Abstract
BackgroundFlight 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.Methodology/Principal FindingsTo 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 (Shits) suggests that synaptic function in serotonergic neurons is required both during development and in adults. Depletion of IP3R 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.ConclusionsThese 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.
Highlights
Animal behavior is a complex stimulus-driven process that requires coordinated interaction between specific neural circuits
These studies show that loss of synaptic activity in serotonergic neurons causes a flight deficit
Reduced flight ability due to loss of synaptic activity in serotonergic neurons Previously, the role of evoked synaptic activity in aminergic neurons has been studied in the context of flight, by expressing tetanus toxin in the aminergic domain [8] with DdcGAL4, which expresses in both dopaminergic and serotonergic neurons [21]
Summary
Animal behavior is a complex stimulus-driven process that requires coordinated interaction between specific neural circuits. Escape response pathways are activated under conditions perceived as a threat by the animal, such as a bright flash of light The organization of these circuits is usually less complex because speed of response is critical for survival. A requirement for the biogenic amines, octopamine and tyramine in modulation of insect flight has been shown from studies in locusts, Manduca and other moths [9,10,11]. The neural components of air-puff stimulated flight, measured in tethered flies, remain largely unknown, previous studies have shown that serotonergic and dopaminergic neurons, which are another subset of aminergic neurons, could play a role in the function/ modulation of this circuit [8]. We have investigated the requirement of neuronal activity in serotonergic neurons, during development and in adults, on air-puff induced flight in Drosophila
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