MK-801 prevents cognitive and behavioral deficits produced by NMDA receptor overstimulation in the rat hippocampus.
The overstimulation of receptors for L-glutamate, particularly those of the N-methyl-D-aspartate (NMDA) type, has been suggested to play a role in mediating damage in a variety of neurodegenerative conditions or disorders ranging from ischemia/hypoxia to senile dementia of the Alzheimer's type (SDAT). We report here that the functional deficits and histological damage mediated by the overactivation of NMDA receptors in the Fischer 344 rat hippocampus can be blocked effectively by systemic administration of the noncompetitive NMDA antagonist, MK-801. These results suggest that MK-801 may be effective clinically in attenuating memory loss and hippocampal damage in disorders associated with the overstimulation of NMDA receptors.
Rogers
B C
BC
Laboratory of Molecular and Integrative Neuroscience, National Institute of Environmental Health Science, Research Triangle Park, North Carolina 27709.
Tilson
H A
HA
D000818:Animals; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000037:antagonists & inhibitors; D001522:Behavior, Animal / Q000187:drug effects*; D003072:Cognition Disorders / Q000139:chemically induced / Q000517:prevention & control*; D003986:Dibenzocycloheptenes / Q000494:pharmacology*; D016291:Dizocilpine Maleate; D006624:Hippocampus / Q000187:drug effects* / Q000473:pathology; D008297:Male; D016202:N-Methylaspartate; D051381:Rats; D011916:Rats, Inbred F344; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter / Q000187:drug effects*
D003986:Dibenzocycloheptenes; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter; D001224:Aspartic Acid; D016202:N-Methylaspartate; D016291:Dizocilpine Maleate