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The Journal of Neuroscience, July 23, 2003, 23(16):6617-6626

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Identification of Upregulated SCG10 mRNA Expression Associated with Late-Phase Long-Term Potentiation in the Rat Hippocampal Schaffer-CA1 Pathway In Vivo

Haixiang Peng, Brian E. Derrick, and Joe L. Martinez, Jr

Cajal Neuroscience Institute, Department of Biology, University of Texas, San Antonio, Texas 78249-0662

The maintenance of long-term potentiation (LTP) depends on alteration of gene transcription. By screening a subtracted cDNA library that is enriched in upregulated transcripts in rat hippocampus 3 hr after Schaffer-CA1 LTP induction in vivo, we identified a neural growth-associated protein SCG10 (superior cervical ganglia clone 10) gene. The semiquantitative reverse transcription-PCR and Northern blot experiments confirmed that SCG10 mRNA levels were elevated in tetanized rat hippocampi compared with those of sham controls that received only low-frequency stimulation. Both 1 and 2 kb forms of SCG10 mRNAs contributed to the increased expression. Using a riboprobe with a sequence specific to the 3'-untranslated region of rat SCG10 mRNA, in situ hybridization further revealed a significant increase of the SCG10 mRNA 2 kb form in the ipsilateral CA3 and CA1 regions of LTP animals. In addition, we systemically injected the competitive NMDA receptor antagonist D,L-3[(±)-2-carboxypiperazine-4-yl]-propyl-1-phosphonic acid (CPP) to determine whether the alteration of SCG10 expression depends on NMDA receptor activation or tetanus alone. Administration of CPP 1 hr before tetanus completely blocked LTP induction and the increase of SCG10 mRNA levels. Thus, these results suggest that the transcription of SCG10 in vivo is regulated by long-lasting synaptic activity and may contribute to the maintenance of long-term synaptic plasticity via a presynaptic remodeling mechanism.

Key words: long-term potentiation; SCG10; gene expression; transcription; hippocampus; synaptic plasticity; NMDA receptor; CA1; CA3; neural growth-associated protein

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Received Oct. 28, 2002; revised May. 29, 2003; accepted May. 29, 2003.

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