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. 2015 Mar 10;9:8. doi: 10.3389/fncir.2015.00008

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Copyright © 2015 Chambers, Androschuk, Rosenfelt, Langer, Harding and Bolduc.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Pan-neuronal disruption of Insulin signaling results in memory defects. (A) Learning is significantly defective in Drosophila expressing UAS-RNAi against the insulin receptor substrate, chico pan-neuronally. We expressed 2 different RNAi constructs: [Elav>ChicoRNAi⁷⁷⁷⁶] (P = 0.005, N = 6 PI per genotype) and [Elav>ChicoRNAi⁷⁷⁷⁷] (P = 0.0104, N = 6 PI per genotype). In addition, pan-neuronal overexpression of chico [Elav>UAS-chico] led to a significant (P = 0.0015, N = 8 PI per genotype) defect in learning. The genetic controls ElavGAL4 [Elav/+], chicoRNAi [chicoRNAi⁷⁷⁷⁶], [chicoRNAi⁷⁷⁷⁷] and InRRNAi [InRRNAi⁹⁹²] show no defects compared to wild-type flies [WT]. (B) 1-day memory after spaced training is impaired by loss or gain of function of chico in neurons. RNAi against chico resulted in significant defect in 1 day memory for both constructs [Elav>ChicoRNAi⁷⁷⁷⁶] (P < 0.00001, N = 8 PI per genotype); [Elav>ChicoRNAi⁷⁷⁷⁷] (P < 0.00001, N = 8 PI per genotype). Overexpression of chico [Elav>UAS-chico] also resulted in significant defect in 1 day memory (P = 0.0004, N = 8 PI per genotype) (C) No significant defects in 1 day memory after massed training were observed between Chico RNAi or UAS-chico expressing flies compared to genetic controls (N = 8 PI per genotype). (D) Similarly, pan-neuronal disruption of Insulin receptor leads to learning defects either via expression of UAS-InR RNAi [Elav>InR RNAi⁹⁹²] (P = 0.0082, N = 4 PI per genotype) or with the expression of a dominant negative InR [Elav>InR^DN] (P < 0.00001, N = 4 PI per genotype). There was no significant defect in any of the genetic appropriate controls. (E) Significant defects in 1 day memory after spaced training were also observed in transgenic flies expressing [Elav>InR RNAi⁹⁹²] (P < 0.00001, N = 8 PI per genotype) or [Elav>InR^DN] (P = 0.0052, N = 8 PI per genotype). (F) No significant defects were seen in flies expressing InR RNAi or DN or in the appropriate genetic controls. (G) Representative level of p70S6K in the brain of WT and flies expressing InR^DN pan-neuronally [Elav>InR^DN]. (H) Significant decreased level of p70S6K is observed in Elav>InR^DN flies (N = 5 brains per genotype, P = 0.0022) All graphs depict mean ± s.e.m. ^*p < 0.05; ^**p < 0.001; ^***p < 0.0001.