NDLI: Modification of NMDA responses by tri-n-butyltin in rat brain neurons

Content Provider	PubMed Central
Author	Kanemoto, Yumiko Ishibashi, Hitoshi Matsuo, Shinichiro Oyama, Yasuo Akaike, Norio
Copyright Year	2002
Abstract	The effects of the organotin, tri-n-butyltin (TBT), on N-methyl-D-aspartate (NMDA) induced membrane currents were investigated in order to evaluate possible neuronal actions of this toxic environmental pollutant. Experiments were conducted on neurons acutely dissociated from the rat dorsal motor nucleus of vagus (DMV) using the nystatin-perforated patch clamp recording technique. In Mg2+-free physiological recording solutions, the application of NMDA to single DMV neurons held at a holding potential (VH) of −40 mV evoked an inward current which rapidly reached a peak before declining to a steady-state inward current. This was followed, immediately after NMDA washout, by a transient outward current. TBT (100 nM) reversibly caused a slight reduction in the inward currents and greatly increased the amplitude of the outward currents. The reversal potential of the NMDA-induced outward current in the presence of TBT was −86.7 mV, close to the theoretical K+ equilibrium potential of −85.7 mV. The NMDA-induced outward current was completely blocked when the K+ in the internal solution was replaced with equimolar Cs+. Under these conditions, the NMDA induced current was more sustained and was unaffected by TBT. The NMDA-induced outward current was markedly inhibited by 5 mM tetraethylammonium chloride and 300 nM charybdotoxin, and it was abolished by removal of extracellular Ca2+, suggesting that the outward current was due to the activation of Ca2+-activated K+ channels by Ca2+ influx through NMDA receptors. In conclusion, in rat DMV neurons, TBT potentiates the Ca2+-activated K+ current induced by NMDA application without having any direct effects on the NMDA-induced inward current. Given the significant role of NMDA receptor mediated excitation in various physiological and pathological processes, the modulation of this response by TBT may have an important influence on neuronal function.
Related Links	http://dx.doi.org/10.1038/sj.bjp.0704707
Ending Page	206
Page Count	6
Starting Page	201
File Format	PDF
ISSN	00071188
Journal	British Journal of Pharmacology
Issue Number	2
Volume Number	136
Language	English
Publisher Date	2002-05-01
Access Restriction	Open
Subject Keyword	Pharmacology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Pharmacology

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