Abstract
Disruption of the fiber connections between the temporal cortex (TC) and lateral entorhinal cortex (LEC) results in impaired memory and decrease of glutamate in both denervated areas. Administration of glutamatergic agonists fully restores the mnemonic function in rats with TC/LEC lesions. The purpose of the present study was to examine whether the pharmacologically supported recovery of function may act via NMDA receptors. Rats with TC/LEC lesions either received saline, the NMDA antagonist HA-966, the NMDA agonist glycine or HA-966 + glycine. The results show that saline-treated rats are severely impaired in retention, whereas rats treated with glycine perform like normal controls. Rats pretreated with HA-966 are not able to profit from the beneficial effects of glycine. These data support the notion that the restoration of memory function obtained by glycine in lesioned animals involves activation of NMDA receptors.
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