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University of British Columbia (1993)

Ion transport in the ileum of the desert locust Schistocerca gregaria, forskal

Richardson, Naomi Dinah

Titre : Ion transport in the ileum of the desert locust Schistocerca gregaria, forskal

Auteur : Richardson, Naomi Dinah

Grade : Master of Science – MSc 1993

Université de soutenance : University of British Columbia

Résumé
Recently, Audsley (1991) purified a neuropeptide factor - scgITP from the copora cardiaca of Shistocerca gregaria. ScgITP stimulates ileal reabsorption of Cl⁻, K⁺, Na⁺ and fluid and inhibits acid secretion. Stimulation with scgITP causes an increase in both Cl⁻ dependent short-circuit current and transepithelial voltage (Vt) and a decrease in transepithelial resistance (Rt ; Irvine et al 1988). There is evidence to suggest that cAMP acts as the second messenger for scgITP (Audsley 1990). In this thesis the mechanisms underlying ileal ion transport and the effects of cAMP were investigated. Intracellular microelectrodes were used to measure apical and basolateral membrane potentials. Brief transepithelial current pulses (13.3 μA) and ion substitutions permitted the estimation of specific ion conductances. In nonstimualted ilea, Vt was slightly positive (to the lumen side) and the inside of the cell was negative with respect to both haemolymph and lumen side bathing media. The apical membrane potential (Va) was slightly more negative than the basolateral membrane potential (Vb). Apical membrane resistance (Ra) was much higher than the basolateral membrane resitance (Rb). Stimulation of ileal ion transport with cAMP resulted in an increase in Vt. There was no change in Va after cAMP stimulation but Vb depolarized. Addition of cAMP caused a large decrease in Rt, due solely to a decrease in Ra with Rb remaining at control values. In nonstimulated ilea, a small apical Na⁺ conductance was measured. Voltage measurements indicated an increase in apical Na⁺ conductance after cAMP addition. However, resistance measurements were not consistent with a cAMP stimualted apical Na⁺ conductance. In nonstimulated ilea the conductance of the apical membrane to K⁺ was very small. After stimulation with cAMP a large increase in apical K⁺ conductance was observed. The cAMP stimulated apical K⁺ conductance was not inhibited by high luminal [K⁺]. The basolateral membrane displayed a very high conductance to K⁺ and to a lesser extent Cl⁻. There is no evidence for cAMP stimualtion of basolateral Cl⁻ conductance. These results are formulated into a model of the mechanism of cAMP control of ileal ion transport.

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