We have investigated the intracellular mechanisms by which dopamine induced a biphasic modulation of the BA2+ current amplitude through the high voltage-activated Ca2+ channel (HVA-IBa) in identified Helix aspersa neurons. We used the two electrode voltage clamp technique on a group of identified neurons of the right parietal anglion in situ, and the whole cell patch clamp technique on these same neurons in primary culture. Brief application of dopamine induced an initial fast reduction of the HVA-IBa followed by a slower enhancement of HVA-IBa. This enhancement was not due to a shift of the current-voltage curve. Repetitive application of dopamine did not attenuate this phase of the response. During longer application, the inhibition began to 'sag' and returned towards control levels. These results indicate that the enhancement was not due to a desensitization of the receptor or a relief from tonic G-protein mediated inhibition of the current. Manipulations of the levels of intracellular second messengers such, Ca2+, cGMP, cAMP and arachidonic acid, as well as inhibition of protein kinases and phosphatases, had no effec on the dopamine induced biphasic effect on HVA-IBa. Pertussis toxin added to the patch pipette had a slow but simultaneous blocking effect on both phases of the dopamine action on HVA-IBa. Since our results show that pertussis toxin affects both phases of the dopamine action on this current, we suggest that both phases of the dopamine action on HVA-IBa are mediated by a pertussis toxin-sensitive G-protein. If a second messenger is implicated, it is none of the 'classical' second messenger systems.
ASJC Scopus subject areas
- Developmental Neuroscience
- Cellular and Molecular Neuroscience