Abstract
Juvenile hormone (JH), which is synthesized by and released from the corpora allatum (CA) regulates the growth, metamorphosis and reproduction of insects. The JH biosynthesis is regulated by a complex of neural and humoral signals. Recently, glutamatergic terminals were found in the CA of the cockroach, Diploptera punctata. Rates of JH synthesis were elevated by the application of glutamate (Glu) and Glu receptor (GluR) agonsits such as N-methyl-D-aspartate (NMDA), kainate (KA), and quisqulate (Quis). In contrast, ibotenate, a GluR agonsit, resulted in the decline of JH synthesis. Additionally, it was also found that the cytosolic calcium concentration in CA cells was elevated after the exposure of Glu, NMDA, or KA. However, the electrophysiological mechanisms regulating CA cells by Glu and these GluR agonists are unclear. In this study, intracellular recording were used to investigate changes in membrane potential of CA cells in response to Glu and GluR agonsits. I found that the application of Glu caused changes in membrane potential of 87% tested CA cells (47% hyperpolarizations, 20% depolarizations and 20% hyperpolarizations followed by depolarizations). KA, similar to Glu, caused changes in membrane potential of 70 % tested CA cells (30% hyperpolarizations, 20% depolarizations and 20% hyperpolarizations followed by depolarizations). Quis treatment induced depolarization in about 50% of the tested CA cells; no hyperpolarization was found. Ibotenate led hyperpolarizations in 67% tested CA cells, despite the depolarizations followed or not; no depolarization was found. The hyperpolarizing responses were significantly blocked by the nonselective chloride channels blocker, picrotoxin. NMDA caused hyperpolarizations in 60% tested cells; only one of the tested cells was depolarized. Its percentage of potential responses is similar to those by NMDA and ibotenate cotreatment. Additionally, the magnitudes of the depolarized response to NMDA were increased in Mg2+ free saline and were blocked by Mg2+ and a NMDA receptor specific blocker, MK-801. These data indicated that functional GluR existed in CA cells, the hyperpolarization response to ibotenate was likely due to an influx of chloride ions, and the hyperpolarization response to NMDA and ibotenate might activate the same pathway. The implication of Glu-mediated regulation of JH synthesis in controlling insect reproduction is discussed.IntroductionEnglish Abstract………………………………2Introduction……………………………………3Material and Methods…………………………7Results…………………………………………10Discussion……………………………………12Reference………………………………………17Figures…………………………………………24Tables……………………………………………26Appendix…………………………………………28Acknowledgement………………………………34