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The Journal of Neuroscience, June 14, 2006, 26(24):6439-6449; doi:10.1523/JNEUROSCI.1844-06.2006

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Development/Plasticity/Repair
Synaptogenesis Regulates Axotomy-Induced Activation of c-Jun–Activator Protein-1 Transcription

Ying-Ju Sung,¹ Fang Wu,² Samuel Schacher,² and Richard T. Ambron¹

¹Department of Anatomy and Cell Biology and ²Center for Neurobiology and Behavior, New York State Psychiatric Institute, Columbia University College of Physicians and Surgeons, New York, New York 10032

Correspondence should be addressed to Ying-Ju Sung, Department of Anatomy and Cell Biology, Columbia University College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032. Email: yjs8{at}columbia.edu

The activator protein-1 (AP1) transcription complex remains active for long periods after axotomy, but its activity diminishes during target contact. This raises the possibility that the function of this complex is regulated by the synaptic connections. Using Aplysia californica, we found that crushing peripheral nerves in vivo enhanced AP1 binding in the sensory neurons that lasted for weeks and then declined as regeneration was completed. The AP1 complex in Aplysia is a c-Jun homodimer. Its activation, after axotomy, is mediated by Aplysia c-Jun–N-terminal kinase (apJNK), which enters the nucleus of sensory neurons and phosphorylates c-Jun at Ser-73 (p73-c-Jun). Active AP1 in the sensory neurons did not mediate apoptosis and was not involved in the appearance of the long-term hyperexcitability that develops in these cells after axotomy, and blocking the activation of apJNK in vitro did not influence neurite outgrowth. In contrast, the levels of activated apJNK and p73-c-Jun declined markedly when sensory neurons formed synapses with motor neuron L7 in vitro. Furthermore, inhibiting the pathway accelerated synaptogenesis between sensory neurons and L7. These data suggest that positive and negative modulation of the JNK–c-Jun–AP1 pathway functions in alerting the nucleus to the loss and gain of synapses, respectively.

Key words: nerve injury; signal transduction pathway; regeneration; synapse formation; sensory neurons; synaptic plasticity

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Received Oct. 17, 2005; accepted May 2, 2006.

Correspondence should be addressed to Ying-Ju Sung, Department of Anatomy and Cell Biology, Columbia University College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032. Email: yjs8{at}columbia.edu

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