Allatostatin A-like immunoreactivity in the nervous system and gut of the larval midge Chironomus riparius: modulation of hindgut motility, rectal K+ transport and implications for exposure to salinity.

Evidence for the presence of allatostatin (AST) A-like neuropeptides in the larval midge Chironomus riparius is reported. Immunohistochemical studies on the nervous system and gut revealed the presence of AST A-like immunoreactive (AST-IR) cells and processes. The nerve cord contained AST-IR processes that originated from cells in the brain and travelled the length of nerve cord to the terminal ganglion. Within each ganglion, these processes gave rise to varicosities, suggesting that they formed synapses with neurons in the ganglia. Endocrine cells containing AST-IR were present in three regions of the midgut: near the attachment of the Malpighian tubules, between the anterior and posterior midgut, and in the vicinity of the gastric caecae. The terminal ganglion also contained four AST-IR cells that gave rise to axons that projected onto the hindgut and posterior midgut. Application of a cockroach AST to the semi-isolated hindgut of larval C. riparius led to dose-dependent inhibition of muscle contractions with an EC50 of ~10 nmol l(-1) and a decrease in rectal K(+) reabsorption resulting from reduced rectal Na(+)/K(+)-ATPase and vacuolar type H(+)-ATPase activities. The results suggest the presence of endogenous AST-like neuropeptides in larval C. riparius, where these factors play a role in the function of the gut. Furthermore, regulation of ion reabsorption by ASTs at the rectum could serve as an ideal mechanism of ion regulation in the face of abrupt and acute elevated salt levels.

Pharmacological characterisation of apical Na+ and Cl- transport mechanisms of the anal papillae in the larval mosquito Aedes aegypti.

The anal papillae of freshwater mosquito larvae are important sites of NaCl uptake, thereby acting to offset the dilution of the hemolymph by the dilute habitat. The ion-transport mechanisms in the anal papillae are not well understood. In this study, the scanning ion-selective electrode technique (SIET) was utilized to measure ion fluxes at the anal papillae, and pharmacological inhibitors of ion transport were utilized to identify ion-transport mechanisms. Na(+) uptake by the anal papillae was inhibited by bafilomycin and phenamil but not by HMA. Cl(-) uptake was inhibited by methazolamide, SITS and DIDS but not by bafilomycin. H(+) secretion was inhibited by bafilomycin and methazolamide. Ouabain and bumetanide had no effect on NaCl uptake or H(+) secretion. Together, the results suggest that Na(+) uptake at the apical membrane occurs through a Na(+) channel that is driven by a V-type H(+)-ATPase and that Cl(-) uptake occurs through a Cl(-)/HCO(3)(-) exchanger, with carbonic anhydrase providing H(+) and HCO(3)(-) to the V-type H(+)-ATPase and exchanger, respectively.