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  • 1
    Online Resource
    Online Resource
    Roles and Regulation of Ketogenesis in Cultured Astroglia and Neurons Under Hypoxia and Hypoglycemia
    SAGE Publications ; 2014
    In:  ASN Neuro Vol. 6, No. 5 ( 2014-07-01), p. 175909141455099-
    Details
    In: ASN Neuro, SAGE Publications, Vol. 6, No. 5 ( 2014-07-01), p. 175909141455099-
    Abstract: Exogenous ketone bodies (KBs), acetoacetate (AA), and β-hydroxybutyrate (BHB) act as alternative energy substrates in neural cells under starvation. The present study examined the endogenous ketogenic capacity of astroglia under hypoxia with/without glucose and the possible roles of KBs in neuronal energy metabolism. Cultured neurons and astroglia were prepared from Sprague-Dawley rats. Palmitic acid (PAL) and l-carnitine (LC) were added to the assay medium. The 4- to 24-hr production of AA and BHB was measured using the cyclic thio-NADH method. 14 C-labeled acid-soluble products (KBs) and 14 CO 2 produced from [1- 14 C]PAL were also measured. l-[U- 14 C]lactic acid ([ 14 C]LAC), [1- 14 C]pyruvic acid ([ 14 C]PYR), or β-[1- 14 C]hydroxybutyric acid ([ 14 C]BHB) was used to compare the oxidative metabolism of the glycolysis end products with that of the KBs. Some cells were placed in a hypoxic chamber (1% O 2 ). PAL and LC induced a higher production of KBs in astroglia than in neurons, while the CO 2 production from PAL was less than 5% of the KB production in both astroglia and neurons. KB production in astroglia was augmented by the AMP-activated protein kinase activators, AICAR and metformin, as well as hypoxia with/without glucose. Neuronal KB production increased under hypoxia in the absence of PAL and LC. In neurons, [ 14 C]LAC and [ 14 C]PYR oxidation decreased after 24 hr of hypoxia, while [ 14 C]BHB oxidation was preserved. Astroglia responds to ischemia in vitro by enhancing KB production, and astroglia-produced KBs derived from fatty acid might serve as a neuronal energy substrate for the tricarboxylic acid cycle instead of lactate, as pyruvate dehydrogenase is susceptible to ischemia.
    Type of Medium: Online Resource
    ISSN: 1759-0914 , 1759-0914
    URL: Article
    DOI: 10.1177/1759091414550997
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2014
    detail.hit.zdb_id: 2485467-0
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  • 2
    Online Resource
    Online Resource
    Neuroprotective Role of Astroglia in Parkinson Disease by Reducing Oxidative Stress Through Dopamine-Induced Activation of Pentose-Phosphate Pathway
    SAGE Publications ; 2018
    In:  ASN Neuro Vol. 10 ( 2018-01), p. 175909141877556-
    Details
    In: ASN Neuro, SAGE Publications, Vol. 10 ( 2018-01), p. 175909141877556-
    Abstract: Oxidative stress plays an important role in the onset and progression of Parkinson disease. Although released dopamine at the synaptic terminal is mostly reabsorbed by dopaminergic neurons, some dopamine is presumably taken up by astroglia. This study examined the dopamine-induced astroglial protective function through the activation of the pentose-phosphate pathway (PPP) to reduce reactive oxygen species (ROS). In vitro experiments were performed using striatal neurons and cortical or striatal astroglia prepared from Sprague-Dawley rats or C57BL/6 mice. The rates of glucose phosphorylation in astroglia were evaluated using the [ 14 C]deoxyglucose method. PPP activity was measured using [1- 14 C]glucose and [6- 14 C]glucose after acute (60 min) or chronic (15 hr) exposure to dopamine. ROS production was measured using 2′,7′-dichlorodihydrofluorescein diacetate. The involvement of the Kelch-like ECH-associated protein 1 (Keap1) or nuclear factor-erythroid-2-related factor 2 (Nrf2) system was evaluated using Nrf2 gene knockout mice, immunohistochemistry, and quantitative reverse transcription polymerase chain reaction analysis for heme oxygenase-1. Acute exposure to dopamine elicited increases in astroglial glucose consumption with lactate release. PPP activity in astroglia was robustly enhanced independently of Na + -dependent monoamine transporters. In contrast, chronic exposure to dopamine induced moderate increases in PPP activity via the Keap1/Nrf2 system. ROS production from dopamine increased gradually over 12 hr. Dopamine induced neuronal cell damage that was prevented by coculturing with astroglia but not with Nrf2-deficient astroglia. Dopamine-enhanced astroglial PPP activity in both acute and chronic manners may possibly reduce neuronal oxidative stress.
    Type of Medium: Online Resource
    ISSN: 1759-0914 , 1759-0914
    URL: Article
    DOI: 10.1177/1759091418775562
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2018
    detail.hit.zdb_id: 2485467-0
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  • 3
    Online Resource
    Online Resource
    A possible role of microglia-derived nitric oxide by lipopolysaccharide in activation of astroglial pentose-phosphate pathway via the Keap1/Nrf2 system
    Springer Science and Business Media LLC ; 2016
    In:  Journal of Neuroinflammation Vol. 13, No. 1 ( 2016-12)
    Details
    In: Journal of Neuroinflammation, Springer Science and Business Media LLC, Vol. 13, No. 1 ( 2016-12)
    Type of Medium: Online Resource
    ISSN: 1742-2094
    URL: Article
    DOI: 10.1186/s12974-016-0564-0
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2016
    detail.hit.zdb_id: 2156455-3
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  • 4
    Online Resource
    Online Resource
    Cellular Origin and Regulation of D -and L -Serine in in Vitro and in Vivo Models of Cerebral Ischemia
    SAGE Publications ; 2014
    In:  Journal of Cerebral Blood Flow & Metabolism Vol. 34, No. 12 ( 2014-12), p. 1928-1935
    Details
    In: Journal of Cerebral Blood Flow & Metabolism, SAGE Publications, Vol. 34, No. 12 ( 2014-12), p. 1928-1935
    Abstract: D-Serine is known to be essential for the activation of the N-methyl-D-aspartate (NMDA) receptor in the excitation of glutamatergic neurons, which have critical roles in long-term potentiation and memory formation. D-Serine is also thought to be involved in NMDA receptor-mediated neurotoxicity. The deletion of serine racemase (SRR), which synthesizes D-Serine from L-Serine, was recently reported to improve ischemic damage in mouse middle cerebral artery occlusion model. However, the cell type in which this phenomenon originates and the regulatory mechanism for D-/L-Serine remain elusive. The D-/L-Serine content in ischemic brain increased until 20 hours after recanalization and then leveled off gradually. The results of in vitro experiments using cultured cells suggested that D-Serine is derived from neurons, while L-Serine seems to be released from astroglia. Immunohistochemistry studies of brain tissue after cerebral ischemia showed that SRR is expressed in neurons, and 3-phosphoglycerate dehydrogenase (3-PGDH), which synthesizes L-Serine from 3-phosphoglycerate, is located in astrocytes, supporting the results of the in vitro experiments. A western blot analysis showed that neither SRR nor 3-PGDH was upregulated after cerebral ischemia. Therefore, the increase in D-/L-Serine was not related to an increase in SRR or 3-PGDH, but to an increase in the substrates of SRR and 3-PGDH.
    Type of Medium: Online Resource
    ISSN: 0271-678X , 1559-7016
    URL: Article
    DOI: 10.1038/jcbfm.2014.164
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2014
    detail.hit.zdb_id: 2039456-1
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