Physiological and pathological actions of calpains in glutamatergic neurons.
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.
Liu
Jing
J
Center for Neuroproteomics and Biomarkers Research, Department of Psychiatry, McKnight Brain Institute, Post Office Box 100256, University of Florida, Gainesville, FL 32610, USA. jingl@ufl.edu
Liu
Ming Cheng
MC
Wang
Kevin K W
KK
D000818:Animals; D002154:Calpain / Q000502:physiology*; D016923:Cell Death; D018698:Glutamic Acid / Q000502:physiology*; D006801:Humans; D009411:Nerve Endings / Q000502:physiology; D009473:Neuronal Plasticity; D009474:Neurons / Q000473:pathology / Q000502:physiology*; D013569:Synapses / Q000502:physiology; D009435:Synaptic Transmission
D018698:Glutamic Acid; D002154:Calpain