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Pharmacological sensitivity of the articular capsule of the primary spines of Eucidaris tribuloides
Institution:1. Institute for Nanotechnology and Water Sustainability, College of Science, Engineering and Technology, University of South Africa, Florida Science Campus, 1710, South Africa;2. Department of Chemistry, Sefako Makgatho Health Sciences University, P.O Box 60, Medunsa 0204, South Africa;2. Department of Integrative Biology, University of Guelph, Guelph, ON, Canada;3. Department of Ocean Sciences, Memorial University, St. John''s, NL, Canada;4. Department of Biological Sciences, California State University Long Beach, Long Beach, CA, United States;5. State of Hawai''i, Division of Aquatic Resources, Ānuenue Fisheries Research Center, Honolulu, HI, United States;6. Society for the Exploration and Valuing of the Environment (SEVE), Portugal Cove-St. Philips, NL, Canada;11. School of Medical Sciences and School of Life and Environmental Sciences, University of Sydney, Sydney, NSW, Australia;12. Department of Biology, Georgia Southern University, Statesboro, GA, United States
Abstract:1. This paper describes the effects of several cholinergic agonists and antagonists, and of β-phenylethylamine (PEA) and some of its derivatives, on the articular capsule, or ligament, of the primary spines of Eucidaris tribuloides.2. Carbamylcholine (CCh), methacholine (MeACh), nicotine, and muscarine exert a stiffening effect similar to that of acetylcholine (ACh), although the time course of their actions varies widely.3. Atropine induced stiffening and blocked and responses to muscarine and MeACh. The responses to MeACh were blocked also by 4-diphenylacetoxy-N-methylpiperidine, suggesting the presence in the ligament of type M3 muscarinic receptors, in addition to nicotinic ones. d-Tubocurarine induced stiffness of the ligament and failed to block the responses to ACh and nicotine.4. While ACh induced only a slight desensitization, CCh caused a long-lasting blockade of the stiffening effects of the cholinergic agonists. This shows that the receptors for ACh have a site or sites that recognize the ester moieties of these molecules.5. Eserine and neostigmine potentiate the responses to acetylcholine, indicating the presence of aeetyl-cholinesterase in the ligament.6. β-Phenylethy lamine, epinephrine, norepinephrine, and dopamine induce diphasic responses; usually a brief softening followed by a slow and irreversible stiffening of the ligament.7. In contrast to the above, tyramine and octopamine elicit a simple softening of ligaments which are stiff as a result of handling or by exposure to cholinergic agonists. However, tyramine and octopamine do not soften ligaments which become stiff as a result of exposure to adrenergic agonists.
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