Skip to main content
. 2012 Sep 27;7(9):e46405. doi: 10.1371/journal.pone.0046405

Figure 1. Loss of synaptic activity in serotonergic neurons causes flight defects.

Figure 1

A) Flight deficit, assayed by the cylinder drop test, is significantly higher in animals expressing either tetanus toxin (TNTH) or the hyperpolarizing K+ ion channel (Kir2.1) as compared with controls (*p<0.005; Student's t test). Approximately 100 or more flies were tested for each genotype. Results are expressed as mean ± SEM. B) Electrophysiological recordings from the DLMs of tethered flies after delivery of an air puff stimulus (arrows). Control flies show rhythmic firing throughout flight. Loss of electrical activity is seen in 13/30 animals expressing TNTH. The remaining animals show wild-type like flight pattern. The duration of flight is reduced to <5 secs in 12/30 flies expressing Kir2.1. Intermittent flight patterns are seen in 9/30 flies. The remaining flies show wild-type like flight pattern. C) Quantification of the spike frequency during flight at a bin interval of 5 secs. Control flies (TRHGAL4/+, control 1 and TRHGAL4/TNTvif, control 2) show a spike frequency of 9 Hz in all the bins. The trace is expressed as an average of 15 flies. TNTH expressing flies show either complete loss of flight or normal flight frequency. D) Control flies (Kir2.1/+) show an average spike frequency of 9 Hz (15 flies). Flies expressing Kir2.1 show variable spike frequencies. Expression of either TNTH or Kir2.1 in serotonergic neurons does not affect the frequency of spontaneous firing as recorded from the DLMs. E) Quantification of spontaneous firing. F) Representative traces of electrophysiological recordings from the DLMs.