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@ARTICLE{Arboit:281504,
      author       = {Arboit, Alberto and Krautwald, Karla and Angenstein, Frank},
      title        = {{A}cetaminophen affects the duration but not the occurrence
                      of {BOLD} signal decline in the dorsal hippocampus after
                      induction of neuronal afterdischarges.},
      journal      = {Imaging neuroscience},
      volume       = {3},
      issn         = {2837-6056},
      address      = {Cambridge, MA},
      publisher    = {MIT Press},
      reportid     = {DZNE-2025-01125},
      pages        = {IMAG.a.161},
      year         = {2025},
      abstract     = {Combined in vivo electrophysiological and functional
                      magnetic resonance imaging (fMRI) measurements were used to
                      monitor neuronal and hemodynamic responses in the right
                      dorsal hippocampus during and after electrical stimulation
                      of the right perforant pathway with a short period of 20 Hz
                      pulses. These measurements were performed under two
                      conditions: $1.5\%$ isoflurane (which has a long-term
                      vasodilator effect) or 100 µg/kg medetomidine (which has a
                      long-term vasoconstrictor effect). The stimulation elicited
                      a short period of neuronal afterdischarges (nAD) followed by
                      a sustained decline in fMRI BOLD signals, as previously
                      described (Arboit et al., 2024). While the duration of nAD
                      was similar in presence of isoflurane and medetomidine, the
                      subsequent decline of BOLD signal was significantly longer
                      with isoflurane than with medetomidine. However, when the
                      same experiments were performed in the presence of
                      acetaminophen, the duration of the sustained decline of BOLD
                      signals became similar: acetaminophen significantly
                      prolonged the decline in the presence of medetomidine,
                      whereas it only slightly shortened it in the presence of
                      isoflurane. As acetaminophen did not affect the generation
                      and intensity of nAD, the results indicate that nAD
                      activates at least two different neurovascular coupling
                      (NVC) mechanisms that mediate the sustained BOLD signal
                      decline, of which acetaminophen affects the maintenance.},
      keywords     = {BOLD-fMRI (Other) / dentate gyrus (Other) / in vivo
                      electrophysiology (Other) / negative BOLD response (Other) /
                      neurovascular coupling (Other)},
      cin          = {AG Angenstein},
      ddc          = {610},
      cid          = {I:(DE-2719)1310004},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40995462},
      pmc          = {pmc:PMC12455054},
      doi          = {10.1162/IMAG.a.161},
      url          = {https://pub.dzne.de/record/281504},
}