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J Neurophysiol 89: 1177-1186, 2003. First published November 13, 2002; doi:10.1152/jn.00504.2002
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J Neurophysiol (March 1, 2003). 10.1152/jn.00504.2002
Submitted on Submitted 2 July 2002; accepted in final form 10 November 2002

TRANSLATIONAL PHYSIOLOGY

A Role for Myotonic Dystrophy Protein Kinase in Synaptic Plasticity

Paul E. Schulz,1,2,5 Adeka D. McIntosh,1 Michael R. Kasten,1,2 Berend Wieringa,4 and Henry F. Epstein1,2,3

 1Department of Neurology,  2Division of Neuroscience, and  3Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, Texas 77030;  4Department of Cell Biology and Histology, University of Nijmegen, 6500 HB Nijmegen, The Netherlands; and  5The Houston VA Hospital Neurology Service

Schulz, Paul E., Adeka D. McIntosh, Michael R. Kasten, Berend Wieringa, and Henry F. Epstein. A Role for Myotonic Dystrophy Protein Kinase in Synaptic Plasticity. J. Neurophysiol. 89: 1177-1186, 2003. Myotonic dystrophy (DM) is associated with an expanded triplet repeat in the 3'-untranslated region of the gene for myotonic dystrophy protein kinase (DMPK), which may reduce DMPK expression. It is unclear how reduced DMPK expression might contribute to the symptoms of DM because the normal function of DMPK is not yet understood. Thus we investigated the function of DMPK to gain insight into how reduced DMPK expression might lead to cognitive dysfunction in DM. We recently demonstrated a role for DMPK in modifying the cytoskeleton, and remodeling of the cytoskeleton is thought to be important for cognitive function. Therefore we hypothesized that DMPK might normally contribute to synaptic plasticity and cognitive function via an effect on actin cytoskeletal rearrangements. To test for involvement of DMPK in synaptic plasticity, we utilized the DMPK null mouse. This mouse showed no changes in baseline synaptic transmission in hippocampal area CA1, nor any changes in long-term synaptic potentiation (LTP) measured 3 h after induction. There was a significant decrease, however, in the decremental potentiation with a duration of 30-180 min that accompanies LTP. These results suggest a role for DMPK in synaptic plasticity that could be relevant to the cognitive dysfunction associated with DM.




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