ArticleInvertebrate neuroscience : IN2007
Homeostasis of glutamate neurotransmission is altered in Drosophila Inositol 1,4,5-trisphosphate receptor mutants.
Article in Invertebrate neuroscience : IN, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 8 citations in OpenAlex.
- Article
- Worker honeybee brain proteome.Journal of proteome research · 2012Article
- Reduced odor responses from antennal neurons of G(q)alpha, phospholipase Cbeta, and rdgA mutants in Drosophila support a role for a phospholipid intermediate in insect olfactory transduction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
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Authors and funding
3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Mutants in the Drosophila InsP3R gene (itpr) are flight defective. Expression of the wild-type InsP3R in aminergic interneurons rescues flight. However, molecular and cellular changes in the central nervous system of InsP3R mutants that lead to flightless behavior remain unknown. To understand the molecular basis of flight phenotypes in Drosophila InsP3R mutants a microarray screen was done with RNA isolated from adult heads and thoraces. We found down-regulation of several genes that affect the excitability of neurons and muscles. Among these the role of glutamine synthetase 2 was investigated further. This enzyme reduces glutamate levels at the synapse. Our results show that Gs2 (glutamine synthetase 2) transcripts and glutamate levels correspond precisely but inversely, with InsP3R phenotypes, which can be rescued by a mutant allele for Gs2, namely, Gs2(m13). From measuring axonal branches and synapse number at a glutamatergic synapse--the adult flight neuromuscular junction--of InsP3R mutants, we conclude that glutamate homeostasis is altered through a cell non-autonomous mechanism, and is likely to be an important basis for the observed flight defects.
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