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TGF-1-Induced Long-Term Changes in Neuronal Excitability in Aplysia Sensory Neurons Depend on MAPK

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

Submitted 20 July 2005; accepted in final form 18 January 2006

Transforming growth factor beta-1 (TGF-1) plays important roles in the early development of the nervous system and has been implicated in neuronal plasticity in adult organisms. It induces long-term increases in sensory neuron excitability in Aplysia as well as a long-term enhancement of synaptic efficacy at sensorimotor synapses. In addition, TGF-1 acutely regulates synapsin phosphorylation and reduces synaptic depression induced by low-frequency stimuli. Because of the critical role of MAPK in other forms of long-term plasticity in Aplysia, we examined the role of MAPK in TGF-1-induced long-term changes in neuronal excitability. Prolonged (6 h) exposure to TGF-1 induced long-term increases in excitability. We confirmed this finding and now report that exposure to TGF-1 was sufficient to activate MAPK and increase nuclear levels of active MAPK. Moreover, TGF-1 enhanced phosphorylation of the Aplysia transcriptional activator cAMP response element binding protein (CREB)1, a homologue to vertebrate CREB. Both the TGF-1-induced long-term changes in neuronal excitability and the phosphorylation of CREB1 were blocked in the presence of an inhibitor of the MAPK cascade, confirming a role for MAPK in long-term modulation of sensory neuron function.

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