Glutamate-gated chloride channels inhibit juvenile hormone biosynthesis in the cockroach, Diploptera punctata.

Juvenile hormone (JH) synthesized and released from endocrine gland corpus allatum (CA) plays an important role in insect metamorphosis, vitellogenesis and reproduction. Glutamate is a major neurotransmitter in the nervous system and its activated receptors possess excitatory and inhibitory forms in muscle fibers of invertebrates. Previously, we have shown that the rise of intracellular calcium through excitatory glutamate receptors, N-methyl-d-aspartate (NMDA) and non-NMDA-type channels stimulates JH synthesis in the cockroach, Diploptera punctata. Here, we demonstrate the occurrence of inhibitory chloride permeable glutamate (GluCl) receptors on CA cell membranes. Application of the GluCl channel activators, ibotenic acid (Ibo) and ivermectin, but not gamma-aminobutyric acid caused a decline in JH synthesis in glands of either high or low activity during the gonadotrophic cycle. Also, while recording the membrane potential of the isolated whole CA glands intracellularly, Ibo induced a hyperpolarizated response. Both changes in the membrane potential and inhibition of JH synthesis could be abolished by the application of the chloride channel blocker picrotoxin. Finally, we found both excitatory and inhibitory glutamate receptors cause antagonistic effects on rates of JH synthesis. These results indicate a novel function of GluCl channels in the inhibition of JH synthesis that could be a potential pathway for developing a new generation of insecticides.