Genetic analysis of glutamate receptors in Drosophila reveals a retrograde signal regulating presynaptic transmitter release

Postsynaptic sensitivity to glutamate was genetically manipulated at the Drosophila neuromuscular junction (NMJ) to test whether postsynaptic activity can regulate presynaptic function during development. We cloned the gene encoding a second muscle-specific glutamate receptor, DGluRIIB, which is clo...

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Bibliographic Details
Published in:Neuron (Cambridge, Mass.) Mass.), 1997-12, Vol.19 (6), p.1237-1248
Main Authors: Petersen, S A, Fetter, R D, Noordermeer, J N, Goodman, C S, DiAntonio, A
Format: Article
Language:English
Subjects:
Amino Acid Sequence
Animals
Animals, Genetically Modified
Cloning, Molecular
Crosses, Genetic
Drosophila
Genes, Insect
Genes, Lethal
Larva
Molecular Sequence Data
Muscles - physiology
Mutagenesis, Insertional
Neuromuscular Junction - physiology
Neurotransmitter Agents - physiology
Receptors, Glutamate - chemistry
Receptors, Glutamate - genetics
Receptors, Glutamate - physiology
Sequence Alignment
Sequence Homology, Amino Acid
Signal Transduction
Synaptic Transmission
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Summary:Postsynaptic sensitivity to glutamate was genetically manipulated at the Drosophila neuromuscular junction (NMJ) to test whether postsynaptic activity can regulate presynaptic function during development. We cloned the gene encoding a second muscle-specific glutamate receptor, DGluRIIB, which is closely related to the previously identified DGluRIIA and located adjacent to it in the genome. Mutations that eliminate DGluRIIA (but not DGluRIIB) or transgenic constructs that increase DGluRIIA expression were generated. When DGluRIIA is missing, the response of the muscle to a single vesicle of transmitter is substantially decreased. However, the response of the muscle to nerve stimulation is normal because quantal content is significantly increased. Thus, a decrease in postsynaptic receptors leads to an increase in presynaptic transmitter release, indicating that postsynaptic activity controls a retrograde signal that regulates presynaptic function.
ISSN:0896-6273
DOI:10.1016/s0896-6273(00)80415-8