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Published Online
on April 24, 2002

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The Journal of Neuroscience, 2002, 22:RC220:1-6

RAPID COMMUNICATION
Transforming Growth Factor 1 Alters Synapsin Distribution and Modulates Synaptic Depression in Aplysia

J. Chin¹, A. Angers¹, L. J. Cleary¹, A. Eskin², and J. H. Byrne¹

¹ Department of Neurobiology and Anatomy, W. M. Keck Center for the Neurobiology of Learning and Memory, University of Texas-Houston Medical School, Houston, Texas 77030, and ² Department of Biology and Biochemistry, University of Houston, Houston, Texas 77204

Transforming growth factor 1 (TGF-1) induces long-term synaptic facilitation and long-term increases in excitability in Aplysia. Here we report that this growth factor has acute effects as well. Treatment of pleural-pedal ganglia with TGF-1 for 5 min activated mitogen-activated protein kinase (MAPK) and stimulated the phosphorylation of synapsin in a MAPK-dependent manner. This phosphorylation appeared to modulate synapsin distribution in cultured sensory neurons. Control neurons exhibited a punctate distribution of synapsin along neurites, which appeared to represent high concentration aggregates of synapsin. TGF-1-treated sensory neurons showed a significant reduction in the number of these puncta, an effect that was blocked by the MAP/ERK kinase inhibitor U0126. The functional consequence of TGF-1 was tested by examining its effects on synaptic transmission at the sensorimotor synapse. Application of TGF-1 reduced the magnitude of synaptic depression. This effect was dependent on MAPK, consistent with the hypothesis that TGF-1 mobilizes synaptic vesicles through the phosphorylation of synapsin.

Key words: synapsin; Aplysia; TGF-1; synaptic depression; short-term plasticity; mobilization; phosphorylation; synaptic vesicles; MAPK

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Copyright © Society for Neuroscience  0270-6474//$05.00/0

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