Deficits in water escape performance and alterations in hippocampal cholinergic mechanisms associated with neonatal monosodium glutamate treatment in mice

Pharmacology, Biochemistry, and Behavior
P T WongW H Loke

Abstract

Mice treated neonatally with monosodium glutamate (MSG) were found to have learning and memory deficits in performing a non-spatial water escape task. Scopolamine impaired the water-escape performance of the control mice but not that of the MSG-treated mice. It was suggested that the water-escape performance deficit in the MSG-treated mice was a result of impaired central cholinergic mechanisms. As such, scopolamine was unable to further incapacitate an already impaired cholinergic system. This is strongly supported by the decreased affinity of the sodium-dependent high-affinity choline uptake observed in the hippocampus. D-Cycloserine, a partial agonist at the glycine site of the NMDA receptor, did not affect the water-escape performance of the MSG-treated and control mice; nor did it alter the effects of scopolamine. This lack of effect of D-Cycloserine may imply that the NMDA receptors are not involved in non-spatial learning, in contrast to their reported involvement in spatial learning.

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Citations

Jan 5, 2000·European Journal of Pharmacology·S N SukhanovA T Ferreira
Mar 20, 2002·Pharmacology, Biochemistry, and Behavior·Duo ChenYong-Meng Xu
Oct 10, 2002·Brain Research Bulletin·E R G SanabriaM J S Fernandes
Nov 17, 2009·Cerebral Cortex·Emily A KellyAnia K Majewska
Oct 18, 2005·Pharmacology, Biochemistry, and Behavior·E Olvera-CortésI González-Burgos
Jul 21, 2020·Neurotoxicology·Adejoke Y Onaolapo, Olakunle J Onaolapo

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