Physiological and Pathological Actions of Calpains in Glutamatergic Neurons

Sci. Signal., 10 June 2008
Vol. 1, Issue 23, p. tr3
DOI: 10.1126/scisignal.123tr3

Physiological and Pathological Actions of Calpains in Glutamatergic Neurons

  1. Jing Liu1,*,
  2. Ming Cheng Liu2,3, and
  3. Kevin K. W. Wang1,2,3,*
  1. 1Center for Neuroproteomics and Biomarkers Research, Department of Psychiatry, McKnight Brain Institute, Post Office Box 100256, University of Florida, Gainesville, FL 32610, USA.
  2. 2Center for Traumatic Brain Injury Studies, Department of Neuroscience, McKnight Brain Institute, Post Office Box 100256, University of Florida, Gainesville, FL 32610, USA.
  3. 3Center of Innovative Research, Banyan Biomarkers, Incorporated, 12085 Research Drive, Alachua, FL 32615, USA.
  1. *Corresponding authors.

    E-mail: jingl{at}ufl.edu; kwang{at}banyanbio.com

Abstract

These animations show the activation and actions of neuronal calpains under physiological and pathophysiological conditions. They emphasize how physiological events involved in excitatory neurotransmission and synaptic plasticity—such as glutamate release, calcium influx, and activation of postsynaptic calpains—can become destructive under pathological conditions. These animations would be useful in a neurobiology or neuroscience course, where they could be used to illustrate proteolytic mechanisms underling activity-dependent synaptic plasticity, and how excessive activation of these signaling mechanisms can lead to excitotoxic neuronal death.

Citation:

J. Liu, M. C. Liu, and K. K. Wang, Physiological and Pathological Actions of Calpains in Glutamatergic Neurons. Sci. Signal. 1, tr3 (2008).

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