Effects of 2,3-butanedione monoxime on induction of action potential bursts in central snail neurons: Direct and indirect modulations of ionic currents

Chia Hsien Lin, Chi Lun Wu, Mei Shan Lin, Ming Chang Liu, Pei Jung Lin, Ming Cheng Tsai

研究成果: 雜誌貢獻文章

3 引文 (Scopus)

摘要

The effects of 2,3-butanedione monoxime (BDM) on induction of action potential bursts were studied pharmacologically on the RP4 central neuron of giant African snail (Achatina fulica Ferussac). The effect of okadaic acid on the neuron was also tested. The RP4 neuron showed a spontaneous firing of action potential. Okadaic acid (1 μmol/l) did not alter the frequency of spontaneous action potential while BDM (3 mmol/l) reversibly elicited bursts of potential (BoP) of the RP4 neuron. The BoP elicited by BDM (3 mmol/l) were reversed 20 min after incubation with diazoxide (500 μmol/l) while the BoP were not altered in preparations treated with okadaic acid and BDM. The BDM-elicited BoP were not inhibited after administration with (a) hexamethonium (100 μmol/l), (b) atropine (1 mmol/l), (c) d-tubocurarine (100 μmol/l), (d) prazosin (100 μmol/l), (e) propranolol (100 μmol/l), (f) calcium-free solution, (g) high K+ (12 mmol/l) or (h) with high Mg2+ (30 mmol/l) solutions. The BDM-elicited BoP were inhibited by pretreatment with KT-5720 (10 μmol/l) or H89 (10 μmol/l), the protein kinase A inhibitors. However, the BoP were not affected after application of chelerythrine (10 μmol/l) or Ro 31-8220 (10 μmol/l), the protein kinase C inhibitors. Voltage-clamped studies revealed that BDM elicited a negative slope resistance (NSR) at membrane potentials between -50 and -10 mV. The NSR was not detectable at the same membrane potential in control RP4 neuron. It is suggested that the BoP elicited by BDM were not due to (1) the synaptic effects of neurotransmitters; (2) the activation of cholinergic, adrenergic receptors, or (3) phosphatase activity of the neuron. The BDM-elicited BoP were dependent on the protein kinase A related cAMP in the neuron and the delayed outward K + current may contribute to the BDMelicited BoP.
原文英語
頁(從 - 到)57-69
頁數13
期刊Pharmacology
73
發行號2
DOIs
出版狀態已發佈 - 一月 20 2005

指紋

Snails
Action Potentials
Neurons
Okadaic Acid
Protein Kinase Inhibitors
Cyclic AMP-Dependent Protein Kinases
Membrane Potentials
Diazoxide
diacetylmonoxime
Tubocurarine
Hexamethonium
Protein C Inhibitor
Prazosin
Cholinergic Receptors
Atropine
Phosphoric Monoester Hydrolases
Propranolol
Adrenergic Receptors
Protein Kinase C
Neurotransmitter Agents

Keywords

  • 2,3-Butanedione monoxime
  • Bursts of potential
  • Central neurons
  • Ionic currents of RP4 neurons
  • Negative slope resistance
  • Protein kinase
  • Snail, central neurons

ASJC Scopus subject areas

  • Pharmacology

引用此文

Effects of 2,3-butanedione monoxime on induction of action potential bursts in central snail neurons : Direct and indirect modulations of ionic currents. / Lin, Chia Hsien; Wu, Chi Lun; Lin, Mei Shan; Liu, Ming Chang; Lin, Pei Jung; Tsai, Ming Cheng.

於: Pharmacology, 卷 73, 編號 2, 20.01.2005, p. 57-69.

研究成果: 雜誌貢獻文章

Lin, Chia Hsien ; Wu, Chi Lun ; Lin, Mei Shan ; Liu, Ming Chang ; Lin, Pei Jung ; Tsai, Ming Cheng. / Effects of 2,3-butanedione monoxime on induction of action potential bursts in central snail neurons : Direct and indirect modulations of ionic currents. 於: Pharmacology. 2005 ; 卷 73, 編號 2. 頁 57-69.
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abstract = "The effects of 2,3-butanedione monoxime (BDM) on induction of action potential bursts were studied pharmacologically on the RP4 central neuron of giant African snail (Achatina fulica Ferussac). The effect of okadaic acid on the neuron was also tested. The RP4 neuron showed a spontaneous firing of action potential. Okadaic acid (1 μmol/l) did not alter the frequency of spontaneous action potential while BDM (3 mmol/l) reversibly elicited bursts of potential (BoP) of the RP4 neuron. The BoP elicited by BDM (3 mmol/l) were reversed 20 min after incubation with diazoxide (500 μmol/l) while the BoP were not altered in preparations treated with okadaic acid and BDM. The BDM-elicited BoP were not inhibited after administration with (a) hexamethonium (100 μmol/l), (b) atropine (1 mmol/l), (c) d-tubocurarine (100 μmol/l), (d) prazosin (100 μmol/l), (e) propranolol (100 μmol/l), (f) calcium-free solution, (g) high K+ (12 mmol/l) or (h) with high Mg2+ (30 mmol/l) solutions. The BDM-elicited BoP were inhibited by pretreatment with KT-5720 (10 μmol/l) or H89 (10 μmol/l), the protein kinase A inhibitors. However, the BoP were not affected after application of chelerythrine (10 μmol/l) or Ro 31-8220 (10 μmol/l), the protein kinase C inhibitors. Voltage-clamped studies revealed that BDM elicited a negative slope resistance (NSR) at membrane potentials between -50 and -10 mV. The NSR was not detectable at the same membrane potential in control RP4 neuron. It is suggested that the BoP elicited by BDM were not due to (1) the synaptic effects of neurotransmitters; (2) the activation of cholinergic, adrenergic receptors, or (3) phosphatase activity of the neuron. The BDM-elicited BoP were dependent on the protein kinase A related cAMP in the neuron and the delayed outward K + current may contribute to the BDMelicited BoP.",
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T1 - Effects of 2,3-butanedione monoxime on induction of action potential bursts in central snail neurons

T2 - Direct and indirect modulations of ionic currents

AU - Lin, Chia Hsien

AU - Wu, Chi Lun

AU - Lin, Mei Shan

AU - Liu, Ming Chang

AU - Lin, Pei Jung

AU - Tsai, Ming Cheng

PY - 2005/1/20

Y1 - 2005/1/20

N2 - The effects of 2,3-butanedione monoxime (BDM) on induction of action potential bursts were studied pharmacologically on the RP4 central neuron of giant African snail (Achatina fulica Ferussac). The effect of okadaic acid on the neuron was also tested. The RP4 neuron showed a spontaneous firing of action potential. Okadaic acid (1 μmol/l) did not alter the frequency of spontaneous action potential while BDM (3 mmol/l) reversibly elicited bursts of potential (BoP) of the RP4 neuron. The BoP elicited by BDM (3 mmol/l) were reversed 20 min after incubation with diazoxide (500 μmol/l) while the BoP were not altered in preparations treated with okadaic acid and BDM. The BDM-elicited BoP were not inhibited after administration with (a) hexamethonium (100 μmol/l), (b) atropine (1 mmol/l), (c) d-tubocurarine (100 μmol/l), (d) prazosin (100 μmol/l), (e) propranolol (100 μmol/l), (f) calcium-free solution, (g) high K+ (12 mmol/l) or (h) with high Mg2+ (30 mmol/l) solutions. The BDM-elicited BoP were inhibited by pretreatment with KT-5720 (10 μmol/l) or H89 (10 μmol/l), the protein kinase A inhibitors. However, the BoP were not affected after application of chelerythrine (10 μmol/l) or Ro 31-8220 (10 μmol/l), the protein kinase C inhibitors. Voltage-clamped studies revealed that BDM elicited a negative slope resistance (NSR) at membrane potentials between -50 and -10 mV. The NSR was not detectable at the same membrane potential in control RP4 neuron. It is suggested that the BoP elicited by BDM were not due to (1) the synaptic effects of neurotransmitters; (2) the activation of cholinergic, adrenergic receptors, or (3) phosphatase activity of the neuron. The BDM-elicited BoP were dependent on the protein kinase A related cAMP in the neuron and the delayed outward K + current may contribute to the BDMelicited BoP.

AB - The effects of 2,3-butanedione monoxime (BDM) on induction of action potential bursts were studied pharmacologically on the RP4 central neuron of giant African snail (Achatina fulica Ferussac). The effect of okadaic acid on the neuron was also tested. The RP4 neuron showed a spontaneous firing of action potential. Okadaic acid (1 μmol/l) did not alter the frequency of spontaneous action potential while BDM (3 mmol/l) reversibly elicited bursts of potential (BoP) of the RP4 neuron. The BoP elicited by BDM (3 mmol/l) were reversed 20 min after incubation with diazoxide (500 μmol/l) while the BoP were not altered in preparations treated with okadaic acid and BDM. The BDM-elicited BoP were not inhibited after administration with (a) hexamethonium (100 μmol/l), (b) atropine (1 mmol/l), (c) d-tubocurarine (100 μmol/l), (d) prazosin (100 μmol/l), (e) propranolol (100 μmol/l), (f) calcium-free solution, (g) high K+ (12 mmol/l) or (h) with high Mg2+ (30 mmol/l) solutions. The BDM-elicited BoP were inhibited by pretreatment with KT-5720 (10 μmol/l) or H89 (10 μmol/l), the protein kinase A inhibitors. However, the BoP were not affected after application of chelerythrine (10 μmol/l) or Ro 31-8220 (10 μmol/l), the protein kinase C inhibitors. Voltage-clamped studies revealed that BDM elicited a negative slope resistance (NSR) at membrane potentials between -50 and -10 mV. The NSR was not detectable at the same membrane potential in control RP4 neuron. It is suggested that the BoP elicited by BDM were not due to (1) the synaptic effects of neurotransmitters; (2) the activation of cholinergic, adrenergic receptors, or (3) phosphatase activity of the neuron. The BDM-elicited BoP were dependent on the protein kinase A related cAMP in the neuron and the delayed outward K + current may contribute to the BDMelicited BoP.

KW - 2,3-Butanedione monoxime

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KW - Ionic currents of RP4 neurons

KW - Negative slope resistance

KW - Protein kinase

KW - Snail, central neurons

KW - 2,3-Butanedione monoxime

KW - Bursts of potential

KW - Central neurons

KW - Ionic currents of RP4 neurons

KW - Negative slope resistance

KW - Protein kinase

KW - Snail, central neurons

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