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Rescheduling Behavioral Subunits of a Fixed Action Pattern by Genetic Manipulation of Peptidergic Signaling.

Kim DH, Han MR, Lee G, Lee SS, Kim YJ, Adams ME - PLoS Genet. (2015)

Bottom Line: Activation of CCAP or CAMB neurons through temperature-sensitive TRPM8 gating is sufficient to trigger ecdysis behavior.Our findings demonstrate that kinin and CAMB neurons are direct targets of ETH and play critical roles in scheduling successive behavioral steps in the ecdysis FAP.Moreover, temporal organization of the FAP is likely a function of ETH receptor density in target neurons.

View Article: PubMed Central - PubMed

Affiliation: Department of Entomology, University of California, Riverside, Riverside, California, United States of America.

ABSTRACT
The ecdysis behavioral sequence in insects is a classic fixed action pattern (FAP) initiated by hormonal signaling. Ecdysis triggering hormones (ETHs) release the FAP through direct actions on the CNS. Here we present evidence implicating two groups of central ETH receptor (ETHR) neurons in scheduling the first two steps of the FAP: kinin (aka drosokinin, leucokinin) neurons regulate pre-ecdysis behavior and CAMB neurons (CCAP, AstCC, MIP, and Bursicon) initiate the switch to ecdysis behavior. Ablation of kinin neurons or altering levels of ETH receptor (ETHR) expression in these neurons modifies timing and intensity of pre-ecdysis behavior. Cell ablation or ETHR knockdown in CAMB neurons delays the switch to ecdysis, whereas overexpression of ETHR or expression of pertussis toxin in these neurons accelerates timing of the switch. Calcium dynamics in kinin neurons are temporally aligned with pre-ecdysis behavior, whereas activity of CAMB neurons coincides with the switch from pre-ecdysis to ecdysis behavior. Activation of CCAP or CAMB neurons through temperature-sensitive TRPM8 gating is sufficient to trigger ecdysis behavior. Our findings demonstrate that kinin and CAMB neurons are direct targets of ETH and play critical roles in scheduling successive behavioral steps in the ecdysis FAP. Moreover, temporal organization of the FAP is likely a function of ETH receptor density in target neurons.

No MeSH data available.


Related in: MedlinePlus

ETHR expression levels affect timing of calcium mobilization in CAMB neurons.(A) Changes in timing of calcium mobilization in CAMB neurons caused by manipulation of ETHR expression. Latency to onset of calcium mobilization in ETHR-RNAi knockdown preparations (ETHR-KD) is delayed in excess of 40 min. Conversely, onset timing of calcium mobilization is accelerated as a consequence of ETHR overexpression (ETHR-OE). (B) Over-expression of ETH receptor increased spontaneous responses in the neurons in absence of ETH. Under conditions of ETHR knockdown, no spontaneous response was observed.
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pgen.1005513.g004: ETHR expression levels affect timing of calcium mobilization in CAMB neurons.(A) Changes in timing of calcium mobilization in CAMB neurons caused by manipulation of ETHR expression. Latency to onset of calcium mobilization in ETHR-RNAi knockdown preparations (ETHR-KD) is delayed in excess of 40 min. Conversely, onset timing of calcium mobilization is accelerated as a consequence of ETHR overexpression (ETHR-OE). (B) Over-expression of ETH receptor increased spontaneous responses in the neurons in absence of ETH. Under conditions of ETHR knockdown, no spontaneous response was observed.

Mentions: Mean latency to onset of calcium dynamics in CAMB neurons of control preparations treated with ETH (300 nM) is 16.6 ± 10.3 min. In preparations from flies in which ETHR expression in CAMB neurons is reduced through expression of ETHR-RNAi, onset of calcium dynamics is eliminated (Fig 4A). In contrast, onset of calcium dynamics in CAMB neurons overexpressing ETHR is greatly accelerated: responses were registered within 5.0 ± 3.6 min. Thus, timing of calcium mobilization in CAMB neurons exposed to ETH depends on the level of ETHR expression in register with behavioral outcomes described in the previous section. We observed a significant rate (~19%) of spontaneous calcium mobilization in CAMB neurons upon isolation and placement of the CNS in the recording chamber, a rate that increased (~40%) in flies overexpressing ETHR in CAMB neurons (Fig 4B). Spontaneous calcium mobilization was entirely absent in ETHR knockdown flies. Preparations that exhibited spontaneous calcium dynamics prior to ETH exposure were discarded.


Rescheduling Behavioral Subunits of a Fixed Action Pattern by Genetic Manipulation of Peptidergic Signaling.

Kim DH, Han MR, Lee G, Lee SS, Kim YJ, Adams ME - PLoS Genet. (2015)

ETHR expression levels affect timing of calcium mobilization in CAMB neurons.(A) Changes in timing of calcium mobilization in CAMB neurons caused by manipulation of ETHR expression. Latency to onset of calcium mobilization in ETHR-RNAi knockdown preparations (ETHR-KD) is delayed in excess of 40 min. Conversely, onset timing of calcium mobilization is accelerated as a consequence of ETHR overexpression (ETHR-OE). (B) Over-expression of ETH receptor increased spontaneous responses in the neurons in absence of ETH. Under conditions of ETHR knockdown, no spontaneous response was observed.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4581697&req=5

pgen.1005513.g004: ETHR expression levels affect timing of calcium mobilization in CAMB neurons.(A) Changes in timing of calcium mobilization in CAMB neurons caused by manipulation of ETHR expression. Latency to onset of calcium mobilization in ETHR-RNAi knockdown preparations (ETHR-KD) is delayed in excess of 40 min. Conversely, onset timing of calcium mobilization is accelerated as a consequence of ETHR overexpression (ETHR-OE). (B) Over-expression of ETH receptor increased spontaneous responses in the neurons in absence of ETH. Under conditions of ETHR knockdown, no spontaneous response was observed.
Mentions: Mean latency to onset of calcium dynamics in CAMB neurons of control preparations treated with ETH (300 nM) is 16.6 ± 10.3 min. In preparations from flies in which ETHR expression in CAMB neurons is reduced through expression of ETHR-RNAi, onset of calcium dynamics is eliminated (Fig 4A). In contrast, onset of calcium dynamics in CAMB neurons overexpressing ETHR is greatly accelerated: responses were registered within 5.0 ± 3.6 min. Thus, timing of calcium mobilization in CAMB neurons exposed to ETH depends on the level of ETHR expression in register with behavioral outcomes described in the previous section. We observed a significant rate (~19%) of spontaneous calcium mobilization in CAMB neurons upon isolation and placement of the CNS in the recording chamber, a rate that increased (~40%) in flies overexpressing ETHR in CAMB neurons (Fig 4B). Spontaneous calcium mobilization was entirely absent in ETHR knockdown flies. Preparations that exhibited spontaneous calcium dynamics prior to ETH exposure were discarded.

Bottom Line: Activation of CCAP or CAMB neurons through temperature-sensitive TRPM8 gating is sufficient to trigger ecdysis behavior.Our findings demonstrate that kinin and CAMB neurons are direct targets of ETH and play critical roles in scheduling successive behavioral steps in the ecdysis FAP.Moreover, temporal organization of the FAP is likely a function of ETH receptor density in target neurons.

View Article: PubMed Central - PubMed

Affiliation: Department of Entomology, University of California, Riverside, Riverside, California, United States of America.

ABSTRACT
The ecdysis behavioral sequence in insects is a classic fixed action pattern (FAP) initiated by hormonal signaling. Ecdysis triggering hormones (ETHs) release the FAP through direct actions on the CNS. Here we present evidence implicating two groups of central ETH receptor (ETHR) neurons in scheduling the first two steps of the FAP: kinin (aka drosokinin, leucokinin) neurons regulate pre-ecdysis behavior and CAMB neurons (CCAP, AstCC, MIP, and Bursicon) initiate the switch to ecdysis behavior. Ablation of kinin neurons or altering levels of ETH receptor (ETHR) expression in these neurons modifies timing and intensity of pre-ecdysis behavior. Cell ablation or ETHR knockdown in CAMB neurons delays the switch to ecdysis, whereas overexpression of ETHR or expression of pertussis toxin in these neurons accelerates timing of the switch. Calcium dynamics in kinin neurons are temporally aligned with pre-ecdysis behavior, whereas activity of CAMB neurons coincides with the switch from pre-ecdysis to ecdysis behavior. Activation of CCAP or CAMB neurons through temperature-sensitive TRPM8 gating is sufficient to trigger ecdysis behavior. Our findings demonstrate that kinin and CAMB neurons are direct targets of ETH and play critical roles in scheduling successive behavioral steps in the ecdysis FAP. Moreover, temporal organization of the FAP is likely a function of ETH receptor density in target neurons.

No MeSH data available.


Related in: MedlinePlus