Effects of l-arginine on the afferent resting activity in the cephalopod statocyst

Abstract

The effects of bath application of the nitric oxide (NO) precursor l-arginine ( l-ARG) on the resting activity (RA) of afferent crista fibers were studied in isolated statocysts of the cuttlefish Sepia officinalis under various experimental conditions. l-ARG (threshold 10 −7 M) had three different effects: inhibition, excitation, and excitation followed by an inhibition; only the inhibitory effect of l-ARG was dose-dependent. d-Arginine ( d-ARG) had no effect. When the preparation was pre-treated with NO synthase inhibitors ( N G-Nitric- l-arginine methyl ester HCl ( l-NAME), N G-Nitro- l-arginine ( l-NOARG)), both the inhibitory and the excitatory effects of l-ARG significantly decreased at higher concentrations (10 −5 to −4 M), or were completely blocked at lower concentrations (10 −7 to −6 M), of l-ARG. When the preparation was pre-treated with guanylate cyclase inhibitors (1 H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one (ODQ), methylene blue (M-BLU), cystamine (CYS)), l-ARG had only excitatory effects, whereas its effects were only inhibitory when the preparation was pre-treated with adenylate cyclase inhibitors 2′,3′-dideoxyadenosine (DDA), MDL-12330A (MDL), nicotinic acid (NIC-A)). l-ARG had no effects when the pre-treatment was with a guanylate cyclase inhibitor and an adenylate cyclase inhibitor combined; in that situation, the RA of the afferent fibers remained. These data indicate that in cephalopod statocysts, a cGMP and a cAMP signal transduction pathway (presumably via the generation of NO) are responsible for the effects of l-ARG on the RA of crista afferent fibers. They also indicate that the l-ARG–cGMP pathway is the dominant pathway and is inhibitory, and that both pathways have only modulatory effects on, but are not essential for, the generation of the RA.