PMC:6891830 / 6055-7469 JSONTXT

{"project":"TEST0","denotations":[{"id":"31208231-97-102-3772","span":{"begin":97,"end":98},"obj":"[\"29044647\"]"},{"id":"31208231-98-103-3773","span":{"begin":344,"end":345},"obj":"[\"29214672\"]"},{"id":"31208231-110-115-3774","span":{"begin":649,"end":650},"obj":"[\"29247482\"]"},{"id":"31208231-229-234-3775","span":{"begin":976,"end":977},"obj":"[\"29247482\"]"}],"text":"The astrocytic proteins downregulated in these cortical patches have been implicated in epilepsy.5 Glutamate transporter 1 and glutamine synthetase are responsible for the uptake and metabolism, respectively, of glutamate released from synapses. Genetic deletion of Glt1 leads to glutamate accumulation at synapses and seizures in other models,6 while glutamine synthetase is a key enzyme in the glutamine-glutamate-gamma aminobutyric acid (GABA) cycle. Kir4.1 channels, on the other hand, are critical for spatial buffering of potassium. Downregulation of these channels can elevate extracellular potassium levels, increasing neuronal excitability.7 The effects of Kir4.1 loss may be compounded by Cx43 downregulation. Channel protein connexin43 mediates gap junction coupling among astrocytes, facilitating movement of potassium through the astrocyte network from regions with high concentrations (eg, synapses) to regions with lower concentrations (eg, capillary networks).7 Notably, Shandra and colleagues introduced the gap junction-permeable tracer biocytin into astrocytes in tissue from the mild TBI animals, but found that the molecule was excluded from cortical patches with abnormal astrocytes. Although not directly tested here, the findings suggest that potassium will accumulate in these regions because of transporter downregulation and decoupling of astrocytes with surrounding astrocytic networks."}

{"project":"0_colil","denotations":[{"id":"31208231-29044647-3772","span":{"begin":97,"end":98},"obj":"29044647"},{"id":"31208231-29214672-3773","span":{"begin":344,"end":345},"obj":"29214672"},{"id":"31208231-29247482-3774","span":{"begin":649,"end":650},"obj":"29247482"},{"id":"31208231-29247482-3775","span":{"begin":976,"end":977},"obj":"29247482"}],"text":"The astrocytic proteins downregulated in these cortical patches have been implicated in epilepsy.5 Glutamate transporter 1 and glutamine synthetase are responsible for the uptake and metabolism, respectively, of glutamate released from synapses. Genetic deletion of Glt1 leads to glutamate accumulation at synapses and seizures in other models,6 while glutamine synthetase is a key enzyme in the glutamine-glutamate-gamma aminobutyric acid (GABA) cycle. Kir4.1 channels, on the other hand, are critical for spatial buffering of potassium. Downregulation of these channels can elevate extracellular potassium levels, increasing neuronal excitability.7 The effects of Kir4.1 loss may be compounded by Cx43 downregulation. Channel protein connexin43 mediates gap junction coupling among astrocytes, facilitating movement of potassium through the astrocyte network from regions with high concentrations (eg, synapses) to regions with lower concentrations (eg, capillary networks).7 Notably, Shandra and colleagues introduced the gap junction-permeable tracer biocytin into astrocytes in tissue from the mild TBI animals, but found that the molecule was excluded from cortical patches with abnormal astrocytes. Although not directly tested here, the findings suggest that potassium will accumulate in these regions because of transporter downregulation and decoupling of astrocytes with surrounding astrocytic networks."}

{"project":"2_test","denotations":[{"id":"31208231-29044647-28640717","span":{"begin":97,"end":98},"obj":"29044647"},{"id":"31208231-29214672-28640718","span":{"begin":344,"end":345},"obj":"29214672"},{"id":"31208231-29247482-28640719","span":{"begin":649,"end":650},"obj":"29247482"},{"id":"31208231-29247482-28640720","span":{"begin":976,"end":977},"obj":"29247482"}],"text":"The astrocytic proteins downregulated in these cortical patches have been implicated in epilepsy.5 Glutamate transporter 1 and glutamine synthetase are responsible for the uptake and metabolism, respectively, of glutamate released from synapses. Genetic deletion of Glt1 leads to glutamate accumulation at synapses and seizures in other models,6 while glutamine synthetase is a key enzyme in the glutamine-glutamate-gamma aminobutyric acid (GABA) cycle. Kir4.1 channels, on the other hand, are critical for spatial buffering of potassium. Downregulation of these channels can elevate extracellular potassium levels, increasing neuronal excitability.7 The effects of Kir4.1 loss may be compounded by Cx43 downregulation. Channel protein connexin43 mediates gap junction coupling among astrocytes, facilitating movement of potassium through the astrocyte network from regions with high concentrations (eg, synapses) to regions with lower concentrations (eg, capillary networks).7 Notably, Shandra and colleagues introduced the gap junction-permeable tracer biocytin into astrocytes in tissue from the mild TBI animals, but found that the molecule was excluded from cortical patches with abnormal astrocytes. Although not directly tested here, the findings suggest that potassium will accumulate in these regions because of transporter downregulation and decoupling of astrocytes with surrounding astrocytic networks."}

{"project":"MyTest","denotations":[{"id":"31208231-29044647-28640717","span":{"begin":97,"end":99},"obj":"29044647"},{"id":"31208231-29214672-28640718","span":{"begin":344,"end":346},"obj":"29214672"},{"id":"31208231-29247482-28640719","span":{"begin":649,"end":651},"obj":"29247482"},{"id":"31208231-29247482-28640720","span":{"begin":976,"end":978},"obj":"29247482"}],"namespaces":[{"prefix":"_base","uri":"https://www.uniprot.org/uniprot/testbase"},{"prefix":"UniProtKB","uri":"https://www.uniprot.org/uniprot/"},{"prefix":"uniprot","uri":"https://www.uniprot.org/uniprotkb/"}],"text":"The astrocytic proteins downregulated in these cortical patches have been implicated in epilepsy.5 Glutamate transporter 1 and glutamine synthetase are responsible for the uptake and metabolism, respectively, of glutamate released from synapses. Genetic deletion of Glt1 leads to glutamate accumulation at synapses and seizures in other models,6 while glutamine synthetase is a key enzyme in the glutamine-glutamate-gamma aminobutyric acid (GABA) cycle. Kir4.1 channels, on the other hand, are critical for spatial buffering of potassium. Downregulation of these channels can elevate extracellular potassium levels, increasing neuronal excitability.7 The effects of Kir4.1 loss may be compounded by Cx43 downregulation. Channel protein connexin43 mediates gap junction coupling among astrocytes, facilitating movement of potassium through the astrocyte network from regions with high concentrations (eg, synapses) to regions with lower concentrations (eg, capillary networks).7 Notably, Shandra and colleagues introduced the gap junction-permeable tracer biocytin into astrocytes in tissue from the mild TBI animals, but found that the molecule was excluded from cortical patches with abnormal astrocytes. Although not directly tested here, the findings suggest that potassium will accumulate in these regions because of transporter downregulation and decoupling of astrocytes with surrounding astrocytic networks."}

{"project":"testtesttest","denotations":[{"id":"T64","span":{"begin":236,"end":244},"obj":"Body_part"},{"id":"T65","span":{"begin":306,"end":314},"obj":"Body_part"},{"id":"T66","span":{"begin":484,"end":488},"obj":"Body_part"},{"id":"T67","span":{"begin":584,"end":597},"obj":"Body_part"},{"id":"T68","span":{"begin":760,"end":768},"obj":"Body_part"},{"id":"T69","span":{"begin":784,"end":794},"obj":"Body_part"},{"id":"T70","span":{"begin":843,"end":852},"obj":"Body_part"},{"id":"T71","span":{"begin":904,"end":912},"obj":"Body_part"},{"id":"T72","span":{"begin":956,"end":974},"obj":"Body_part"},{"id":"T73","span":{"begin":1029,"end":1037},"obj":"Body_part"},{"id":"T74","span":{"begin":1069,"end":1079},"obj":"Body_part"},{"id":"T75","span":{"begin":1083,"end":1089},"obj":"Body_part"},{"id":"T76","span":{"begin":1194,"end":1204},"obj":"Body_part"},{"id":"T77","span":{"begin":1366,"end":1376},"obj":"Body_part"}],"attributes":[{"id":"A64","pred":"uberon_id","subj":"T64","obj":"http://purl.obolibrary.org/obo/GO_0045202"},{"id":"A65","pred":"uberon_id","subj":"T65","obj":"http://purl.obolibrary.org/obo/GO_0045202"},{"id":"A66","pred":"uberon_id","subj":"T66","obj":"http://purl.obolibrary.org/obo/UBERON_0002398"},{"id":"A67","pred":"uberon_id","subj":"T67","obj":"http://purl.obolibrary.org/obo/GO_0005576"},{"id":"A68","pred":"uberon_id","subj":"T68","obj":"http://purl.obolibrary.org/obo/UBERON_0007651"},{"id":"A69","pred":"uberon_id","subj":"T69","obj":"http://purl.obolibrary.org/obo/CL_0000127"},{"id":"A70","pred":"uberon_id","subj":"T70","obj":"http://purl.obolibrary.org/obo/CL_0000127"},{"id":"A71","pred":"uberon_id","subj":"T71","obj":"http://purl.obolibrary.org/obo/GO_0045202"},{"id":"A72","pred":"uberon_id","subj":"T72","obj":"http://purl.obolibrary.org/obo/UBERON_0035753"},{"id":"A73","pred":"uberon_id","subj":"T73","obj":"http://purl.obolibrary.org/obo/UBERON_0007651"},{"id":"A74","pred":"uberon_id","subj":"T74","obj":"http://purl.obolibrary.org/obo/CL_0000127"},{"id":"A75","pred":"uberon_id","subj":"T75","obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"A76","pred":"uberon_id","subj":"T76","obj":"http://purl.obolibrary.org/obo/CL_0000127"},{"id":"A77","pred":"uberon_id","subj":"T77","obj":"http://purl.obolibrary.org/obo/CL_0000127"}],"text":"The astrocytic proteins downregulated in these cortical patches have been implicated in epilepsy.5 Glutamate transporter 1 and glutamine synthetase are responsible for the uptake and metabolism, respectively, of glutamate released from synapses. Genetic deletion of Glt1 leads to glutamate accumulation at synapses and seizures in other models,6 while glutamine synthetase is a key enzyme in the glutamine-glutamate-gamma aminobutyric acid (GABA) cycle. Kir4.1 channels, on the other hand, are critical for spatial buffering of potassium. Downregulation of these channels can elevate extracellular potassium levels, increasing neuronal excitability.7 The effects of Kir4.1 loss may be compounded by Cx43 downregulation. Channel protein connexin43 mediates gap junction coupling among astrocytes, facilitating movement of potassium through the astrocyte network from regions with high concentrations (eg, synapses) to regions with lower concentrations (eg, capillary networks).7 Notably, Shandra and colleagues introduced the gap junction-permeable tracer biocytin into astrocytes in tissue from the mild TBI animals, but found that the molecule was excluded from cortical patches with abnormal astrocytes. Although not directly tested here, the findings suggest that potassium will accumulate in these regions because of transporter downregulation and decoupling of astrocytes with surrounding astrocytic networks."}