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Published on: February 5, 2015
Arsenic trioxide modulates the central snail neuron action potential.
Guan-Ling Lu1, Yu-Chi Chang, Yi-Hung Chen
1Department of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Arsenic trioxide (As2O3) affects snail neuron activity, causing bursts of potential (BoPs) via phospholipase C (PLC) at 10 mM. Higher concentrations irreversibly abolish neuronal action potentials.
Area of Science:
- Neuroscience
- Pharmacology
- Toxicology
Background:
- The electropharmacological effects of arsenic trioxide (As2O3) on neuronal activity are not well understood.
- Investigating As2O3's impact on spontaneous neuronal firing is crucial for understanding its potential neurological effects.
Purpose of the Study:
- To investigate the effects of arsenic trioxide (As2O3) on spontaneous neuronal impulse activity.
- To elucidate the mechanism underlying As2O3-induced changes in neuronal excitability.
Main Methods:
- Utilized intracellular recordings and two-electrode voltage clamp techniques.
- Studied the effects of varying As2O3 concentrations on the RP4 neuron of the giant African snail (Achatina fulica Ferussac).
Main Results:
- As2O3 demonstrated a concentration-dependent effect on neuronal activity.
- 10 mM As2O3 induced bursts of potential (BoPs), which were blocked by phospholipase C (PLC) inhibitors.
- Higher As2O3 concentrations (30 mM) depolarized the resting membrane potential and abolished spontaneous action potentials.
- Voltage-clamp data indicated As2O3 decreased fast inward current without affecting steady-state outward current.
Conclusions:
- Arsenic trioxide (As2O3) at 10 mM elicits BoPs in central snail neurons, potentially mediated by PLC activity.
- The observed BoPs are not dependent on protein kinase A activity or calcium influx.
- High concentrations of As2O3 cause irreversible abolition of spontaneous neuronal action potentials.
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