title: Characteristic features of inhibitory junction potentials evoked by single stimuli in the guinea-pig isolated taenia caeci.
abstract: 1. Changes in membrane potential of the guinea-pig isolated taenia caeci evoked by single stimuli have been investigated using intracellular recording techniques. Nifedipine (10 microM) was used to arrest spontaneous muscle action potentials. Single stimuli elicited complex junction potentials which consisted of both excitatory and inhibitory components. 2. The excitatory component of the compound junction potential was unaffected by hexamethonium (100 microM) but abolished by atropine (1 microM) and omega-conotoxin GVIA (10-100 nM). 3. In the presence of atropine, single stimuli elicited fast inhibitory junction potentials (IJPs). IJPs were sometimes biphasic during repolarization with a noticeable 'slow tail'. Apamin (30-100 nM) potently inhibited the fast IJP and revealed an underlying slow IJP. 4. The fast IJP was also abolished by omega-conotoxin GVIA (100 nM). However, the slow IJP was insensitive to omega-conotoxin GVIA but was abolished by cadmium (30 microM). 5. Guanethidine (3 microM) and N omega-nitro-L-arginine (10-100 microM) had no detectable effects on either of the IJPs. The dye Reactive Blue 2 reduced the amplitude of the fast IJP but this reduction was associated with a membrane hyperpolarization. 6. The existence of two distinct IJPs in the guinea-pig taenia caeci has been demonstrated. The ability of omega-conotoxin GVIA to selectively abolish the fast IJP leaving the slow IJP intact suggests that separate nerves are involved in mediating these responses.
authors.affiliation: University Department of Pharmacology, Oxford, UK.
authors.forename: M
authors.initials: M
authors.lastname: Bridgewater
authors.forename: T C
authors.initials: TC
authors.lastname: Cunnane
authors.forename: A F
authors.initials: AF
authors.lastname: Brading
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001030:Apamin / Q000494:pharmacology; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D001285:Atropine / Q000494:pharmacology; D002104:Cadmium / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002432:Cecum / Q000187:drug effects / Q000502:physiology*; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology; D006145:Guanethidine / Q000494:pharmacology; D006168:Guinea Pigs; D018738:Hexamethonium / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D009469:Neuromuscular Junction / Q000187:drug effects / Q000502:physiology*; D018377:Neurotransmitter Agents / Q000502:physiology; D009569:Nitric Oxide / Q000037:antagonists & inhibitors; D019335:Nitroarginine; D010455:Peptides / Q000494:pharmacology; D020960:omega-Conotoxins
chemical_list: D002121:Calcium Channel Blockers; D018377:Neurotransmitter Agents; D010455:Peptides; D020960:omega-Conotoxins; D002104:Cadmium; C053423:Conus magus toxin; D019335:Nitroarginine; D001030:Apamin; D009569:Nitric Oxide; D018738:Hexamethonium; D001285:Atropine; D001120:Arginine; D006145:Guanethidine