You are not currently logged in.
Access your personal account or get JSTOR access through your library or other institution:
If You Use a Screen ReaderThis content is available through Read Online (Free) program, which relies on page scans. Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Early Age-Related Cognitive Impairment in Mice Lacking Cannabinoid CB1 Receptors
A. Bilkei-Gorzo, I. Racz, O. Valverde, M. Otto, K. Michel, M. Sarstre and A. Zimmer
Proceedings of the National Academy of Sciences of the United States of America
Vol. 102, No. 43, Residential Mobility of Low-Income Populations (Oct. 25, 2005), pp. 15670-15675
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/4143493
Page Count: 6
Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Preview not available
The molecular mechanisms contributing to the normal age-related decline of cognitive functions or to pathological learning and memory impairment are largely unknown. We demonstrate here that young mice (6-7 weeks) with a genetic deletion of the cannabinoid CB1 receptor performed as well as WT mice, or often better, in a number of learning and memory paradigms, including animal models of skill-learning, partner recognition, and operant conditioning. In contrast, the performance of mature mice (3-5 months) lacking CB1 receptors was much worse than that of age-matched WT animals. In most tests, these mice performed at the same level as old animals (14-17 months), suggesting that the decline in cognitive functions is accelerated in the absence of CB1 receptors. This rapid decline in CB1 -deficient animals is accompanied by a loss of neurons in the CA1 and CA3 regions of the hippocampus.
Proceedings of the National Academy of Sciences of the United States of America © 2005 National Academy of Sciences