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Title | : | Characteristic development of the GABA-removal system in the mouse spinal cord |
Authors | : | Kim, J. Kosaka, Y. Shimizu-Okabe, C. Niizaki, A. Takayama, C. |
Issue Date | : | 14-Mar-2014 |
Abstract | : | 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. |
URL | : | https://doi.org/10.1016/j.neuroscience.2013.12.066 |
Type Local | : | 雑誌掲載論文 |
ISSN | : | 0306-4522 |
Publisher | : | Elsevier |
URI | : | http://hdl.handle.net/20.500.12000/46548 |
Citation | : | Neuroscience Vol.262 p.129 -142 |
Appears in Collections | : | Peer-reviewed Journal Articles (Faculty of Medicine)
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