LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 79

Search options

  1. 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
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  2. Article ; Online: Loss of Astrocytic µ Opioid Receptors Exacerbates Aversion Associated with Morphine Withdrawal in Mice: Role of Mitochondrial Respiration.

    Murlanova, Kateryna / Jouroukhin, Yan / Novototskaya-Vlasova, Ksenia / Huseynov, Shovgi / Pletnikova, Olga / Morales, Michael J / Guan, Yun / Kamiya, Atsushi / Bergles, Dwight E / Dietz, David M / Pletnikov, Mikhail V

    Cells

    2023  Volume 12, Issue 10

    Abstract: Astrocytes express mu/µ opioid receptors, but the function of these receptors remains poorly understood. We evaluated the effects of astrocyte-restricted knockout of µ opioid receptors on reward- and aversion-associated behaviors in mice chronically ... ...

    Abstract Astrocytes express mu/µ opioid receptors, but the function of these receptors remains poorly understood. We evaluated the effects of astrocyte-restricted knockout of µ opioid receptors on reward- and aversion-associated behaviors in mice chronically exposed to morphine. Specifically, one of the floxed alleles of the
    MeSH term(s) Mice ; Animals ; Morphine/adverse effects ; Astrocytes ; Receptors, Opioid ; Narcotic Antagonists/pharmacology ; Naloxone/pharmacology ; Mice, Knockout ; Receptors, Opioid, mu/genetics
    Chemical Substances Morphine (76I7G6D29C) ; Receptors, Opioid ; Narcotic Antagonists ; Naloxone (36B82AMQ7N) ; Receptors, Opioid, mu
    Language English
    Publishing date 2023-05-17
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells12101412
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  3. 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
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  4. Article: Microglial cannabinoid receptor type 1 mediates social memory deficits 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

    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. ...

    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
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  5. Article ; Online: Neuronal Histone Methyltransferase EZH2 Regulates Neuronal Morphogenesis, Synaptic Plasticity, and Cognitive Behavior in Mice.

    Zhang, Mei / Zhang, Yong / Xu, Qian / Crawford, Joshua / Qian, Cheng / Wang, Guo-Hua / Qian, Jiang / Dong, Xin-Zhong / Pletnikov, Mikhail V / Liu, Chang-Mei / Zhou, Feng-Quan

    Neuroscience bulletin

    2023  Volume 39, Issue 10, Page(s) 1512–1532

    Abstract: The histone methyltransferase enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2)-mediated trimethylation of histone H3 lysine 27 (H3K27me3) regulates neural stem cell proliferation and fate specificity through silencing different gene sets ... ...

    Abstract The histone methyltransferase enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2)-mediated trimethylation of histone H3 lysine 27 (H3K27me3) regulates neural stem cell proliferation and fate specificity through silencing different gene sets in the central nervous system. Here, we explored the function of EZH2 in early post-mitotic neurons by generating a neuron-specific Ezh2 conditional knockout mouse line. The results showed that a lack of neuronal EZH2 led to delayed neuronal migration, more complex dendritic arborization, and increased dendritic spine density. Transcriptome analysis revealed that neuronal EZH2-regulated genes are related to neuronal morphogenesis. In particular, the gene encoding p21-activated kinase 3 (Pak3) was identified as a target gene suppressed by EZH2 and H3K27me3, and expression of the dominant negative Pak3 reversed Ezh2 knockout-induced higher dendritic spine density. Finally, the lack of neuronal EZH2 resulted in impaired memory behaviors in adult mice. Our results demonstrated that neuronal EZH2 acts to control multiple steps of neuronal morphogenesis during development, and has long-lasting effects on cognitive function in adult mice.
    MeSH term(s) Animals ; Mice ; Enhancer of Zeste Homolog 2 Protein/metabolism ; Histone Methyltransferases/metabolism ; Histones/genetics ; Morphogenesis ; Neuronal Plasticity ; Neurons/metabolism
    Chemical Substances Enhancer of Zeste Homolog 2 Protein (EC 2.1.1.43) ; Histone Methyltransferases (EC 2.1.1.-) ; Histones
    Language English
    Publishing date 2023-06-16
    Publishing country Singapore
    Document type Journal Article
    ZDB-ID 2419741-5
    ISSN 1995-8218 ; 1673-7067
    ISSN (online) 1995-8218
    ISSN 1673-7067
    DOI 10.1007/s12264-023-01074-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  6. Article ; Online: Microvascular anomaly conditions in psychiatric disease. Schizophrenia - angiogenesis connection.

    Katsel, Pavel / Roussos, Panos / Pletnikov, Mikhail / Haroutunian, Vahram

    Neuroscience and biobehavioral reviews

    2017  Volume 77, Page(s) 327–339

    Abstract: Schizophrenia (SZ) is a severe mental disorder with unknown etiology and elusive neuropathological and neurobiological features have been a focus of many theoretical hypotheses and empirical studies. Current genetic and neurobiology information relevant ... ...

    Abstract Schizophrenia (SZ) is a severe mental disorder with unknown etiology and elusive neuropathological and neurobiological features have been a focus of many theoretical hypotheses and empirical studies. Current genetic and neurobiology information relevant to SZ implicates neuronal developmental and synaptic plasticity abnormalities, and neurotransmitter, microglial and oligodendrocytes dysfunction. Several recent theories have highlighted the neurovascular unit as a potential contributor to the pathophysiology of SZ. We explored the biological plausibility of a link between SZ and the neurovascular system by examining insights gained from genetic, neuroimaging and postmortem studies, which include gene expression and neuropathology analyses. We also reviewed information from animal models of cerebral angiogenesis in order to understand better the complex interplay between angiogenic and neurotrophic factors in development, vascular endothelium/blood brain barrier remodeling and maintenance, all of which contribute to sustaining adequate regional blood flow and safeguarding normal brain function. Microvascular and hemodynamic alterations in SZ highlight the importance of further research and reveal the neurovascular unit as a potential therapeutic target in SZ.
    MeSH term(s) Animals ; Brain/blood supply ; Humans ; Microvessels/anatomy & histology ; Neuroimaging ; Schizophrenia
    Language English
    Publishing date 2017-04-08
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S. ; 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.2017.04.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  7. Article ; Online: Homeostatic regulation of neuronal excitability by probiotics in male germ-free mice.

    Kim, Juhyun / Kim, Dong Won / Lee, Adrian / Mason, Madisen / Jouroukhin, Yan / Woo, Hyewon / Yolken, Robert H / Pletnikov, Mikhail V

    Journal of neuroscience research

    2021  Volume 100, Issue 2, Page(s) 444–460

    Abstract: Emerging evidence indicates that probiotics can influence the gut-brain axis to ameliorate somatic and behavioral symptoms associated with brain disorders. However, whether probiotics have effects on the electrophysiological activities of individual ... ...

    Abstract Emerging evidence indicates that probiotics can influence the gut-brain axis to ameliorate somatic and behavioral symptoms associated with brain disorders. However, whether probiotics have effects on the electrophysiological activities of individual neurons in the brain has not been evaluated at a single-neuron resolution, and whether the neuronal effects of probiotics depend on the gut microbiome status have yet to be tested. Thus, we conducted whole-cell patch-clamp recording-assisted electrophysiological characterizations of the neuronal effects of probiotics in male germ-free (GF) mice with and without gut microbiome colonization. Two weeks of treatment with probiotics (Lactobacillus rhamnosus and Bifidobacterium animalis) significantly and selectively increased the intrinsic excitability of hippocampal CA1 pyramidal neurons, whereas reconstituting gut microbiota in GF mice reversed the effects of the probiotics leading to a decreased intrinsic excitability in hippocampal neurons. This bidirectional modulation of neuronal excitability by probiotics was observed in hippocampal neurons with corresponding basal membrane property and action potential waveform changes. However, unlike the hippocampus, the amygdala excitatory neurons did not show any electrophysiological changes to the probiotic treatment in either GF or conventionalized GF mice. Our findings demonstrate for the first time how probiotic treatment can have a significant influence on the electrophysiological properties of neurons, bidirectionally modulating their intrinsic excitability in a gut microbiota and brain area-specific manner.
    MeSH term(s) Animals ; Gastrointestinal Microbiome/physiology ; Hippocampus ; Male ; Mice ; Neurons ; Probiotics/pharmacology ; Pyramidal Cells/physiology
    Language English
    Publishing date 2021-12-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 195324-2
    ISSN 1097-4547 ; 0360-4012
    ISSN (online) 1097-4547
    ISSN 0360-4012
    DOI 10.1002/jnr.24999
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  8. Article ; Online: Cannabis and the Developing Brain: Insights into Its Long-Lasting Effects.

    Hurd, Yasmin L / Manzoni, Olivier J / Pletnikov, Mikhail V / Lee, Francis S / Bhattacharyya, Sagnik / Melis, Miriam

    The Journal of neuroscience : the official journal of the Society for Neuroscience

    2019  Volume 39, Issue 42, Page(s) 8250–8258

    Abstract: The recent shift in sociopolitical debates and growing liberalization of cannabis use across the globe has raised concern regarding its impact on vulnerable populations, such as pregnant women and adolescents. Epidemiological studies have long ... ...

    Abstract The recent shift in sociopolitical debates and growing liberalization of cannabis use across the globe has raised concern regarding its impact on vulnerable populations, such as pregnant women and adolescents. Epidemiological studies have long demonstrated a relationship between developmental cannabis exposure and later mental health symptoms. This relationship is especially strong in people with particular genetic polymorphisms, suggesting that cannabis use interacts with genotype to increase mental health risk. Seminal animal research directly linked prenatal and adolescent exposure to delta-9-tetrahydrocannabinol, the major psychoactive component of cannabis, with protracted effects on adult neural systems relevant to psychiatric and substance use disorders. In this article, we discuss some recent advances in understanding the long-term molecular, epigenetic, electrophysiological, and behavioral consequences of prenatal, perinatal, and adolescent exposure to cannabis/delta-9-tetrahydrocannabinol. Insights are provided from both animal and human studies, including
    MeSH term(s) Adolescent ; Animals ; Cannabis/adverse effects ; Cognition/physiology ; Female ; Humans ; Marijuana Use/adverse effects ; Mental Disorders/etiology ; Mental Disorders/psychology ; Pregnancy ; Prenatal Exposure Delayed Effects/psychology
    Language English
    Publishing date 2019-10-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 604637-x
    ISSN 1529-2401 ; 0270-6474
    ISSN (online) 1529-2401
    ISSN 0270-6474
    DOI 10.1523/JNEUROSCI.1165-19.2019
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  9. Article ; Online: Increased novelty-induced locomotion, sensitivity to amphetamine, and extracellular dopamine in striatum of Zdhhc15-deficient mice.

    Mejias, Rebeca / Rodriguez-Gotor, Juan J / Niwa, Minae / Krasnova, Irina N / Adamczyk, Abby / Han, Mei / Thomas, Gareth M / Xi, Zheng-Xiong / Huganir, Richard L / Pletnikov, Mikhail V / Sawa, Akira / Cadet, Jean-Lud / Wang, Tao

    Translational psychiatry

    2021  Volume 11, Issue 1, Page(s) 65

    Abstract: Novelty-seeking behaviors and impulsivity are personality traits associated with several psychiatric illnesses including attention deficits hyperactivity disorders. The underlying neural mechanisms remain poorly understood. We produced and characterized ... ...

    Abstract Novelty-seeking behaviors and impulsivity are personality traits associated with several psychiatric illnesses including attention deficits hyperactivity disorders. The underlying neural mechanisms remain poorly understood. We produced and characterized a line of knockout mice for zdhhc15, which encodes a neural palmitoyltransferase. Genetic defects of zdhhc15 were implicated in intellectual disability and behavioral anomalies in humans. Zdhhc15-KO mice showed normal spatial learning and working memory but exhibited a significant increase in novelty-induced locomotion in open field. Striatal dopamine content was reduced but extracellular dopamine levels were increased during the habituation phase to a novel environment. Administration of amphetamine and methylphenidate resulted in a significant increase in locomotion and extracellular dopamine levels in the ventral striatum of mutant mice compared to controls. Number and projections of dopaminergic neurons in the nigrostriatal and mesolimbic pathways were normal. No significant change in the basal palmitoylation of known ZDHHC15 substrates including DAT was detected in striatum of zdhhc15 KO mice using an acyl-biotin exchange assay. These results support that a transient, reversible, and novelty-induced elevation of extracellular dopamine in ventral striatum contributes to novelty-seeking behaviors in rodents and implicate ZDHHC15-mediated palmitoylation as a novel regulatory mechanism of dopamine in the striatum.
    MeSH term(s) Amphetamine/pharmacology ; Animals ; Corpus Striatum/metabolism ; Dopamine ; Dopamine Plasma Membrane Transport Proteins/genetics ; Dopamine Plasma Membrane Transport Proteins/metabolism ; Locomotion ; Mice ; Mice, Knockout
    Chemical Substances Dopamine Plasma Membrane Transport Proteins ; Amphetamine (CK833KGX7E) ; Dopamine (VTD58H1Z2X)
    Language English
    Publishing date 2021-01-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; 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/s41398-020-01194-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  10. Article ; Online: MCT1 Deletion in Oligodendrocyte Lineage Cells Causes Late-Onset Hypomyelination and Axonal Degeneration.

    Philips, Thomas / Mironova, Yevgeniya A / Jouroukhin, Yan / Chew, Jeannie / Vidensky, Svetlana / Farah, Mohamed H / Pletnikov, Mikhail V / Bergles, Dwight E / Morrison, Brett M / Rothstein, Jeffrey D

    Cell reports

    2021  Volume 34, Issue 2, Page(s) 108610

    Abstract: Oligodendrocytes (OLs) are important for myelination and shuttling energy metabolites lactate and pyruvate toward axons through their expression of monocarboxylate transporter 1 (MCT1). Recent studies suggest that loss of OL MCT1 causes axonal ... ...

    Abstract Oligodendrocytes (OLs) are important for myelination and shuttling energy metabolites lactate and pyruvate toward axons through their expression of monocarboxylate transporter 1 (MCT1). Recent studies suggest that loss of OL MCT1 causes axonal degeneration. However, it is unknown how widespread and chronic loss of MCT1 in OLs specifically affects neuronal energy homeostasis with aging. To answer this, MCT1 conditional null mice were generated that allow for OL-specific MCT1 ablation. We observe that MCT1 loss from OL lineage cells is dispensable for normal myelination and axonal energy homeostasis early in life. By contrast, loss of OL lineage MCT1 expression with aging leads to significant axonal degeneration with concomitant hypomyelination. These data support the hypothesis that MCT1 is important for neuronal energy homeostasis in the aging central nervous system (CNS). The reduction in OL MCT1 that occurs with aging may enhance the risk for axonal degeneration and atrophy in neurodegenerative diseases.
    MeSH term(s) Animals ; Axons/metabolism ; Female ; Male ; Mice ; Mice, Transgenic ; Monocarboxylic Acid Transporters/deficiency ; Monocarboxylic Acid Transporters/metabolism ; Myelin Sheath/metabolism ; Myelin Sheath/pathology ; Nerve Degeneration/metabolism ; Oligodendroglia/metabolism ; Oligodendroglia/pathology ; Symporters/deficiency ; Symporters/metabolism
    Chemical Substances Monocarboxylic Acid Transporters ; Symporters ; monocarboxylate transport protein 1
    Language English
    Publishing date 2021-01-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2020.108610
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

To top