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|Title:||Deficits in water escape performance and alterations in hippocampal cholinergic mechanisms associated with neonatal monosodium glutamate treatment in mice||Authors:||Wong, P.T.-H.
|Keywords:||Hippocampal cholinergic mechanisms
Learning and memory
NMDA receptors D-Cycloserine
Water escape task
|Issue Date:||1997||Citation:||Wong, P.T.-H., Teo, W.L., Feng, H., Xue, Y.D., Neo, L.H., Loke, W.H. (1997). Deficits in water escape performance and alterations in hippocampal cholinergic mechanisms associated with neonatal monosodium glutamate treatment in mice. Pharmacology Biochemistry and Behavior 57 (1-2) : 383-388. ScholarBank@NUS Repository. https://doi.org/10.1016/S0091-3057(96)00338-3||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.||Source Title:||Pharmacology Biochemistry and Behavior||URI:||http://scholarbank.nus.edu.sg/handle/10635/23572||ISSN:||00913057||DOI:||10.1016/S0091-3057(96)00338-3|
|Appears in Collections:||Staff Publications|
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