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. 2019 Jul 10;5(7):eaaw4099. doi: 10.1126/sciadv.aaw4099

Fig. 5. Preventing GABAergic cell death blocks changes in the nociception circuit and suppresses neuropathic allodynia.

Fig. 5

(A) Blocking GABAergic cell death after leg injury by Gad1-Gal4–driven expression of UAS-p35 prevents GABA loss. (B) Quantification of (A), n ≥ 9. (C and D) GABAergic-specific expression of p35 (Gad1-Gal4>UAS-p35) rescues contralateral sensitization of the escape response circuit measured by (C) escape circuit velocity, n ≥ 9; (D) escape response duration, n ≥ 9; and (E) prevents neuropathic allodynia behavior (n = 9 replicates, 10 animals per replicate). (F) Nociceptive sensory neuron–specific (ppk-Gal4) knockdown of GABA receptor D-GABA-B-R2 is sufficient to cause thermal allodynia (38°C) in uninjured flies (n ≥ 9 replicates, 10 animals per replicate). (G) Knockdown of nAChRα1 in GABAergic neurons (Gad1-Gal4>nAChRα1-IR) prevents GABA loss after injury. (H) Quantification of active caspase in GABAergic neurons (active caspase/Gad1+ cells) in control intact and injured flies expressing Lamin-GFP and nAChRα1-IR (Gad1-Gal4>UAS-Lamin-GFP; UAS-nAChRα1-IR). (I) Knockdown of nAChRα1 in GABAergic neurons prevents neuropathic allodynia behavior (n ≥ 9 replicates, 10 animals per replicate). Data are represented as means ± SEM. **P < 0.01; ***P < 0.001, two-way ANOVA followed by Tukey’s post hoc test.