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Article ; Online: Modeling psychotic disorders: Environment x environment interaction.

Murlanova, Kateryna / Pletnikov, Mikhail V

2023 Volume 152, Page(s) 105310

Abstract: Schizophrenia is a major psychotic disorder with multifactorial etiology that includes interactions between genetic vulnerability and environmental risk factors. In addition, interplay of multiple environmental adversities affects neurodevelopment and ... ...

Abstract	Schizophrenia is a major psychotic disorder with multifactorial etiology that includes interactions between genetic vulnerability and environmental risk factors. In addition, interplay of multiple environmental adversities affects neurodevelopment and may increase the individual risk of developing schizophrenia. Consistent with the two-hit hypothesis of schizophrenia, we review rodent models that combine maternal immune activation as the first hit with other adverse environmental exposures as the second hit. We discuss the strengths and pitfalls of the current animal models of environment x environment interplay and propose some future directions to advance the field.
MeSH term(s)	Animals ; Gene-Environment Interaction ; Psychotic Disorders/genetics ; Schizophrenia/complications ; Environmental Exposure/adverse effects ; Rodentia
Language	English
Publishing date	2023-07-10
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	282464-4
ISSN	1873-7528 ; 0149-7634
ISSN (online)	1873-7528
ISSN	0149-7634
DOI	10.1016/j.neubiorev.2023.105310
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Article ; Online: Neuronal metabolism in learning and memory: The anticipatory activity perspective.

Alexandrov, Yuri I / Pletnikov, Mikhail V

Neuroscience and biobehavioral reviews

2022 Volume 137, Page(s) 104664

Abstract: Current research on the molecular mechanisms of learning and memory is based on the "stimulus-response" paradigm, in which the neural circuits connecting environmental events with behavioral responses are strengthened. By contrast, cognitive and systems ... ...

Abstract	Current research on the molecular mechanisms of learning and memory is based on the "stimulus-response" paradigm, in which the neural circuits connecting environmental events with behavioral responses are strengthened. By contrast, cognitive and systems neuroscience emphasize the intrinsic activity of the brain that integrates information, establishes anticipatory actions, executes adaptive actions, and assesses the outcome via regulatory feedback mechanisms. We believe that the difference in the perspectives of systems and molecular studies is a major roadblock to further progress toward understanding the mechanisms of learning and memory. Here, we briefly overview the current studies in molecular mechanisms of learning and memory and propose that studying the predictive properties of neuronal metabolism will significantly advance our knowledge of how intrinsic, predictive activity of neurons shapes a new learning event. We further suggest that predictive metabolic changes in the brain may also take place in non-neuronal cells, including those of peripheral tissues. Finally, we present a path forward toward more in-depth studies of the role of cell metabolism in learning and memory.
MeSH term(s)	Brain/physiology ; Humans ; Learning/physiology ; Memory/physiology ; Neurons/physiology
Language	English
Publishing date	2022-04-16
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	282464-4
ISSN	1873-7528 ; 0149-7634
ISSN (online)	1873-7528
ISSN	0149-7634
DOI	10.1016/j.neubiorev.2022.104664
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Article ; Online: Experimental and computational analyses of calcium dynamics in 22q11.2 deletion model astrocytes.

Maly, Ivan V / Hofmann, Wilma A / Pletnikov, Mikhail V

Neuroscience letters

2022 Volume 783, Page(s) 136711

Abstract: Methods for deriving mechanistic information from intracellular calcium dynamics have largely been applied to neuronal data despite the knowledge of roles of glial cells in behavior, cognition, and psychiatric disorders. Using calcium imaging, computer ... ...

Abstract	Methods for deriving mechanistic information from intracellular calcium dynamics have largely been applied to neuronal data despite the knowledge of roles of glial cells in behavior, cognition, and psychiatric disorders. Using calcium imaging, computer vision, and Bayesian kinetic inference (BKI), we analyzed calcium dynamics in primary astrocytes derived from control or Df1/
MeSH term(s)	Animals ; Astrocytes ; Bayes Theorem ; Calcium ; DiGeorge Syndrome ; Disease Models, Animal ; Humans ; Mice
Chemical Substances	Calcium (SY7Q814VUP)
Language	English
Publishing date	2022-06-06
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	194929-9
ISSN	1872-7972 ; 0304-3940
ISSN (online)	1872-7972
ISSN	0304-3940
DOI	10.1016/j.neulet.2022.136711
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Article ; Online: Contributions of nonneuronal brain cells in substance use disorders.

Reissner, Kathryn J / Pletnikov, Mikhail V

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2019 Volume 45, Issue 1, Page(s) 224–225

MeSH term(s)	Animals ; Brain/cytology ; Brain/pathology ; Brain/physiology ; Drug-Seeking Behavior/physiology ; Humans ; Neuroglia/physiology ; Substance-Related Disorders/pathology ; Substance-Related Disorders/physiopathology
Language	English
Publishing date	2019-09-02
Publishing country	England
Document type	News
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/s41386-019-0494-5
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Article: Astrocyte Bioenergetics and Major Psychiatric Disorders.

Maly, Ivan V / Morales, Michael J / Pletnikov, Mikhail V

Advances in neurobiology

2021 Volume 26, Page(s) 173–227

Abstract: Ongoing research continues to add new elements to the emerging picture of involvement of astrocyte energy metabolism in the pathophysiology of major psychiatric disorders, including schizophrenia, mood disorders, and addictions. This review outlines what ...

Abstract	Ongoing research continues to add new elements to the emerging picture of involvement of astrocyte energy metabolism in the pathophysiology of major psychiatric disorders, including schizophrenia, mood disorders, and addictions. This review outlines what is known about the energy metabolism in astrocytes, the most numerous cell type in the brain, and summarizes the recent work on how specific perturbations of astrocyte bioenergetics may contribute to the neuropsychiatric conditions. The role of astrocyte energy metabolism in mental health and disease is reviewed on the organism, organ, and cell level. Data arising from genomic, metabolomic, in vitro, and neurobehavioral studies is critically analyzed to suggest future directions in research and possible metabolism-focused therapeutic interventions.
MeSH term(s)	Astrocytes ; Brain ; Energy Metabolism ; Humans ; Mental Disorders ; Schizophrenia
Language	English
Publishing date	2021-12-10
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2190-5215
ISSN	2190-5215
DOI	10.1007/978-3-030-77375-5_9
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Book: Modeling the psychopathological dimensions of schizophrenia

Pletnikov, Mikhail V / Waddington, John L

from molecules to behavior

(Handbook of behavioral neuroscience ; volume 23)

2016

Author's details	edited by Mikhail V. Pletnikov, John L. Waddington
Series title	Handbook of behavioral neuroscience ; volume 23
MeSH term(s)	Schizophrenia ; Disease Models, Animal
Language	English
Size	xv, 531 pages :, illustrations (some color) ;, 28 cm.
Document type	Book
ISBN	9780128009819 ; 0128009810
Database	Catalogue of the US National Library of Medicine (NLM)

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Article ; Online: Deficient mitochondrial respiration in astrocytes impairs trace fear conditioning and increases naloxone-precipitated aversion in morphine-dependent mice.

Murlanova, Kateryna / Jouroukhin, Yan / Huseynov, Shovgi / Pletnikova, Olga / Morales, Michael J / Guan, Yun / Baraban, Jay M / Bergles, Dwight E / Pletnikov, Mikhail V

Glia

2022 Volume 70, Issue 7, Page(s) 1289–1300

Abstract: Mitochondria are abundant in the fine processes of astrocytes, however, potential roles for astrocyte mitochondria remain poorly understood. In the present study, we performed a systematic examination of the effects of abnormal oxidative phosphorylation ... ...

Abstract	Mitochondria are abundant in the fine processes of astrocytes, however, potential roles for astrocyte mitochondria remain poorly understood. In the present study, we performed a systematic examination of the effects of abnormal oxidative phosphorylation in astrocytes on several mouse behaviors. Impaired astrocyte oxidative phosphorylation was produced by astrocyte-specific deletion of the nuclear mitochondrial gene, Cox10, that encodes an accessory protein of complex IV, the protoheme:heme-O-farnesyl transferase. As expected, conditional deletion of the Cox10 gene in mice (cKO mice) significantly reduced expression of COX10 and Cytochrome c oxidase subunit I (MTCO1) of Complex IV, resulting in decreased oxidative phosphorylation without significantly affecting glycolysis. No effects of the deletion were observed on locomotor activity, anxiety-like behavior, nociception, or spontaneous alternation. Cox10 cKO female mice exhibited mildly impaired novel object recognition, while Cox10 cKO male mice were moderately deficient in trace fear conditioning. No group-related changes were observed in conditional place preference (CPP) that assessed effects of morphine on reward. In contrast to CPP, Cox10 cKO mice demonstrated significantly increased aversive behaviors produced by naloxone-precipitated withdrawal following chronic exposure to morphine, that is, jumping and avoidance behavior as assessed by conditional place aversion (CPA). Our study suggests that astrocyte oxidative phosphorylation may contribute to behaviors associated with greater cognitive load and/or aversive and stressful conditions.
MeSH term(s)	Alkyl and Aryl Transferases/metabolism ; Animals ; Astrocytes/metabolism ; Fear ; Female ; Male ; Membrane Proteins/metabolism ; Mice ; Mitochondria/metabolism ; Morphine/metabolism ; Morphine/pharmacology ; Morphine Dependence/metabolism ; Morphine Dependence/psychology ; Naloxone/metabolism ; Naloxone/pharmacology ; Narcotic Antagonists/metabolism ; Narcotic Antagonists/pharmacology ; Respiration ; Substance Withdrawal Syndrome/metabolism ; Substance Withdrawal Syndrome/psychology
Chemical Substances	Membrane Proteins ; Narcotic Antagonists ; Naloxone (36B82AMQ7N) ; Morphine (76I7G6D29C) ; Alkyl and Aryl Transferases (EC 2.5.-) ; COX10 protein, mouse (EC 2.5.1.-)
Language	English
Publishing date	2022-03-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.24169
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Article ; Online: Inducible and conditional transgenic mouse models of schizophrenia.

Pletnikov, Mikhail V

Progress in brain research

2009 Volume 179, Page(s) 35–47

Abstract: Schizophrenia is a devastating disorder. Despite the advance in research techniques in the last couple of decades, the pathogenesis of the disorder still remains poorly understood. Given the lack of pathognomonic feature of the disease and difficulty to ... ...

Abstract	Schizophrenia is a devastating disorder. Despite the advance in research techniques in the last couple of decades, the pathogenesis of the disorder still remains poorly understood. Given the lack of pathognomonic feature of the disease and difficulty to analyze molecular pathways in patients, animal models have been instrumental in advancing our understanding of the disease. Recent progress in genetics has identified candidate susceptibility genes for schizophrenia, and generation of new genetic animal models has begun to provide valuable insights into the disease development. However, the complex neurodevelopmental and heterogeneous nature of schizophrenia still poses tremendous challenges for creating credible mouse models. In this review, we will discuss how current genetic systems of temporal and conditional regulation of gene expression have shed lights on the functions of the candidate genes in mouse models of schizophrenia. We also consider the strength and weaknesses of each model. We will argue that further development of more sophisticated genetic animal models is crucial for clarifying the unknowns of schizophrenia.
MeSH term(s)	Animals ; Disease Models, Animal ; Estrogen Receptor alpha/genetics ; GTP-Binding Proteins/genetics ; Gene Expression Regulation/genetics ; Gene Transfer Techniques ; Humans ; Mice ; Mice, Transgenic/genetics ; Nerve Tissue Proteins/genetics ; Receptors, Dopamine D2/genetics ; Schizophrenia/genetics ; Tetracycline/pharmacology
Chemical Substances	DISC1 protein, human ; Estrogen Receptor alpha ; Nerve Tissue Proteins ; Receptors, Dopamine D2 ; GTP-Binding Proteins (EC 3.6.1.-) ; Tetracycline (F8VB5M810T)
Language	English
Publishing date	2009
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ISSN	1875-7855 ; 0079-6123
ISSN (online)	1875-7855
ISSN	0079-6123
DOI	10.1016/S0079-6123(09)17905-0
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Article ; Online: Microglial cannabinoid receptor type 1 mediates social memory deficits in mice produced by adolescent THC exposure and 16p11.2 duplication.

Hasegawa, Yuto / Kim, Juhyun / Ursini, Gianluca / Jouroukhin, Yan / Zhu, Xiaolei / Miyahara, Yu / Xiong, Feiyi / Madireddy, Samskruthi / Obayashi, Mizuho / Lutz, Beat / Sawa, Akira / Brown, Solange P / Pletnikov, Mikhail V / Kamiya, Atsushi

Nature communications

2023 Volume 14, Issue 1, Page(s) 6559

Abstract: Adolescent cannabis use increases the risk for cognitive impairments and psychiatric disorders. Cannabinoid receptor type 1 (Cnr1) is expressed not only in neurons and astrocytes, but also in microglia, which shape synaptic connections during adolescence. ...

Abstract	Adolescent cannabis use increases the risk for cognitive impairments and psychiatric disorders. Cannabinoid receptor type 1 (Cnr1) is expressed not only in neurons and astrocytes, but also in microglia, which shape synaptic connections during adolescence. However, the role of microglia in mediating the adverse cognitive effects of delta-9-tetrahydrocannabinol (THC), the principal psychoactive constituent of cannabis, is not fully understood. Here, we report that in mice, adolescent THC exposure produces microglial apoptosis in the medial prefrontal cortex (mPFC), which was exacerbated in a model of 16p11.2 duplication, a representative copy number variation (CNV) risk factor for psychiatric disorders. These effects are mediated by microglial Cnr1, leading to reduction in the excitability of mPFC pyramidal-tract neurons and deficits in social memory in adulthood. Our findings suggest the microglial Cnr1 may contribute to adverse effect of cannabis exposure in genetically vulnerable individuals.
MeSH term(s)	Animals ; Mice ; Cannabinoid Receptor Agonists ; DNA Copy Number Variations ; Dronabinol/adverse effects ; Memory Disorders/chemically induced ; Memory Disorders/genetics ; Microglia ; Receptors, Cannabinoid/genetics
Chemical Substances	Cannabinoid Receptor Agonists ; Dronabinol (7J8897W37S) ; Receptors, Cannabinoid
Language	English
Publishing date	2023-10-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-42276-5
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Article: Microglial cannabinoid receptor type 1 mediates social memory deficits produced by adolescent THC exposure and 16p11.2 duplication.

bioRxiv : the preprint server for biology

2023

Abstract	Adolescent cannabis use increases the risk for cognitive impairments and psychiatric disorders. Cannabinoid receptor type 1 (Cnr1) is expressed not only in neurons and astrocytes, but also in microglia, which shape synaptic connections during adolescence. Nonetheless, until now, the role of microglia in mediating the adverse cognitive effects of delta-9-tetrahydrocannabinol (THC), the principal psychoactive constituent of cannabis, has been unexplored. Here, we report that adolescent THC exposure produces microglial apoptosis in the medial prefrontal cortex (mPFC), which was exacerbated in the mouse model of 16p11.2 duplication, a representative copy number variation (CNV) risk factor for psychiatric disorders. These effects are mediated by microglial Cnr1, leading to reduction in the excitability of mPFC pyramidal-tract neurons and deficits in social memory in adulthood. Our findings highlight the importance of microglial Cnr1 to produce the adverse effect of cannabis exposure in genetically vulnerable individuals.
Language	English
Publishing date	2023-07-26
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.07.24.550212
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