Reference Report

Reference
Citation	Sadaf, S., Birman, S., Hasan, G. (2012). Synaptic Activity in Serotonergic Neurons Is Required for Air-Puff Stimulated Flight in Drosophila melanogaster. PLoS ONE 7(9): e46405. (Export to RIS)
FlyBase ID	FBrf0219558
Publication Type	Research paper
PubMed ID	23029511
PubMed Abstract	Flight is an integral component of many complex behavioral patterns in insects. The giant fiber circuit has been well studied in several insects including Drosophila. However, components of the insect flight circuit that respond to an air-puff stimulus and comprise the flight central pattern generator are poorly defined. Aminergic neurons have been implicated in locust, moth and Drosophila flight. Here we have investigated the requirement of neuronal activity in serotonergic neurons, during development and in adults, on air-puff induced flight in Drosophila.To target serotonergic neurons specifically, a Drosophila strain that contains regulatory regions from the TRH (Tryptophan Hydroxylase) gene linked to the yeast transcription factor GAL4 was used. By blocking synaptic transmission from serotonergic neurons with a tetanus toxin transgene or by hyperpolarisation with Kir2.1, close to 50% adults became flightless. Temporal expression of a temperature sensitive Dynamin mutant transgene (Shi(ts)) suggests that synaptic function in serotonergic neurons is required both during development and in adults. Depletion of IP(3)R in serotonergic neurons via RNAi did not affect flight. Interestingly, at all stages a partial requirement for synaptic activity in serotonergic neurons was observed. The status of serotonergic neurons was investigated in the central nervous system of larvae and adults expressing tetanus toxin. A small but significant reduction was observed in serotonergic cell number in adult second thoracic segments from flightless tetanus toxin expressing animals.These studies show that loss of synaptic activity in serotonergic neurons causes a flight deficit. The temporal focus of the flight deficit is during pupal development and in adults. The cause of the flight deficit is likely to be loss of neurons and reduced synaptic function. Based on the partial phenotypes, serotonergic neurons appear to be modulatory, rather than an intrinsic part of the flight circuit.
DOI	10.1371/journal.pone.0046405
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Language of Publication	English
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Publication Type	Journal
Abbreviation	PLoS ONE
Title	PLoS ONE
Publication Year	2006-
ISBN/ISSN	1932-6203
Data from Reference
Alleles (9)
	Ctet\TeTxLC^{IMPTNT-V.Scer\UAS} Ctet\TeTxLC^TNT.Scer\UAS Hsap\KCNJ2^{Scer\UAS.T:Avic\GFP-EGFP} Itp-r83A^NIG.1063R Mmus\Cd8a^{Scer\UAS.T:Avic\GFP} olf186-F^GD3554 Scer\GAL4^Trh.PB shi^1.Scer\UAS Stim^GD16187
Constructs (9)
	P{GD3554} P{GD16187} P{NIG.1063R} P{Trh-GAL4.B} P{UAS-Hsap\KCNJ2.EGFP} P{UAS-mCD8::GFP.L} P{UAS-shi^ts1.K} P{UAS-TeTxLC.(-)V} P{UAS-TeTxLC.tnt}
Genes (9)
	Ctet\TeTxLC Hsap\KCNJ2 Itp-r83A Mmus\Cd8a olf186-F Scer\GAL4 shi Stim Trh
Natural transposons (1)
	P-element