ABSTRACT
The C3 neurone of Helix aspersa is known to induce contraction of the ipsilateral tentacle retractor muscle. It is immunoreactive for peptides of the FMRFamide series and immunoreactive FMRFamide nerve fibres occur in the muscle.
Here we found that FMRFamide-like immunoreactivity was released from the isolated muscle following depolarization with high-potassium saline and that such release was calcium-dependent. HPLC characterization of the immunoreactive material in the muscle showed that FMRFamide itself, rather than the other FMRFamide-related peptides known from Helix, accounted for most of the immunoreactivity. Parallel radioimmunoassay (RIA) also showed that FMRFamide predominates in the C3 neurone.
The nicotinic acetylcholine (ACh) receptor antagonists benzoquinonium (10−5mol l−1) and trimetaphan (5×10−5mol l−1) reversibly reduced tension evoked in the muscle by C3 stimulation. These drugs also blocked the muscle response to bath-applied ACh. Physostigmine (5×10−8mol l−1), an acetylcholinesterase antagonist, potentiated the C3-evoked muscle response. Depolarizing excitatory junction potentials recorded in the muscle cells in response to C3 neurone stimulation corresponded 1:1 with action potentials in the C3 neurone. Whereas locally applied ACh evoked a depolarizing response in the muscle fibres, similar to that evoked by C3 neurone activation, locally applied FMRFamide, even at very high doses, did not affect the membrane potential of the muscle cells. Also, exposure of the cerebral ganglia to high-Mg2+/low-Ca2+ saline did not block the C3 neurone-evoked muscle tension. Taken together, these findings indicate that the C3 neurone makes monosynaptic connections with the tentacle retractor muscle cells and that the contraction of the muscle it induces is due, at least in part, to the release of ACh at the neuromuscular junction. The role of the FMRFamide contained in the neurone is not yet clear.
