Christopher M. Norris, Ph.D.
Assistant Professor
University of Virginia, 1998
Office: 131 Sanders-Brown Center on Aging (0230)
Lab: (859) 257-1412 Ext. 246
Tel: (859) 257-1412 Ext. 249
The ultimate goal of our work is to identify causal mechanisms for deteriorating neural and cognitive function associated with aging and Alzheimer's Disease (AD). Our particular interest is in Ca2+ signaling mechanisms, including Ca2+ channels and Ca2+ dependent second messengers, such as the multifunctional Ca2+/calmodulin-dependent protein phosphatase, calcineurin. Our work, and work by others, indicates that calcineurin activity is increased during aging and linked to several bio-markers of cognitive decline including altered synaptic plasticity, increased voltage-sensitive Ca2+ channel function, astrocyte activation, and upregulation of gene expression programs involved in immune/inflammatory signaling. As such, one of our major projects is directed at reversing, or limiting the neural and cognitive changes that result from aging and AD by targeting calcineurin-dependent signaling pathways.
Selected Publications
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Sama MA, Mathis DM, Furman JL, Artiushin IA, Mohmmad Abdul H, Kraner SD, Norris CM (2008)
Interleukin-1-dependent signaling between glia and neurons depends critically on astrocytic calcineurin/NFAT activity Journal of Biological Chemistry, in press.
Norris CM, Blalock EM, Chen K-C, Porter, NM, Thibault O, Kraner SD, Landfield PW (2008)
Hippocampal 'zipper' slice studies reveal a necessary role for calcineurin in the increased activity of L-type Ca2+ channels with aging Neurobiology of Aging, in press.
Jeftinija DM, Hebert SL, Norris CM, Wang QB, Rich MM, Kraner SD (2007)
The CaV 1.2 Ca2+ channel is expressed in the sarcolemma of type I and IIa skeletal muscle fibers. Muscle and Nerve, 36: 482-490.
Norris CM*, Blalock EM*, Thibault O, Brewer LD, Clodfelter GV, Porter NM, Landfield PW (2006)
Electrophysiological Mechanisms of Delayed Excitotoxicity: Positive Feedback Loop Between NMDA Receptor Current and Depolarization-Mediated Glutamate Release.
Journal of Neurophysiology 96:2488-2500.
*authors contributed equally
Norris CM, Kadish I, Blalock EM, Chen KC, Thibault V, Porter NM, Landfield PW, and Kraner SD (2005)
Calcineurin Triggers Reactive/Inflammatory Processes in
Astrocytes and is Upregulated in Aging and Alzheimer's Models.
The Journal of Neuroscience 25:4649-4658.
Norris CM, Blalock EM, Porter, NM, Chen, K-C, Landfield PW (2002)
Calcineurin enhances L-type Ca2+ channel activity in hippocampal neurons: Increased
effect with age in culture.
Neuroscience.110:213-225.
Foster TC, Sharrow KM, Masse JR, Norris CM, Kumar A (2001)
Calcineurin links Ca2+ dysregulation with brain aging.
The Journal of Neuroscience 21:4066-4073.
Norris CM, Halpain S, Foster TC (1998)
Alterations in the balance of protein kinase/phosphatase activities parallel reduced synaptic strength during aging.
Journal of Neurophysiology 80:1567-1570.
Norris CM, Halpain S, Foster TC (1998)
Reversal of age-related alterations in synaptic plasticity by blockade of L-type Ca2+ channels.
The Journal of Neuroscience 18:3171-3179.
Norris CM, Korol DL, Foster TC (1996)
Increased susceptibility to induction of long- term depression and long-term potentiation reversal during aging.
The Journal of Neuroscience 16:5382-5392.
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