Subcellular Mechanism and Site of Action of Ionic Lanthanum at the Motor Nerve Terminal
Document Type
Article
Publication Date
1-1-1992
Description
The mechanism by which ionic lanthanum (La3+) increases and subsequently decreases spontaneous transmitter release was investigated by recording miniature endplate potentials (MEPPs) at frog neuromuscular junctions. Addition of tetrodotoxin and Co2+ delayed the onset of MEPP frequency increase but did not otherwise prevent the response. Dinitrophenol substantially reduced but did not eliminate the increase, whereas 3,4,5-trimethoxybenzoic acid8-(diethylamino) octyl ester (TMB-8) completely abolished it. Thus, La3+ does not act by depolarizing the terminal or by substituting for Ca2+ at transmitter release sites. Instead, it appears to enter the terminal through Na+ channels and promote Ca2+ release from intracellular organelles. The profound depletion of transmitter with time may be due to the high turnover of transmitter coupled with the inhibition of metabolic processes by La3+.
Citation Information
Provan, Spencer D.; and Miyamoto, Michael D.. 1992. Subcellular Mechanism and Site of Action of Ionic Lanthanum at the Motor Nerve Terminal. NeuroReport. Vol.3(1). 101-104. https://doi.org/10.1097/00001756-199201000-00027 PMID: 1319225 ISSN: 0959-4965