Effects of ammonium ions on synaptic transmission and on responses to @entity14425 and XXXX in hippocampal @entity1249 pyramidal neurons in vitro.

@entity8777 @entity1024 @entity14425 @entity1025 @entity1249 @entity841 @entity140 @entity143 @entity35
Effects of @entity8777 on @entity1249 pyramidal neurons and synaptic transmission were investigated with intracellular recording in fully submerged @entity35 hippocampal slices. Superfusion with 1-4 mM @entity8777 reversibly depolarized the membrane by 15.1 +/- 1.4 mV, reduced the amplitude and broadened the duration of action potentials due to a slower rate of repolarization, without significant change in membrane conductance. When membrane potential was returned to control level by the injection of a steady outward current, action potential amplitude recovered but repolarization remained slow. The extent of depolarization was not dependent on the concentration of @entity8777 between 1 and 4 mM. @entity8777 greatly depressed orthodromic transmission evoked by the stimulation of Schaffer collateral/commissural fibers several minutes after depolarizing the @entity1249 neuron. Interruption of transmission began with a decrease in excitatory postsynaptic potential (EPSP) amplitude and eventually EPSPs were almost eliminated. When @entity8777 was removed, it took 2-3 min for membrane potential and 10-15 min for transmission to recover. Inward currents induced by bath application of @entity14425 acting on @entity140 ( @entity140 ) receptors were also depressed. In contrast, @entity8777 enhanced @entity1024 ( @entity143 )-induced currents. This @entity841 disappeared in the absence of added @entity1025 . A reduction in @entity14425 -induced responses provided a possible explanation for the inhibition of excitatory transmission by @entity8777 .
