The postweaning housing environment determines expression of learning deficit associated with neonatal monosodium glutamate (M.S.G.)

Kim N. Fisher, Ruth A. Turner, Gaby Pineault, Jeff Kleim, Matti J. Saari

Research output: Contribution to journalArticle

20 Scopus citations


Perinatal M.S.G. treatment causes a syndrome characterized by damage to the hypothalamic arcuate nucleus, other circumventricular areas, parts of the visual system and the dentate gyrus of the hippocampus. The resulting hormonal dysfunction may be responsible for developmental anomalies of organ systems, obesity, and alterations in sensory/motor performance. We have shown that some behavioral indicators of M.S.G. toxicity in rats can be masked by rearing them in enriched housing conditions. Here, we evaluated the impact of six housing conditions on M.S.G.-induced alterations of organ systems and behavior. Perinatal M.S.G. treatment reduced adrenal, heart and testes weights, as well as total white blood cell (WBC) counts, and increased tail flick latencies. These measures were unaffected by the housing condition. M.S.G.-induced reductions in body weight, grip strength, water maze and dominance task performance varied as a function of housing. Deficits in water maze performance were most evident following social and isolated single-cage housing. We propose that deficits in water maze performance following perinatal M.S.G. may be attributable to hippocampal damage that can be alleviated by rearing the rats in stimulating environments.

Original languageEnglish (US)
Pages (from-to)507-513
Number of pages7
JournalNeurotoxicology and Teratology
Issue number5
StatePublished - Jan 1 1991
Externally publishedYes



  • Neonatal monosodium glutamate (M.S.G.)
  • Postweaning housing environment

ASJC Scopus subject areas

  • Toxicology
  • Developmental Neuroscience
  • Cellular and Molecular Neuroscience

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