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@ARTICLE{Tascio:282573,
      author       = {Tascio, Dario and Gebril, Nehal and Jabs, Ronald and
                      Henneberger, Christian and Steinhäuser, Christian and
                      Seifert, Gerald},
      title        = {{AMPA} {R}eceptors in {NG}2 {G}lia {D}ifferently {A}ffect
                      {S}ignal {T}ransduction in the {H}ippocampus and
                      {C}erebellum.},
      journal      = {Glia},
      volume       = {74},
      number       = {2},
      issn         = {0894-1491},
      address      = {Bognor Regis [u.a.]},
      publisher    = {Wiley-Liss},
      reportid     = {DZNE-2025-01333},
      pages        = {e70107},
      year         = {2026},
      abstract     = {Gray matter NG2 glia constitute a heterogeneous population
                      of cells whose functions remain incompletely understood. In
                      the hippocampus, Schaffer collaterals activate AMPA
                      receptors (AMPARs) in NG2 glia, giving rise to small
                      excitatory post-synaptic currents (EPSCs). Climbing fibers
                      of the cerebellum also form synapses with NG2 glia, although
                      producing much larger EPSCs. We aimed to identify mechanisms
                      generating these regional differences in the efficacy of
                      neuron-glia synapses. Combined patch-clamp and RT-PCR
                      analyses allowed for determining structural and functional
                      differences of AMPARs expressed by the glial cells.
                      Comparing pharmacological and molecular data in both regions
                      revealed stronger expression of Ca2+ permeable AMPARs in
                      cerebellar NG2 glia. Different expression patterns were
                      found both for AMPAR subunits and their auxiliary proteins.
                      Moreover, experiments using the low-affinity AMPAR
                      antagonist γ-DGG pointed towards higher synaptic glutamate
                      concentrations at cerebellar synapses, likely due to
                      multivesicular release, which contributed to enhanced
                      synaptic efficacy. Finally, we examined short-term
                      plasticity and showed that pre- and postsynaptic mechanisms
                      contributed to paired-pulse depression at climbing fiber-NG2
                      glia synapses. Together, our data provide new insights into
                      the molecular and functional specialization of NG2 glia and
                      improve our understanding of the mechanisms underlying
                      neuron-glia synaptic signaling, by highlighting how
                      region-specific differences in AMPAR composition and
                      presynaptic release properties shape this communication in
                      the central nervous system.},
      keywords     = {Animals / Cerebellum: cytology / Cerebellum: metabolism /
                      Cerebellum: physiology / Receptors, AMPA: metabolism /
                      Receptors, AMPA: genetics / Neuroglia: metabolism /
                      Neuroglia: physiology / Neuroglia: drug effects /
                      Hippocampus: cytology / Hippocampus: metabolism /
                      Hippocampus: physiology / Signal Transduction: physiology /
                      Signal Transduction: drug effects / Excitatory Postsynaptic
                      Potentials: physiology / Excitatory Postsynaptic Potentials:
                      drug effects / Synapses: physiology / Mice, Inbred C57BL /
                      Male / Rats / Patch-Clamp Techniques / Mice / Antigens /
                      Proteoglycans / AMPA receptor (Other) / NG2 glia (Other) /
                      cerebellum (Other) / hippocampus (Other) / patch clamp
                      (Other) / subunit composition (Other) / Receptors, AMPA (NLM
                      Chemicals) / chondroitin sulfate proteoglycan 4 (NLM
                      Chemicals) / Antigens (NLM Chemicals) / Proteoglycans (NLM
                      Chemicals)},
      cin          = {AG Henneberger},
      ddc          = {610},
      cid          = {I:(DE-2719)1013029},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41331743},
      pmc          = {pmc:PMC12672973},
      doi          = {10.1002/glia.70107},
      url          = {https://pub.dzne.de/record/282573},
}