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The Journal of Neuroscience, March 16, 2005, 25(11):2832-2837; doi:10.1523/JNEUROSCI.4260-04.2005

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BRIEF COMMUNICATION
The Role of Extracellular Adenosine in Regulating Mossy Fiber Synaptic Plasticity

Maria Kukley,¹ Maximilian Schwan,¹ Bertil B. Fredholm,² and Dirk Dietrich¹

¹Department of Neurosurgery, University Clinic Bonn, D-53105 Bonn, Germany, and ²Department of Physiology and Pharmacology, Karolinska Institutet, S-17177 Stockholm, Sweden

Hippocampal mossy fiber synapses show unique molecular features and dynamic range of plasticity. A recent paper proposed that the defining features of mossy fiber synaptic plasticity are caused by a local buildup of extracellular adenosine (Moore et al., 2003). In this study, we reassessed the role of ambient adenosine in regulating mossy fiber synaptic plasticity in mouse and rat hippocampal slices. Synaptic transmission was highly sensitive to activation of presynaptic adenosine A₁ receptors (A₁Rs), which reduced transmitter release by >75%. However, most of A₁Rs were not activated by ambient adenosine. Field potentials increased only by 20-30% when A₁Rs were fully blocked with the A₁R antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) (1 µM). Moreover, blocking A₁Rs hardly altered paired-pulse facilitation, frequency facilitation, or posttetanic potentiation. Frequency facilitation was similar in A₁R^-/- mice and when measured with NMDA receptor-mediated EPSCs in CA3 pyramidal cells in the presence of DPCPX. Additional experiments suggested that the results obtained by Moore et al. (2003) can partially be explained by their usage of a submerged recording chamber and elevated divalent cation concentrations. In conclusion, a reduction of the basal release probability by ambient adenosine does not underlie presynaptic forms of plasticity at mossy fiber synapses.

Key words: CA3; granule cells; synaptic transmission; hippocampus; interface chamber; submerged chamber; high divalent cation concentration

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Received Oct 13, 2004; revised January 28, 2005; accepted January 30, 2005.

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