PUBLICATION
A genetic basis for molecular asymmetry at vertebrate electrical synapses
- Authors
- Miller, A.C., Whitebirch, A.C., Shah, A.N., Marsden, K.C., Granato, M., O'Brien, J., Moens, C.B.
- ID
- ZDB-PUB-170523-6
- Date
- 2017
- Source
- eLIFE 6: e25364 (Journal)
- Registered Authors
- Granato, Michael, Marsden, Kurt, Miller, Adam, Moens, Cecilia, O'Brien, John
- Keywords
- neuroscience, zebrafish
- MeSH Terms
-
- Animals
- Connexins/genetics*
- Connexins/metabolism*
- Electrical Synapses*
- Gap Junctions/physiology*
- Neurons/physiology*
- Zebrafish
- PubMed
- 28530549 Full text @ Elife
Citation
Miller, A.C., Whitebirch, A.C., Shah, A.N., Marsden, K.C., Granato, M., O'Brien, J., Moens, C.B. (2017) A genetic basis for molecular asymmetry at vertebrate electrical synapses. eLIFE. 6:e25364.
Abstract
Neural network function is based upon the patterns and types of connections made between neurons. Neuronal synapses are adhesions specialized for communication and they come in two types, chemical and electrical. Communication at chemical synapses occurs via neurotransmitter release whereas electrical synapses utilize gap junctions for direct ionic and metabolic coupling. Electrical synapses are often viewed as symmetrical structures, with the same components making both sides of the gap junction. By contrast, we show that a broad set of electrical synapses in zebrafish, Danio rerio, require two gap-junction-forming Connexins for formation and function. We find that one Connexin functions presynaptically while the other functions postsynaptically in forming the channels. We also show that these synapses are required for the speed and coordination of escape responses. Our data identify a genetic basis for molecular asymmetry at vertebrate electrical synapses and show they are required for appropriate behavioral performance.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping