Dopaminergic control of corpora allata activity in the larval tobacco hornworm, Manduca sexta.

The corpora allata (CA) of insects are innervated by axons of non-neurosecretory cerebral neurons, and of the various known neurotransmitters in the brain of the tobacco hornworm, Manduca sexta, only dopamine is detected in the CA by electrochemical detection HPLC. This neurotransmitter stimulates the biosynthetic activity of the CA in vitro for the first 2 days of the last larval stadium, but inhibits CA from day 3 through day 6, the beginning of the prepupal period. Stimulation of JH synthesis has previously been linked with an increase in the production of cyclic AMP (cAMP) in the CA, and dopamine stimulates the adenylyl cyclase system of CA from larvae early in the fifth stadium, while on day 6, its effect is inhibitory. These results suggest: (1) the existence in the CA of both D1- and D2-like dopamine receptors, which in vertebrates stimulate and inhibit, respectively, adenylyl cyclase; and (2) the developmental control of their expression. A potent D1 agonist, (+/-)-SKF 82958-HBr, did not stimulate JH biosynthesis by day 0 CA as expected, but appeared to inhibit it at a concentration of 10(-5)M. Thus the apparent D1-like receptor in Manduca CA may be pharmacologically distinct from vertebrate D1 receptors. The existence of D2-like receptors is supported by the finding that a vertebrate D2 receptor agonist, (+/-) PPHT-HCl, and an antagonist, eticlopride, have the predicted effects on JH acid biosynthesis and cAMP production by day 6 Manduca CA. However, the D1 agonist also significantly reduces JH acid biosynthesis and cAMP production, indicating that while the Manduca D2-like receptor is pharmacologically similar to the vertebrate D2, it shares some characteristics with D1 receptors. The developmental regulation of these receptors by ecdysteroids is suggested by the fact that when day 0 larvae are treated in vivo with exogenous ecdysone:20-hydroxyecdysone, the biosynthetic activity of the CA in vitro 24 h later is no longer stimulated by dopamine.