Key result
Corpus cardiacum extracts and forskolin elevate locust recta cAMP, coinciding with maximal short-circuit current increases.
Stimulation of active ion transport in locust rectum is likely induced by a rapid rise in cyclic AMP, whereas cyclic GMP is not involved in the early stages of stimulation.
Supports cAMP mediation of epithelial ion transport in insect models; leaves open translation to mammalian systems.
A variety of agents stimulate the chloride‐dependent short‐circuit current (Isc) across isolated locust recta. In this study, the role of cyclic nucleotides in mediating this stimulation was examined by measuring levels of cyclic AMP and cyclic GMP in tissues exposed to these agents. After bathing recta in saline, there is a decline in Isc, and this is accompanied by a fall in cellular levels of cyclic AMP and cyclic GMP. Stimulants of Isc across locust recta, corpus cardiacum (CC) extracts containing chloride transport‐stimulating hormone (CTSH) and forskolin, also elevate cellular levels of cyclic AMP. Between 5 and 10 min after addition of CC extract, there is an increase in cyclic AMP levels. During this same time period, the Isc rises at its maximal rate. The Isc remains elevated for at least another 20 min, even though tissue cyclic‐AMP levels decline rapidly by 15 min. These results suggest that stimulation of Isc is induced by a rise in cyclic AMP, but the cessation of stimulated active ion transport is controlled by other biochemical processes. In contrast to the relatively rapid rise in cyclic‐AMP levels, a 60‐min exposure to CC extract was required to elicit a rise in cyclic GMP, and therefore it may not be involved in the early stages of Isc stimulation.
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Chamberlin et al. (1988) studied this question. Corpus cardiacum (CC) extracts and forskolin was evaluated on Levels of cyclic AMP and cyclic GMP and short-circuit current (Isc). Exposure of isolated locust recta to corpus cardiacum extracts and forskolin elevated cellular levels of cyclic AMP, which coincided with the maximal rate of rise in short-circuit current.
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