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Photolysis of Postsynaptic Caged Ca²⁺ Can Potentiate and Depress Mossy Fiber Synaptic Responses in Rat Hippocampal CA3 Pyramidal Neurons

¹ Department of Molecular and Cell Biology, University of California, Berkeley, California 94720; ² Department of Neurobiology, Yale University School of Medicine, New Haven, Connecticut 06520; ³ Division of Neuroscience, Baylor College of Medicine, Houston, Texas 77030

Submitted 4 November 2003; accepted in final form 22 November 2003

The induction of mossy fiber-CA3 long-term potentiation (LTP) and depression (LTD) has been variously described as being dependent on either pre- or postsynaptic factors. Some of the postsynaptic factors for LTP induction include ephrin-B receptor tyrosine kinases and a rise in postsynaptic Ca²⁺ ([Ca²⁺]_i). Ca²⁺ is also believed to be involved in the induction of the various forms of LTD at this synapse. We used photolysis of caged Ca²⁺ compounds to test whether a postsynaptic rise in [Ca²⁺]_i is sufficient to induce changes in synaptic transmission at mossy fiber synapses onto rat hippocampal CA3 pyramidal neurons. We were able to elevate postsynaptic [Ca²⁺]_i to approximately 1 µm for a few seconds in pyramidal cell somata and dendrites. We estimate that CA3 pyramidal neurons have approximately fivefold greater endogenous Ca²⁺ buffer capacity than CA1 neurons, limiting the rise in [Ca²⁺]_i achievable by photolysis. This [Ca²⁺]_i rise induced either a potentiation or a depression at mossy fiber synapses in different preparations. Neither the potentiation nor the depression was accompanied by consistent changes in paired-pulse facilitation, suggesting that these forms of plasticity may be distinct from synaptically induced LTP and LTD at this synapse. Our results are consistent with a postsynaptic locus for the induction of at least some forms of synaptic plasticity at mossy fiber synapses.

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