A Study of Synaptic Plasticity in the Rat Hippocampal Field CA1 in Conditions of Deficiency of Acetylcholine and Other Neurotransmitters

Abstract

Experiments showed that high-amplitude, long-lasting tetanic potentiation could be induced in synaptic terminals formed by Schaffer collaterals on field CA1 pyramidal cells in rat hippocampal slices in which acetylcholine deficiency was modeled by application of the choline reuptake inhibitor hemicholine and the vesicular acetylcholine uptake inhibitor vesamicol. Deficiencies of different neurotransmitters were modeled by 5-min incubation of slices in solution containing an elevated potassium concentration, which led, as demonstrated previously, to depletion of the release of these neurotransmitters from nerve endings. The result of this procedure was that synapses formed by Schaffer collaterals developed long-term potentiation. Long-term post-tetanic potentiation was also induced in slices on this background in the model of neurotransmitter deficiency. Its amplitude was not significantly different from the amplitude of long-term potentiation in controls but was less than that obtained using vesamicol or hemicholine. As deficiency of serotonin, noradrenaline, and dopamine is known to be able to decrease the extent of long-term potentiation of synaptic transmission between fields CA3 and CA1, these result points to the possibility that acetylcholine deficiency partially compensates for this decrease. Considering known data on the locations of different types of nicotinic and muscarinic cholinoreceptors both on pyramidal cells and on inhibitory interneurons, the possible effects of acetylcholine on the efficiency of the inputs formed by Schaffer collaterals were studied. This analysis and consideration of the data obtained here led to the hypothesis that in conditions of acetylcholine deficiency, the main influence on the efficiency of excitation of pyramidal cells in field CA1 by field CA3 is exerted by disinhibition via a network of interacting interneurons.