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First published online January 19, 2006
Journal of Experimental Biology 209, 531-540 (2006)
Published by The Company of Biologists 2006
doi: 10.1242/jeb.02011

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The neuropeptide proctolin potentiates contractions and reduces cGMP concentration via a PKC-dependent pathway

Berit Philipp, Nicole Rogalla and Sabine Kreissl^*

Department of Biology, University of Konstanz, 78457 Konstanz, Germany

View larger version (16K): [in a new window]   Fig. 1. Effects of proctolin and octopamine on the cAMP concentration in Idotea muscle fibres. (A) Without preequilibration in ASW, the cAMP concentration does not change significantly after 15 min of exposure to 1 µmol l-1 proctolin (N=8), whereas 15 min of exposure to 10 µmol l-1 octopamine increases the cAMP concentration significantly (N=5). (B) In fibres equilibrated for 10 min in ASW after dissection, 3 min of simultaneous exposure to 1 µmol l-1 proctolin and the phosphodiesterase inhibitor 0.5 mmol l-1 IBMX (N=8) does not change the cAMP concentration compared to controls with IBMX alone (N=8). *P<0.05.

View larger version (27K): [in a new window]   Fig. 2. Proctolin enhances the amplitude of high (30 mmol l-1) K+-induced contractures of Idotea muscle fibres. (A) Membrane potential (top) and tension (bottom) measured simultaneously before application of proctolin (control), in the presence of 1 µmol l-1 proctolin, and after washing off proctolin for 30 min. Control shows one of three K+-contractures prior to the peptide tests. (B) Normalised membrane potentials and tensions (N=8) of the experiments as shown in A, indicating no significant change in membrane potential (top) and a 47% increase in the amplitudes of K+-contractures with the peptide (bottom). (C) K+-induced contractures measured before exposure to proctolin (control), after a 5 min application of 1 µmol l-1 proctolin in the presence of the PKA inhibitor H89 (1 µmol l-1) for 5 min, and after washing off proctolin and H89 for 30 min. (D) Summary of independent experiments showing the maximal amplitude of contractures normalised to the controls. 1 µmol l-1 proctolin increases the amplitudes of contractures significantly (N=8). In the presence of 20 µmol l-1 H89, proctolin increases the amplitudes of contractures significantly compared to controls without H89 (N=4). H89 alone significantly increases the amplitudes of contractures (N=6). *P<0.05.

View larger version (18K): [in a new window]   Fig. 3. Effect of proctolin on the cGMP concentration of Idotea muscle fibres. (A) The cGMP concentration is not reduced significantly after 15 min exposure to 1 µmol l-1 proctolin (N=6). In the presence of the PKC inhibitor BIM-1 (10 nmol l-1), 15 min application of proctolin has no effect on the cGMP concentration (N=6). The cGMP concentration is not reduced in the presence of BIM-1 (N=8). (B) After a preincubation for 10 min with the unselective phosphodiesterase inhibitor IBMX (0.5 nmol l-1), application of proctolin in the presence of IBMX for 3 min reduces the cGMP concentration in the fibres significantly compared to the cGMP concentration of control with IBMX (N=4, N=3, respectively). *P<0.05.

View larger version (16K): [in a new window]   Fig. 4. The cGMP-analogue 8-bromo-cGMP reduces K+-induced contractures and the proctolin-induced increase. Summary of independent experiments showing the maximum amplitude of contractures normalised to the controls: in the presence of 1 µmol l-1 proctolin (N=8), in the presence of proctolin and 20 nmol l-1 8-bromo-cGMP (N=8) and in the presence of the cGMP analogue (N=8) during high K+-saline application for 5 min. *Significantly different from controls, P<0.05.

View larger version (16K): [in a new window]   Fig. 5. The proctolin-induced potentiation of K+-induced contracture is prevented by the PKC inhibitor BIM-1 and mimicked by the PKC activator PMA. Summary of independent experiments showing the maximum amplitude of contractures normalised to controls: in the presence of 1 µmol l-1 proctolin (N=8), in the presence of proctolin and 10 nmol l-1 BIM-1 (N=5), in the presence of BIM-1 (N=4) and in the presence of 1 µmol l-1 of the PKC activator PMA (N=7) during high K+-saline application for 5 min. *Significantly different from controls, P<0.05.