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The Journal of Neuroscience, September 1, 2004, 24(35):7740-7744; doi:10.1523/JNEUROSCI.1796-04.2004

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The Type IV-Specific Phosphodiesterase Inhibitor Rolipram and Its Effect on Hippocampal Long-Term Potentiation and Synaptic Tagging

Sheeja Navakkode, Sreedharan Sajikumar, and Julietta Uta Frey

Leibniz Institute for Neurobiology, Department of Neurophysiology, D-39118 Magdeburg, Germany

We investigated the effects of rolipram, a selective cAMP phosphodiesterase (PDE) inhibitor, on late plastic events during functional CA1 plasticity in vitro in rat hippocampal slices. We present data showing that an early form of long-term potentiation (LTP) (early-LTP) that normally decays within 2-3 hr can be converted to a lasting LTP (late-LTP) if rolipram is applied during tetanization. This rolipram-reinforced LTP (RLTP) was NMDA receptor and protein synthesis dependent. cAMP formation in region CA1 during late-LTP requires dopaminergic receptor activity (Frey et al., 1989, 1990). Thus, we studied whether RLTP was influenced by inhibitors of the D₁/D₅ receptor. Application of the specific D₁/D₅ antagonist SCH23390(0.1 µM) did not prevent RLTP, suggesting that the phosphodiesterase inhibitor acts downstream of the D₁/D₅ receptors. We also studied whether rolipram can interact with processes of synaptic tagging, because RLTP was also dependent on protein synthesis, similar to late-LTP. Inhibition of PDE and subsequent induction of RLTP in one synaptic population were able to transform early-LTP into late-LTP in a second, independent synaptic population of the same neurons. This supports our hypothesis that cAMP-dependent processes are directly involved in the synthesis of plasticity-related proteins.

Key words: rolipram-reinforced LTP (RLTP); synaptic tagging; protein synthesis; long-term potentiation; functional plasticity; phosphodiesterases

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Received May 10, 2004; revised July 8, 2004; accepted July 13, 2004.

This article has been cited by other articles:

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