Neurochemical and electrophysiological studies on the inhibitory effect of ammonium ions on synaptic transmission in slices of rat hippocampus: Evidence for a postsynaptic action
There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.
Abstract
To elucidate the mechanisms involved in the inhibition of synaptic transmission by
ammonium ions, the effects of NH4Cl on glutamate release and on synaptic transmission
from Schaffer collaterals to CA1 pyramidal cells were measured in fully submerged
slices of rat hippocampus. The large, Ca(2+)-dependent release of glutamate evoked
by electrical-field stimulation or by 56 mM K+ was not reduced by 5 mM NH4Cl. In contrast,
5 mM NH4Cl decreased the smaller, field stimulation-induced release of glutamate observed
in the presence of low concentrations of Ca2+ (0.1 mM), as well as the spontaneous
release of glutamate both in normal and low Ca2+. Unlike the Ca(2+)-dependent release
of glutamate, synaptic transmission was reversibly depressed even by 1 mM NH4 Cl.
Firing of CA1 pyramidal cells evoked by iontophoretically applied glutamate was significantly
inhibited by 2 or 5 mM NH4Cl. This depression was increased in the presence of 25
microM bicuculline. Results suggest that ammonium ions do not depress the Ca(2+)-dependent
release of glutamate originating from synaptic vesicles, which is involved in synaptic
transmission. Rather, ammonium ions inhibit synaptic transmission by a postsynaptic
action, a conclusion strengthened by the inhibitory effect of NH4Cl on glutamate-induced
firing. However, NH4Cl may inhibit the formation of cytoplasmic glutamate, the source
of spontaneous and Ca(2+)-independent release.