Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

Aged rats are known to have deficits in spatial learning behavior in the Morris water maze. We have found that aged rats also have deficits in NR2B protein expression and that the protein expression deficit is correlated with their performance in the Morris water maze. To test whether this NR2B deficit was sufficient to account for the behavioral deficit, we used antisense oligonucleotides to specifically knock down NR2B subunit expression in the hippocampus of young rats. NR2B antisense treatment diminished NMDA receptor responses, abolished NMDA-dependent long-term potentiation (LTP), and impaired spatial learning. These data demonstrate the important role of NR2B in LTP and learning and memory and suggest a role for reduced NR2B expression in age-related cognitive decline.

Type

Journal article

Journal

J Neurosci

Publication Date

01/05/2002

Volume

22

Pages

3628 - 3637

Keywords

Action Potentials, Aging, Animals, Behavior, Animal, Blotting, Western, Calcium Channel Blockers, Catheterization, Electric Stimulation, Excitatory Amino Acid Antagonists, Excitatory Postsynaptic Potentials, Gene Expression, Hippocampus, In Vitro Techniques, Kynurenic Acid, Long-Term Potentiation, Male, Maze Learning, Microinjections, Oligonucleotides, Antisense, Rats, Rats, Inbred F344, Receptors, N-Methyl-D-Aspartate, Spermine