title: Action potential bursts in central snail neurons elicited by procaine: roles of ionic currents.
abstract: The role of ionic currents on procaine-elicited action potential bursts was studied in an identifiable RP1 neuron of the African snail, Achatina fulica Ferussac, using the two-electrode voltage clamp method. The RP1 neuron generated spontaneous action potentials and bath application of procaine at 10 mM reversibly elicited action potential bursts in a concentration-dependent manner. Voltage clamp studies revealed that procaine at 10 mM decreased [1] the Ca2+ current, [2] the Na+ current, [3] the delayed rectifying K+ current I(KD), and [4] the fast-inactivating K+ current (I(A)). Action potential bursts were not elicited by 4-aminopyridine (4-AP), an inhibitor of I(A), whereas they were seen after application of tetraethylammonium chloride (TEA), a blocker of the I(K)(Ca) and I(KD) currents, and tacrine, an inhibitor of I(KD). Pretreatment with U73122, a phospholipase C inhibitor, blocked the action potential bursts elicited by procaine. U73122 did not affect the I(KD) of the RP1 neuron; however, U73122 decreased the inhibitory effect of procaine on the I(KD). Tacrine decreased the TEA-sensitive I(KD) of RP1 neuron but did not significantly affect the I(A). Tacrine also successfully induced action potential bursts in the RP1 neuron. It is concluded that the inhibition on the I(KD) is responsible for the generation of action potential bursts in the central snail RP1 neuron. Further, phospholipase C activity is involved in the procaine-elicited I(KD) inhibition and action potential bursts.
authors.affiliation: Department of Nursing, Ching-Kuo Institute of Management and Health, Keelung 20301, Taiwan, Republic of China.
authors.forename: Chia-Hsien
authors.initials: CH
authors.lastname: Lin
authors.forename: Pei-Lin
authors.initials: PL
authors.lastname: Lin
authors.forename: Ming-Cheng
authors.initials: MC
authors.lastname: Tsai
authors.forename: Hui-Yu
authors.initials: HY
authors.lastname: Hsu
authors.forename: Han-Yin
authors.initials: HY
authors.lastname: Yang
authors.forename: Chieh-Min
authors.initials: CM
authors.lastname: Chuang
authors.forename: Yi-Hung
authors.initials: YH
authors.lastname: Chen
mesh_terms: D015761:4-Aminopyridine / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects* / Q000502:physiology*; D000779:Anesthetics, Local / Q000494:pharmacology; D000818:Animals; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D004963:Estrenes / Q000494:pharmacology; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology*; D023421:Models, Animal; D009474:Neurons / Q000187:drug effects* / Q000502:physiology*; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology; D011343:Procaine / Q000494:pharmacology*; D011760:Pyrrolidinones / Q000494:pharmacology; D012908:Snails / Q000502:physiology*; D015222:Sodium Channels / Q000187:drug effects / Q000502:physiology; D013619:Tacrine / Q000494:pharmacology; D019789:Tetraethylammonium / Q000494:pharmacology; D010738:Type C Phospholipases / Q000037:antagonists & inhibitors / Q000187:drug effects / Q000502:physiology
chemical_list: D000779:Anesthetics, Local; D015220:Calcium Channels; D004963:Estrenes; D007473:Ion Channels; D015221:Potassium Channels; D011760:Pyrrolidinones; D015222:Sodium Channels; C060229:1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione; D013619:Tacrine; D011343:Procaine; D019789:Tetraethylammonium; D015761:4-Aminopyridine; D010738:Type C Phospholipases