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Neuromodulation in molluscan smooth muscle: the action of 5-HT, FMRFamide and purine compounds.

Research output: Contribution to Journal/MagazineJournal articlepeer-review

  • I. D. Nelson
  • H. Huddart
<mark>Journal publication date</mark>1994
<mark>Journal</mark>General Pharmacology
Issue number3
Number of pages14
Pages (from-to)539-552
Publication StatusPublished
<mark>Original language</mark>English


1. 1. The RR, OR, RS and RP muscles of Buccinum did not respond directly to 5-HT, but this monoamine converted their normally tonic ACh responses to fast twitch contractions with lowered tonic force. This action was not accompanied by significant membrane potential changes. 2. 2. Pre-treatment with dibutyryl cAMP potentiated ACh responses and enhanced 5-HT modification of the responses. 3. 3. All muscles responded strongly to FMRFamide with twitch contractions but this was not accompanied by significant membrane potential changes. 4. 4. FMRFamide enhanced ACh contracture force and converted the responses into fast twitch activity. FMRFamide responses were dramatically inhibited by 5-HT with loss of all tonic force and fast twitch activity. 5. 5. While dibutyryl cAMP did not affect FMRFamide responses, the IP3 inhibitor lithium, at very high concentrations, caused a significant diminution of FMRFamide responses. 6. 6. All four muscles were unresponsive to adenosine and ATP but all except the RP responded in a dose-dependent manner to GTP and GTP-γ-S over the 10−7-10−4 mol 1−1 range. The responses showed moderate fast twich activity which was unaccompanied by action potential discharges. Guanosine was without effect, except at very high concentrations where it inhibited FMRFamide responses. 7. 7. ACh and GTP acted additively to increase muscle force and to enhance ACh-induced depolarization. Similarly both GTP and GTP-γ-S acted additively, considerably enhancing FMRFamide responses. 8. 8. It is proposed that 5-HT, FMRFamide and GTP may, via their separate receptors or by possible interaction with ion channels, activate secondary messenger systems to modify the calcium released by ACh-induced depolarization to modulate excitation-contraction coupling and force generation in these muscles.