HOME HELP FEEDBACK SUBSCRIPTIONS ALL ISSUES SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a Colleague Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Murphy, G. G. Articles by Silva, A. J. Search for Related Content PubMed PubMed Citation Articles by Murphy, G. G. Articles by Silva, A. J.

Investigation of Age-Related Cognitive Decline Using Mice as a Model System: Neurophysiological Correlates

From the Departments of Neurobiology, Psychology, Psychiatry and Brain Research Institute, University of California, Los Angeles, Los Angeles, CA (GGM, AJS); and the Department of Pharmacology, University of Iowa, Iowa City, IA (VS, JWH).

Objective: Learning and memory impairments without overt pathology often accompany advancing age. To gain a better understanding of the underlying neuronal substrates associated with this age-related cognitive decline, the authors have begun to use mice as an animal model system. As described in the companion paper, mice exhibit age-related impairments in cognition. Here, the authors explore the possibility that age-related changes in neuronal function may be the result of deregulation of cytosolic free calcium homeostasis.

Methods: Calcium homeostasis in young and aged mice was examined by measuring the slow afterhyperpolarization (sAHP) in hippocampal neurons as well as assessing voltage-dependent calcium channel mediated long-term potentiation (vdccLTP). In addition, putative changes in phosphorylation of the L-type channel Ca_V1.2 by cAMP-dependent protein kinase were examined.

Results: Both neurophysiological measures of calcium homeostasis indicated an increase in activity-dependent calcium influx. This increase was not the result of an age-related increase in phosphorylation of the L-type channel Ca_V1.2 by cAMP-dependent protein kinase.

Conclusions: Like in other areas of biomedical research, mice have become an invaluable research tool in the investigation of learning and memory. It is expected that similar benefits can be realized by developing mouse models for age-related cognitive decline.

Key Words: Mice • learning and memory • aging • calcium • synaptic plasticity

This article has been cited by other articles:

				D. J. Smith From Depression to Where Are My Keys: Unlocking the Behavioral Disorders of Old Age Am J Geriatr Psychiatry, December 1, 2006; 14(12): 989 - 992. [Full Text] [PDF]

				G. G. Murphy, N. P. Rahnama, and A. J. Silva Investigation of Age-Related Cognitive Decline Using Mice as a Model System: Behavioral Correlates Am J Geriatr Psychiatry, December 1, 2006; 14(12): 1004 - 1011. [Abstract] [Full Text] [PDF]