Skip to main content
. 2018 Jan 23;7:e29915. doi: 10.7554/eLife.29915

Figure 6. Activation of premotor INs AVA potentiates A-MN-dependent rPSC bursts.

Figure 6.

(A) The evoked and spontaneous rPSC bursts share frequency spectrum characteristics. Black traces: frequency spectrum analyses (upper panel) for three rPSC traces upon the optogenetic activation of AVA premotor INs (lower panel); Yellow traces: frequency spectrum analyses (upper panel) for three spontaneous rPSC bursts exhibited by animals upon the co-ablation of premotor INs and B-MNs (lower panel). (B) Representative traces of AVA-evoked rPSC bursts in respective genotypic backgrounds, both in the presence (Control) or absence (Ablated) of specific neuronal groups. +: hpIs270 (AVA-specific ChR2 activation upon exposure to LED, in wildtype background); - AVA: hpIs270; hpIs321 (upon expsure to LED, after a subset of premotor INs including AVA were ablated); - AVB: hp270; hpIs331 (upon exposure to LED, after several INs including AVB were ablated); - A: hpIs270; hpIs371 (upon exposure to LED, after A-MNs were ablated); - B: hpIs270; hpIs604 (upon exposure to LED, after B-MNs were ablated). (C) Quantification of rPSC burst frequencies evoked by AVA activation in respective genetic backgrounds. (D) Quantification of total discharge of rPSC bursts evoked by AVA in respective genetic backgrounds. Both are diminished upon the ablation of AVA, but are not affected by ablation of the AVB premotor INs. They are both significantly decreased in A-, but not B-MN-ablated animals (n ≥ 5 in each data set). ns, not significant (p>0.05), ***p<0.001 against the respective non-ablated Control group by the students’ t - test. Error bars, SEM.