1998年11月
GABAergic neuron-to-astrocyte signaling regulates dendritic branching in coculture
JOURNAL OF NEUROBIOLOGY
- ,
- 巻
- 37
- 号
- 2
- 開始ページ
- 251
- 終了ページ
- 264
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1002/(SICI)1097-4695(19981105)37:2<251::AID-NEU5>3.0.CO;2-S
- 出版者・発行元
- JOHN WILEY & SONS INC
Effects of neurotransmitters on dendritic morphology were analyzed in cocultures of neurons and astrocytes from the neonatal rat olfactory bulb by means of immunocytochemical staining and morphometry. About 70% of the neurons were gamma-aminobutyric acid (GABA)-immunoreactive on day 7 of the coculture. Morphometric analysis of neurons having no contact with other neurons revealed that incubation of the coculture with either a sodium channel blocker, tetrodotoxin, or GABA, receptor antagonists such as bicuculline or picrotoxin resulted in a decreased number of dendritic branch points as compared to neurons in control cultures, while the same treatment did not affect radial dendritic outgrowth or the number of primary dendrites. Application of a GABA, receptor antagonist, phaclofen, or an AMPA-type glutamate receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione, had no detectable effect on dendritic morphology. Incubation of the coculture with a GABA, receptor agonist, muscimol, enhanced branching and reversed the inhibitory effect of tetrodotoxin. Branching was also enhanced by increasing extracellular K+. The inhibitory effect of tetrodotoxin or bicuculline and the stimulatory effect of muscimol or elevated K+ were abolished when neurons were grown on a monolayer of dead astrocytes, indicating that the morphoregulatory action of GABA requires living astrocytes to operate. Astrocytes pretreated with muscimol before the addition of neurons supported branching better than those without pretreatment. These results suggest that various aspects of dendritic growth are regulated by distinct mechanisms, and that neuron-to-astrocyte signaling mediated by GABA promotes dendritic branching. (C) 1998 John Wiley & Sons, Inc.
- リンク情報
-
- DOI
- https://doi.org/10.1002/(SICI)1097-4695(19981105)37:2<251::AID-NEU5>3.0.CO;2-S
- CiNii Articles
- http://ci.nii.ac.jp/naid/10014520885
- PubMed
- https://www.ncbi.nlm.nih.gov/pubmed/9805271
- Web of Science
- https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000076492200005&DestApp=WOS_CPL
- ID情報
-
- DOI : 10.1002/(SICI)1097-4695(19981105)37:2<251::AID-NEU5>3.0.CO;2-S
- ISSN : 0022-3034
- CiNii Articles ID : 10014520885
- PubMed ID : 9805271
- Web of Science ID : WOS:000076492200005