• Francois Trudeau, Sylvain Gagnon, and Guy Massicotte.
• Département des Sciences de l'activité physique, Université du Québec à Trois-Rivières, Trois-Rivières, Québec, Canada.
• Eur. J. Pharmacol. 2004 Apr 19; 490 (1-3): 177-86.

AbstractDiabetes mellitus is an endocrine disorder of carbohydrate metabolism resulting primarily from inadequate insulin release (Type 1 insulin-dependent diabetes mellitus) or insulin insensitivity coupled with inadequate compensatory insulin release (Type 2 non-insulin-dependent diabetes mellitus). Previous studies involving behavioural and electrophysiological analysis indicate that diabetes mellitus induces cognitive impairment and defects of long-term potentiation in the hippocampus. Considered to be an important mechanism of learning and memory in mammals, long-term potentiation is known to require regulation of the glutamate receptor properties. According to many studies, defects of long-term potentiation in the hippocampus of diabetic animals are due to abnormal glutamate receptors. We review here the changes in glutamate receptors that may account for modifications of long-term potentiation in various models of diabetes mellitus. As glutamate receptors are also involved in the appearance of neurodegenerative states, we discuss the possibility that deficits in long-term potentiation during chronic diabetes might arise from dysfunction of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors in early stages of the disease. This review addresses the possible role of hyperglycaemia and insulin in regulating these receptors.

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