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The Journal of Neuroscience, January 3, 2007, 27(1):84-92; doi:10.1523/JNEUROSCI.4385-06.2007

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Development/Plasticity/Repair
Synaptic Protein Dynamics in Hibernation

Christina G. von der Ohe,¹ Craig C. Garner,³ Corinna Darian-Smith,² and H. Craig Heller¹

Departments of ¹Biological Sciences, ²Comparative Medicine, and ³Psychiatry and Behavioral Sciences, Stanford University, Stanford, California 94305

Correspondence should be addressed to Christina G. von der Ohe, Department of Biological Sciences, Stanford University, Stanford, CA 94305-5020. Email: vonderohe{at}stanford.edu

Neurons in hibernating mammals exhibit a dramatic form of plasticity during torpor, with dendritic arbors retracting as body temperature cools and then regrowing rapidly as body temperature rises. In this study, we used immunohistochemical imaging and Western blotting of several presynaptic and postsynaptic proteins to determine the synaptic changes that accompany torpor and to investigate the mechanisms behind these changes. We show torpor-related alterations in synaptic protein localization that occur rapidly and uniformly across several brain regions in a temperature-dependent manner. Entry into torpor is associated with a 50–65% loss of synapses, as indicated by changes in the extent of colocalization of presynaptic and postsynaptic markers. We also show that the loss of synaptic protein clustering occurring during entry into torpor is not attributable to protein loss. These findings suggest that torpor-related changes in synapses stem from dissociation of proteins from the cytoskeletal active zone and postsynaptic density, creating a reservoir of proteins that can be quickly mobilized for rapid rebuilding of dendritic spines and synapses during the return to euthermia. A mechanism of neural plasticity based on protein dissociation rather than protein breakdown could explain the hibernator's capacity for large, rapid, and repeated microstructural changes, providing a fascinating contrast to neuropathologies that are dominated by protein breakdown and cell death.

Key words: synapse; protein; hibernation; torpor; temperature; plasticity

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Received July 6, 2006; revised Nov. 16, 2006; accepted Nov. 21, 2006.

Correspondence should be addressed to Christina G. von der Ohe, Department of Biological Sciences, Stanford University, Stanford, CA 94305-5020. Email: vonderohe{at}stanford.edu

This article has been cited by other articles:

				C. Darian-Smith Synaptic Plasticity, Neurogenesis, and Functional Recovery after Spinal Cord Injury Neuroscientist, April 1, 2009; 15(2): 149 - 165. [Abstract] [PDF]

				D. Turina, V. M. Loitto, K. Bjornstrom, T. Sundqvist, and C. Eintrei Propofol causes neurite retraction in neurones Br. J. Anaesth., September 1, 2008; 101(3): 374 - 379. [Abstract] [Full Text] [PDF]

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