ribosomal, 16S ; Receptors, Glucocorticoid ; Serotonin (333DO1RDJY) ; Tph2 protein, mouse (EC 1.14.16.4) ; Tryptophan Hydroxylase (EC 1.14.16.4) ; Corticosterone (W980KJ009P)
Language	English
Publishing date	2020-11-02
Publishing country	Netherlands
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1200-2
ISSN	1872-6240 ; 0006-8993
ISSN (online)	1872-6240
ISSN	0006-8993
DOI	10.1016/j.brainres.2020.147190
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