title: Palytoxin-induced transmitter release in the autonomic nervous system of the rat.
abstract: A combination of pharmacological, histochemical, immunocytochemical, neurochemical and microscopic techniques has been used to test the hypothesis that smooth muscle contractions caused by palytoxin are primarily a response to toxin-induced release of transmitter from motor nerve terminals. In the anococcygeus, palytoxin caused a dose-dependent contraction; the dose-response curve was particularly steep in the dose range 0.3-100 nM. This part of the response was abolished by phentolamine and absent in the muscles of reserpinized animals. A single, large dose of palytoxin (100 nM) caused a biphasic contraction. Phentolamine blocked the first phase by 50% and the second by > 80%. Transmitter overflow studies showed that the toxin enhanced the release of 3H after loading with 3H-NA, and immunofluorescence showed the loss of adrenergic transmitters from the innervation. In the vas deferens, palytoxin caused a biphasic contraction of the muscle. Phentolamine blocked first phase by > 80% and the second by 47%. Immunofluorescence studies showed that stores of adrenergic transmitter were depleted but stores of NPY were not greatly affected. Indirect evidence suggested that palytoxin did not cause the release of purinergic transmitters. A direct component to the contraction was apparently present in most preparations, but though variable in extent it was usually slight. It is concluded that the contractions of smooth muscle caused by palytoxin are primarily the result of toxin-induced transmitter release.
authors.affiliation: School of Neurosciences, University of Newcastle, Newcastle upon Tyne, U.K.
authors.forename: J
authors.initials: J
authors.lastname: Posangi
authors.forename: J B
authors.initials: JB
authors.lastname: Harris
authors.forename: M A
authors.initials: MA
authors.lastname: Zar
mesh_terms: D000178:Acrylamides / Q000633:toxicity*; D000818:Animals; D001341:Autonomic Nervous System / Q000187:drug effects / Q000378:metabolism; D003064:Cnidarian Venoms / Q000633:toxicity*; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D004357:Drug Synergism; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D008297:Male; D008856:Microscopy, Fluorescence; D009046:Motor Neurons / Q000187:drug effects / Q000378:metabolism; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects* / Q000294:innervation; D009411:Nerve Endings / Q000187:drug effects / Q000378:metabolism; D009478:Neuropeptide Y / Q000378:metabolism; D018377:Neurotransmitter Agents / Q000378:metabolism*; D009543:Nifedipine / Q000494:pharmacology; D009638:Norepinephrine / Q000378:metabolism; D010646:Phentolamine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013779:Tetrodotoxin / Q000633:toxicity; D014649:Vas Deferens / Q000187:drug effects / Q000294:innervation; D000095702:Polyether Toxins
chemical_list: D000178:Acrylamides; D003064:Cnidarian Venoms; D009478:Neuropeptide Y; D018377:Neurotransmitter Agents; D009543:Nifedipine; D009638:Norepinephrine; D010646:Phentolamine; D013779:Tetrodotoxin; C010272:palytoxin; D000095702:Polyether Toxins