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Abstract

We hypothesized that presynaptic glutamate regulates postsynaptic ionotropic glutamate receptor number during synaptogenesis. To test this idea, we genetically manipulated presynaptic glutamate levels at the glutamatergic Drosophila neuromuscular junction (NMJ), then microscopically and electrophysiologically measured postsynaptic glutamate receptor field size and function. Our data show that presynaptic glutamate is a strong negative regulator of postsynaptic receptor field size and function during development. Glutamate-triggered receptor downregulation was not affected by block of synaptic vesicle fusion, demonstrating that receptors are regulated by nonvesicular glutamate release. Our results reveal an elegant mechanism for receptor field regulation during synaptogenesis and reveal a nonpathological role for nonvesicular glutamate release at the synapse.

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Targeted expression of tetanus toxin light chain in Drosophila specifically eliminates synaptic transmission and causes behavioral defects.

S. Sweeney, K Broadie, J. Keane … (1995)

Tetanus toxin cleaves the synaptic vesicle protein synaptobrevin, and the ensuing loss of neurotransmitter exocytosis has implicated synaptobrevin in this process. To further the study of synaptic function in a genetically tractable organism and to generate a tool to disable neuronal communication for behavioural studies, we have expressed a gene encoding tetanus toxin light chain in Drosophila. Toxin expression in embryonic neurons removes detectable synaptobrevin and eliminates evoked, but not spontaneous, synaptic vesicle release. No other developmental or morphological defects are detected. Correspondingly, only synaptobrevin (n-syb), but not the ubiquitously expressed syb protein, is cleaved by tetanus toxin in vitro. Targeted expression of toxin can produce specific behavioral defects; in one case, the olfactory escape response is reduced.

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

S Petersen, R Fetter, J Noordermeer … (1997)

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.

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Glutamate receptor expression regulates quantal size and quantal content at the Drosophila neuromuscular junction.

Aaron DiAntonio, Sophie A Petersen, Manfred Heckmann … (1999)

At the Drosophila glutamatergic neuromuscular junction, the postsynaptic cell can regulate synaptic strength by both changing its sensitivity to neurotransmitter and generating a retrograde signal that regulates presynaptic transmitter release. To investigate the molecular mechanisms underlying these forms of plasticity, we have undertaken a genetic analysis of two postsynaptic glutamate receptors that are expressed at this synapse. Deletion of both genes results in embryonic lethality that can be rescued by transgenic expression of either receptor. Although these receptors are redundant for viability, they have important differences. By transgenically rescuing the double mutant, we have investigated the relationship of receptor gene dosage and composition to synaptic function. We find that the receptor subunit composition regulates quantal size, Argiotoxin sensitivity, and receptor desensitization kinetics. Finally, we show that the activity of the receptor can regulate the retrograde signal functioning at this synapse. Thus, the diversity of receptors expressed at this synapse provides the cell with mechanisms for generating synaptic plasticity.

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PubMed ID:: 11753421

DOI:: 10.1038/nn789

ScienceOpen disciplines: Chemistry

Keywords: Aging,metabolism,Animals,Down-Regulation,physiology,Drosophila,embryology,Electrophysiology,Embryo, Nonmammalian,Glutamic Acid,Neuromuscular Junction,Presynaptic Terminals,Receptors, Glutamate,Synapses,Tissue Distribution

Developmental regulation of glutamate receptor field size by nonvesicular glutamate release.

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Most cited references 39

Targeted expression of tetanus toxin light chain in Drosophila specifically eliminates synaptic transmission and causes behavioral defects.

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

Glutamate receptor expression regulates quantal size and quantal content at the Drosophila neuromuscular junction.

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