본 연구는 피레스로이드계 살충제인 퍼메트린이 Heliothis virescens의 중추신경세포의 나트륨채널에 어떻게 작용하는 가를 전기생리학적으 로 관찰하였다. 퍼메트린은 나트륨채널의 꼬리전류(INa-tail)를 지속적으로 증가시켰으며 이러한 비정상적인 나트륨 전류증가가 나방류의 신경계에 과도한 흥분을 일으겨 살충작용을 하는 것으로 생각된다. 이러한 살충작용은 전갈독과 함께 사용했을때 약 8배의 증가가 있었음을 확인하였다. 전 갈독이 살충제의 독성을 강화하는 분자생리학적 기전연구가 계속되면 해충방제에 많은 기여를 할 것으로 생각된다.

During insect development from embryo to adult, airway clearance in tracheal system occurs episodically each time the molt is completed by performance of the ecdysis sequence. We found that the neuropeptide Kinin is required for normal respiratory fluid clearance or “tracheal air-filling” in fruit fly Drosophila larvae. Disruption of Kinin signaling leads to defective air-filling during all larval stages. Targeted Kinin receptor silencing in tracheal epithelial cells also shows tracheal air-filling defect. On the other hand, promotion of Kinin signaling in vivo through peptide injection or Kinin neuron activation induces premature tracheal collapse and air-filling. Moreover, direct exposure of epithelial cells in vitro to Kinin leads to calcium mobilization in tracheal epithelial cells. Our findings strongly implicate the neuropeptide Kinin as an important regulator of airway clearance via intracellular calcium mobilization in tracheal epithelial cells of fruit fly Drosophila.

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. Activation of CCAP or CAMB neurons through temperature-sensitive TRPM8 gating is both necessary and 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. Furthermore, temporal organization of the FAP is likely a function of ETH receptor density in target neurons.