title: Photolysis of postsynaptic caged Ca2+ can potentiate and depress mossy fiber synaptic responses in rat hippocampal CA3 pyramidal neurons.
abstract: 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 microm 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.
authors.affiliation: Department of Molecular and Cell Biology, University of California, Berkeley, California 94720, USA.
authors.forename: Jun
authors.initials: J
authors.lastname: Wang
authors.forename: Mark F
authors.initials: MF
authors.lastname: Yeckel
authors.forename: Daniel
authors.initials: D
authors.lastname: Johnston
authors.forename: Robert S
authors.initials: RS
authors.lastname: Zucker
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D000927:Anticonvulsants / Q000494:pharmacology; D052160:Benzothiazoles; D002118:Calcium / Q000378:metabolism*; D003374:Coumarins / Q000378:metabolism; D003521:Cyclopropanes / Q000494:pharmacology; D016572:Cyclosporine / Q000494:pharmacology; D004558:Electric Stimulation / Q000379:methods; D004791:Enzyme Inhibitors / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000502:physiology; D005998:Glycine / Q000031:analogs & derivatives* / Q000378:metabolism / Q000494:pharmacology; D006624:Hippocampus / Q000166:cytology* / Q000502:physiology; D066298:In Vitro Techniques; D017774:Long-Term Potentiation / Q000502:physiology / Q000528:radiation effects; D036881:Long-Term Synaptic Depression / Q000502:physiology* / Q000528:radiation effects; D008387:Marine Toxins; D019599:Mossy Fibers, Hippocampal / Q000502:physiology* / Q000528:radiation effects; D010080:Oxazoles / Q000494:pharmacology; D018408:Patch-Clamp Techniques / Q000379:methods; D010782:Photolysis; D017966:Pyramidal Cells / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013569:Synapses / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology
chemical_list: D000927:Anticonvulsants; D052160:Benzothiazoles; D003374:Coumarins; D003521:Cyclopropanes; D004791:Enzyme Inhibitors; D008387:Marine Toxins; C116748:N-(3-(2-benzothiazolyl)-6-(2-(2-(bis(carboxymethyl)amino)-5-methylphenoxy)ethoxy)-2-oxo-2H-1-benzopyran-7-yl)-N-(carboxymethyl)glycine; D010080:Oxazoles; C082313:2-(2,3-dicarboxycyclopropyl)glycine; C059041:calyculin A; D016572:Cyclosporine; D002118:Calcium; D005998:Glycine