PUBLICATION
Stereotyped initiation of retinal waves by bipolar cells via presynaptic NMDA autoreceptors
- Authors
- Zhang, R.W., Li, X.Q., Kawakami, K., Du, J.L.
- ID
- ZDB-PUB-160903-8
- Date
- 2016
- Source
- Nature communications 7: 12650 (Journal)
- Registered Authors
- Du, Jiu Lin, Kawakami, Koichi
- Keywords
- Neuronal development, Retina
- MeSH Terms
-
- Animals
- Electrical Synapses/physiology
- Glutamic Acid/metabolism
- Larva/growth & development
- Presynaptic Terminals/metabolism
- Receptors, N-Methyl-D-Aspartate/metabolism*
- Retinal Bipolar Cells/metabolism*
- Retinal Ganglion Cells/metabolism*
- Synaptic Transmission/physiology*
- Visual Pathways/physiology*
- Zebrafish/embryology*
- Zebrafish/genetics
- PubMed
- 27586999 Full text @ Nat. Commun.
Citation
Zhang, R.W., Li, X.Q., Kawakami, K., Du, J.L. (2016) Stereotyped initiation of retinal waves by bipolar cells via presynaptic NMDA autoreceptors. Nature communications. 7:12650.
Abstract
Glutamatergic retinal waves, the spontaneous patterned neural activities propagating among developing retinal ganglion cells (RGCs), instruct the activity-dependent refinement of visuotopic maps. However, its initiation and underlying mechanism remain largely elusive. Here using larval zebrafish and multiple in vivo approaches, we discover that bipolar cells (BCs) are responsible for the generation of glutamatergic retinal waves. The wave originates from BC axon terminals (ATs) and propagates laterally to nearby BCs and vertically to downstream RGCs and the optic tectum. Its initiation is triggered by the activation of and consequent glutamate release from BC ATs, and is mediated by the N-methyl-D-aspartate subtype of glutamate receptors (NMDARs) expressed at these ATs. Intercellular asymmetry of NMDAR expression at BC ATs enables the preferential initiation of waves at the temporal retina, where BC ATs express more NMDARs. Thus, our findings indicate that glutamatergic retinal waves are initiated by BCs through a presynaptic NMDA autoreceptor-dependent process.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping