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. Author manuscript; available in PMC: 2019 Aug 15.
Published in final edited form as: ACS Chem Neurosci. 2018 Mar 27;9(8):2041–2053. doi: 10.1021/acschemneuro.7b00513

Figure 5.

Figure 5

apSPTR-GF-DP2 modulates feeding motor programs elicited by CBI-2 through its actions on the interneuron B20, but not B64. (a), apSPTR-GF-DP2 shortens protraction duration in a concentration-dependent manner. (a1–4), a representative example; a single cycle of a motor program was elicited by stimulating CBI-2 at 9 Hz until the end of the protraction phase, detected by the onset of the sharp synaptic inhibition of CPG neuron B31 and the abrupt ending of I2 nerve activity. Protraction phase (open bar) is defined by the activity in the I2 nerve. Retraction phase (filled bar) is defined by a period of hyperpolarization of B31 after the protraction phase is terminated and also by a period of high-frequency activity of the radula closing motoneuron B8. Upon wash, protraction duration returns to its control value. (a5), group data on protraction duration. In contrast, apSPTR-GF-DP2 has no significant effect on the duration of retraction (a6) or B8 activity during either protraction (a7) or retraction (a8). (b), apSPTR-GF-DP2 has no effect on B64 excitability. (b1), a representative example, (b2), group data. (c), apSPTR-GF-DP2 increases B20 excitability and shortens B20 spike latency. (c1), a representative example, (c2, c3), group data. Recordings in (a) were made in ASW, whereas recordings in (b) and (c) were made in high divalent saline. *, p < 0.05; **, p < 0.01; ***, p < 0.001 (Bonferroni post hoc tests). Error bars, S.E.