Triethyltin exposure suppresses synaptic transmission in area CA1 of the rat hippocampal slice.

To examine the effects of TET on the electrophysiology of area CA1 of hippocampus, hippocampal slices were obtained from adult hooded rats and were maintained in vitro using standard techniques. Stimulating and recording electrodes were placed in the Schaffer collaterals and CA1 pyramidal cell body layer, respectively. Following baseline measurements, slices were exposed to either 0, 1, 3, 6, or 10 microM TET in the incubating medium. Both pyramidal cell excitability and recurrent/feedforward inhibition were suppressed in a dose-dependent manner within 3 hr postexposure. The evoked population spike and population excitatory postsynaptic potential (EPSP) were suppressed significantly by 2 hr postexposure for 1 and 3 microM TET exposures, and by 45 min postexposure for 6 and 10 microM exposures. A similar dose-dependency was observed for the suppression of recurrent/feedforward inhibition in hippocampal CA1. A second procedure tested the specificity of TET effects to axonal conduction of Schaffer collaterals. Both the stimulating and recording electrode were placed in the Schaffer collaterals so that both the Schaffer collateral population fiber volley and the CA1 pyramidal cell population EPSP could be recorded. TET exposure suppressed pyramidal cell EPSPs without significantly affecting the amplitude of Schaffer collateral fiber volleys. The results support the view that acute TET exposure suppresses synaptic transmission in area CA1 of hippocampus.

Aspartame exposure and in vitro hippocampal slice excitability and plasticity.

Aspartame (APM) is a low-calorie sweetener recently approved and released for widespread use in the United States. However, concerns still exist that APM consumption may be responsible for adverse neurological and psychological effects in some people. In addition, recent reports indicate that APM exposure may alter regional brain neurotransmitter levels. The present study assessed the effects of APM and its amino acid moieties on rat hippocampal slice excitability and plasticity. Specifically, tests of excitatory systems, inhibitory systems, and synaptic plasticity (induction of long-term potentiation--LTP) were administered postexposure. Exposures of 0.01, 0.1, 1, and 10 mM APM potentiated the response of hippocampal CA1 pyramidal cells, but had no apparent effect on local inhibitory systems. APM exposure did not block the establishment of LTP at any dose despite the potentiation of pyramidal cell response observed postexposure. In addition, 0.1 mM phenylalanine (PHE) produced a greater increase in excitability than that produced by an equivalent dose of APM, 0.1 mM aspartic acid (ASP) and 0.1 mM phenylalanine methyl ester (PM) produced effects comparable to those produced a smaller, but reliable, change in hippocampal CA1 excitability relative to baseline. Like APM, none of the amino acids produced detectable changes in inhibitory systems or neuronal plasticity.