A cGMP-dependent cascade enhances an L-type-like Ca2+ current in identified snail neurons.

We studied the impact of an NO-cGMP dependent signalling pathway on the high-voltage-activated (HVA) Ca(2+) current in identified neurons of the pulmonate snail, Helix pomatia, using Ba(2+) as charge carrier. The 3',5'-cyclic guanosine monophosphate (cGMP) analogues, dibutyryl-cGMP and 8-bromo-cGMP, consistently induced a biphasic response, consisting of an increase superseded by a decline of the Ba(2+) current. The NO donor, sodium nitroprusside (SNP), modulated only in a minority of neurons the Ba(2+) current.

Nitric oxide decreases a calcium-activated potassium current via activation of phosphodiesterase 2 in Helix U-cells.

In the present study, we investigated the underlaying mechanism of nitric oxide (NO) and cGMP on the decline of a Ca2+-activated potassium (KCa) current in U-cells of the right parietal ganglion of the pulmonate snail, Helix pomatia. Using a two-electrode voltage-clamp technique, we activated a KCa-current either by opening of endogenous voltage-gated Ca2+-channels during depolarizing voltage steps or by ionophoretic injection of Ca2+ via a third electrode containing 100 mM Ca2+. KCa-current amplitude in U-cells was sensitive to Ba2+, TEA, iberiotoxin, kaliotoxin and charybdotoxin (ChTX), but not to 4-aminopyridine (4-AP) (up to 30 mM) and apamin (up to 300 nM).