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@ARTICLE{Fai:281864,
      author       = {Faiß, Lukas and Salivara, Aikaterini and Oldani, Silvia
                      and Breustedt, Jörg and Schmitz, Dietmar and Rost, Benjamin
                      R},
      title        = {{H}ippocampal {C}ommissural {C}ircuitry {S}hows
                      {A}symmetric c{AMP}-{D}ependent {S}ynaptic {P}lasticity.},
      journal      = {ACS chemical neuroscience},
      volume       = {16},
      number       = {21},
      issn         = {1948-7193},
      address      = {Washington, DC},
      publisher    = {ACS Publ.},
      reportid     = {DZNE-2025-01237},
      pages        = {4236 - 4245},
      year         = {2025},
      abstract     = {Hemispheric asymmetries in NMDAR-dependent synaptic
                      plasticity have been described in hippocampal area CA1, but
                      it remains unclear whether similar lateralized mechanisms
                      exist for cyclic adenosine monophosphate (cAMP)-dependent
                      plasticity. Here, we investigated whether cAMP-mediated
                      potentiation of synaptic transmission in mouse CA1 exhibits
                      hemisphere-specific properties. In recordings with
                      electrical stimulation of CA1 inputs, a subset of recordings
                      in the left, but not in the right hemisphere CA1, exhibited
                      a pronounced cAMP-induced potentiation of field excitatory
                      postsynaptic potentials (fEPSPs). To isolate input-specific
                      contributions, we expressed the optogenetic actuator
                      ChrimsonR unilaterally in the CA3/CA2 region of wild-type
                      mice. Light-evoked glutamate release from ipsilateral
                      Schaffer collaterals showed no cAMP sensitivity in either
                      hemisphere, while commissures originating from the right
                      (COR) exhibited cAMP-mediated potentiation of transmission
                      in a subset of experiments. Notably, this effect was absent
                      at commissures originating from the left (COL). The
                      selective presence of the effect prompted us to further
                      investigate the underlying cell population using
                      CA3-specific (G32-4 Cre) and CA2-specific (Amigo2-Cre)
                      driver lines. Recordings from synapses of CA3 COR
                      recapitulated the cAMP-induced potentiation of transmitter
                      release observed in wild-type animals. However, the effect
                      was again restricted to a subset of experiments, did not
                      correlate with the age or the sex of the mice, and was
                      absent in recordings with specific stimulation of CA2 COR.
                      Our results demonstrate a variable cAMP sensitivity of
                      synaptic transmission at COR synapses in the left CA1.
                      Altogether, we reveal a hemisphere-specific cAMP-mediated
                      synaptic plasticity at CA3 COR onto CA1, underscoring hidden
                      heterogeneity and lateralization in hippocampal circuit
                      function.},
      keywords     = {Animals / Neuronal Plasticity: physiology / Cyclic AMP:
                      metabolism / Mice / Excitatory Postsynaptic Potentials:
                      physiology / Male / Hippocampus: physiology / Hippocampus:
                      metabolism / CA1 Region, Hippocampal: physiology / CA1
                      Region, Hippocampal: metabolism / Mice, Inbred C57BL /
                      Synaptic Transmission: physiology / CA3 Region, Hippocampal:
                      physiology / Mice, Transgenic / Functional Laterality:
                      physiology / cAMP (Other) / commissural fibers (Other) /
                      hippocampus (Other) / lateralization (Other) / synaptic
                      plasticity (Other) / Cyclic AMP (NLM Chemicals)},
      cin          = {AG Schmitz},
      ddc          = {540},
      cid          = {I:(DE-2719)1810004},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41081426},
      doi          = {10.1021/acschemneuro.5c00454},
      url          = {https://pub.dzne.de/record/281864},
}