| http://purl.uniprot.org/citations/24412234 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/24412234 | http://www.w3.org/2000/01/rdf-schema#comment | "GABA is a predominant inhibitory neurotransmitter in the CNS. Released GABA is removed from the synaptic cleft by two GABA transporters (GATs), GAT-1 and GAT-3, and their dysfunction affects brain functions. The present study aimed to reveal the ontogeny of the GABA-removal system by examining the immunohistochemical localization of GAT-1 and GAT-3 in the embryonic and postnatal mouse cervical spinal cord. In the dorsal horn, GAT-1 was localized within the presynapses of inhibitory axons after embryonic day 15 (E15), a little prior to GABAergic synapse formation. The GAT-1-positive dots increased in density until postnatal day 21 (P21). By contrast, in the ventral horn, GAT-1-positive dots were sparse during development, although many transient GABAergic synapses were formed before birth. GAT-3 was first localized within the radial processes of radial glia in the ventral part on E12 and the dorsal part on E15. The initial localization of the GAT-3 was almost concomitant with the dispersal of GABAergic neurons. GAT-3 continued to be localized within the processes of astrocytes, and increased in expression until P21. These results suggested the following: (1) before synapse formation, GABA may be transported into the processes of radial glia or immature astrocytes by GAT-3. (2) At the transient GABAergic synapses in the ventral horn, GABA may not be reuptaken into the presynapses. (3) In the dorsal horn, GABA may start to be reuptaken by GAT-1 a little prior to synapse formation. (4) After synapse formation, GAT-3 may continue to remove GABA from immature and mature synaptic clefts into the processes of astrocytes. (5) Development of the GABA-removal system may be completed by P21."xsd:string |
| http://purl.uniprot.org/citations/24412234 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.neuroscience.2013.12.066"xsd:string |
| http://purl.uniprot.org/citations/24412234 | http://purl.uniprot.org/core/author | "Kim J."xsd:string |
| http://purl.uniprot.org/citations/24412234 | http://purl.uniprot.org/core/author | "Takayama C."xsd:string |
| http://purl.uniprot.org/citations/24412234 | http://purl.uniprot.org/core/author | "Kosaka Y."xsd:string |
| http://purl.uniprot.org/citations/24412234 | http://purl.uniprot.org/core/author | "Shimizu-Okabe C."xsd:string |
| http://purl.uniprot.org/citations/24412234 | http://purl.uniprot.org/core/author | "Niizaki A."xsd:string |
| http://purl.uniprot.org/citations/24412234 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
| http://purl.uniprot.org/citations/24412234 | http://purl.uniprot.org/core/name | "Neuroscience"xsd:string |
| http://purl.uniprot.org/citations/24412234 | http://purl.uniprot.org/core/pages | "129-142"xsd:string |
| http://purl.uniprot.org/citations/24412234 | http://purl.uniprot.org/core/title | "Characteristic development of the GABA-removal system in the mouse spinal cord."xsd:string |
| http://purl.uniprot.org/citations/24412234 | http://purl.uniprot.org/core/volume | "262"xsd:string |
| http://purl.uniprot.org/citations/24412234 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/24412234 |
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