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 ex...

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Bibliographic Details
Published in:Fundamental and applied toxicology 1988-08, Vol.11 (2), p.221-228
Main Authors: Fountain, Stephen B., Hennes, Steven K., Teyler, Timothy J.
Format: Article
Language:English
Subjects:
ACIDE ASPARTIQUE
ACIDO ASPARTICO
Animals
Aspartame - toxicity
ASPARTIC ACID
Biological and medical sciences
BRAIN
CEREBRO
Dipeptides - toxicity
EDULCORANT
EDULCORANTES
Electric Stimulation
Electrophysiology
ENCEPHALE
Female
FENILALANINA
Food toxicology
Hippocampus - drug effects
Hippocampus - physiopathology
INVESTIGACION
Medical sciences
NERVOUS SYSTEM
Neuronal Plasticity - drug effects
Neurons - drug effects
NUTRICION
NUTRITION
PHENYLALANINE
RAT
RATA
RATS
RECHERCHE
SISTEMA NERVIOSO
SWEETENERS
SYSTEME NERVEUX
Time Factors
Toxicology
TOXINAS
TOXINE
TOXINS
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Summary: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 m m 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 m m phenylalanine (PHE) produced a greater increase in excitability than that produced by an equivalent dose of APM, 0.1 m m aspartic acid (ASP) and 0.1 m m phenylalanine methyl ester (PM) produced effects comparable to those produced by an equivalent dose of APM, and combined exposure of 0.1 m m ASP and 0.1 m m PHE 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.
ISSN:0272-0590
1095-6832
DOI:10.1016/0272-0590(88)90146-7