Differential properties of tetrodotoxin-sensitive and tetrodotoxin- resistant sodium channels in rat dorsal root ganglion neurons
- M. Roy, T. Narahashi
- BiologyJournal of Neuroscience
- 1 June 1992
TTX-sensitive and TTX-resistant sodium channel currents were analyzed in acutely dissociated dorsal root ganglion (DRG) neurons isolated from 3–12-d-old and adult rats, and several external divalent cations exerted different effects on these current types.
Differential mechanism of action of the pyrethroid tetramethrin on tetrodotoxin-sensitive and tetrodotoxin-resistant sodium channels.
- H. Tatebayashi, T. Narahashi
- BiologyJournal of Pharmacology and Experimental…
- 1 August 1994
Rat dorsal root ganglion neurons are endowed with tetrodotoxin-sensitive (TTX-S) and tetrodOToxin-resistant ( TTX-R) sodium channels, and the pyrethroid insecticides cause differential effects on the two types of sodium channels.
Neuronal ion channels as the target sites of insecticides.
- T. Narahashi
- BiologyActa Pharmacologica et Toxicologica
- 1 July 1996
It appears that the sodium channel and the GABA system merit continuing efforts for development of newer and better insecticides.
Neuroreceptors and ion channels as the basis for drug action: past, present, and future.
- T. Narahashi
- BiologyJournal of Pharmacology and Experimental…
- 1 July 2000
This article summarizes the development of cellular neuropharmacology and neurotoxicology, based primarily on my own research, and emphasis is placed on the three-dimensional structure-activity relationship, in particular how changes in the molecular structure of drugs and receptors/channels result in kineticChanges in the function of receptors/Channels.
Chemicals as tools in the study of excitable membranes.
- T. Narahashi
- EngineeringPhysiological Reviews
- 1 October 1974
Tetrodotoxin Blockage of Sodium Conductance Increase in Lobster Giant Axons
- T. Narahashi, JOHN W. Moore, W. R. Scott
- BiologyThe Journal of General Physiology
- 1 May 1964
Observations have been made of sodium and potassium currents in the lobster giant axons treated with tetrodotoxin by means of the sucrose-gap voltage-clamp technique, and it is concluded that tetrodOToxin blocks the action potential production through its selective inhibition of the sodium-carrying mechanism while keeping the potassium- Carrying mechanism intact.
Characterization of two types of calcium channels in mouse neuroblastoma cells.
- T. Narahashi, A. Tsunoo, M. Yoshii
- BiologyJournal of Physiology
- 1 February 1987
Calcium channel currents as carried by Ba2+ (50 mM) were recorded using the whole‐cell variation of the patch‐electrode voltage‐clamp technique and were considered to be two different entities, equally sensitive to the temperature.
Modulation of sodium channels of rat cerebellar Purkinje neurons by the pyrethroid tetramethrin.
- J. H. Song, T. Narahashi
- BiologyJournal of Pharmacology and Experimental…
- 1 April 1996
The selective toxicity of pyrethroids between mammals and insects could be explained quantitatively on the basis of sodium channel factors that include temperature dependence, intrinsic sensitivity and recovery rate and detoxication factors.
Effects of the neuroprotective agent riluzole on the high voltage-activated calcium channels of rat dorsal root ganglion neurons.
- C. S. Huang, J. H. Song, K. Nagata, J. Yeh, T. Narahashi
- BiologyJournal of Pharmacology and Experimental…
- 1 September 1997
Riluzole inhibition of N- and P/Q-type calcium channels may result in reduced calcium influx at presynaptic terminals, which thereby decreases excessive excitatory neurotransmitter release, especially glutamate, a mechanism known to cause neuronal death in ischemic conditions.
Differential action of riluzole on tetrodotoxin-sensitive and tetrodotoxin-resistant sodium channels.
- J. H. Song, C. S. Huang, K. Nagata, J. Yeh, T. Narahashi
- BiologyJournal of Pharmacology and Experimental…
- 1 August 1997
One of the mechanisms by which riluzole exerts its neuroprotective action is to preferentially block the inactivated sodium channel of damaged or depolarized neurons under ischemic conditions, thereby suppressing excess stimulation of the glutamatergic receptors and massive influx of Ca++.
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