PUBLICATION
Vesicular Glutamate Transport at a Central Synapse Limits the Acuity of Visual Perception in Zebrafish
- Authors
- Smear, M.C., Tao, H.W., Staub, W., Orger, M.B., Gosse, N.J., Liu, Y., Takahashi, K., Poo, M.M., and Baier, H.
- ID
- ZDB-PUB-070122-7
- Date
- 2007
- Source
- Neuron 53(1): 65-77 (Journal)
- Registered Authors
- Baier, Herwig, Gosse, Nathan, Liu, Yan, Orger, Mike, Smear, Matt, Staub, Wendy
- Keywords
- none
- MeSH Terms
-
- Synaptic Transmission/genetics*
- Superior Colliculi/abnormalities
- Superior Colliculi/metabolism
- Superior Colliculi/physiopathology
- Vesicular Glutamate Transport Protein 2/genetics
- PubMed
- 17196531 Full text @ Neuron
Abstract
The neural circuitry that constrains visual acuity in the CNS has not been experimentally identified. We show here that zebrafish blumenkohl (blu) mutants are impaired in resolving rapid movements and fine spatial detail. The blu gene encodes a vesicular glutamate transporter expressed by retinal ganglion cells. Mutant retinotectal synapses release less glutamate, per vesicle and per terminal, and fatigue more quickly than wild-type in response to high-frequency stimulation. In addition, mutant axons arborize more extensively, thus increasing the number of synaptic terminals and effectively normalizing the combined input to postsynaptic cells in the tectum. This presumably homeostatic response results in larger receptive fields of tectal cells and a degradation of the retinotopic map. As predicted, mutants have a selective deficit in the capture of small prey objects, a behavior dependent on the tectum. Our studies successfully link the disruption of a synaptic protein to complex changes in neural circuitry and behavior.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping