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@ARTICLE{Arboit:163678,
      author       = {Arboit, Alberto and Ku, Shih-Pi and Krautwald, Karla and
                      Angenstein, Frank},
      title        = {{B}rief neuronal afterdischarges in the rat hippocampus
                      lead to transient changes in oscillatory activity and to a
                      very long-lasting decline in {BOLD} signals without inducing
                      a hypoxic state.},
      journal      = {NeuroImage},
      volume       = {245},
      issn         = {1053-8119},
      address      = {Orlando, Fla.},
      publisher    = {Academic Press},
      reportid     = {DZNE-2022-00424},
      pages        = {118769},
      year         = {2021},
      abstract     = {The effects of hippocampal neuronal afterdischarges (nAD)
                      on hemodynamic parameters, such as
                      blood-oxygen-level-dependent (BOLD) signals) and local
                      cerebral blood volume (CBV) changes, as well as neuronal
                      activity and metabolic parameters in the dentate gyrus, was
                      investigated in rats by combining in vivo electrophysiology
                      with functional magnetic resonance imaging (fMRI) or
                      1H-nuclear magnetic resonance spectroscopy (1H-NMRS). Brief
                      electrical high-frequency pulse-burst stimulation of the
                      right perforant pathway triggered nAD, a seizure-like
                      activity, in the right dentate gyrus with a high incidence,
                      a phenomenon that in turn caused a sustained decrease in
                      BOLD signals for more than 30 min. The decrease was
                      associated with a reduction in CBV but not with signs of
                      hypoxic metabolism. nAD also triggered transient changes
                      mainly in the low gamma frequency band that recovered within
                      20 min, so that the longer-lasting altered hemodynamics
                      reflected a switch in blood supply rather than transient
                      changes in ongoing neuronal activity. Even in the presence
                      of reduced baseline BOLD signals, neurovascular coupling
                      mechanisms remained intact, making long-lasting vasospasm
                      unlikely. Subsequently generated nAD did not further alter
                      the baseline BOLD signals. Similarly, nAD did not alter
                      baseline BOLD signals when acetaminophen was previously
                      administered, because acetaminophen alone had already caused
                      a similar decrease in baseline BOLD signals as observed
                      after the first nAD. Thus, at least two different blood
                      supply states exist for the hippocampus, one low and one
                      high, with both states allowing similar neuronal activity.
                      Both acetaminophen and nAD switch from the high to the low
                      blood supply state. As a result, the hemodynamic response
                      function to an identical stimulus differed after nAD or
                      acetaminophen, although the triggered neuronal activity was
                      similar.},
      keywords     = {Animals / Brain Waves: drug effects / Brain Waves:
                      physiology / Disease Models, Animal / Electrocorticography /
                      Hippocampus: drug effects / Hippocampus: physiology /
                      Magnetic Resonance Imaging / Male / Neuroimaging /
                      Neurovascular Coupling: drug effects / Neurovascular
                      Coupling: physiology / Proton Magnetic Resonance
                      Spectroscopy / Rats / Rats, Wistar / Seizures: metabolism /
                      Seizures: physiopathology / 1H-NMR spectroscopy (Other) /
                      Electrophysiology (Other) / Gamma oscillations (Other) /
                      Negative BOLD (Other) / Postictal state (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:34861394},
      doi          = {10.1016/j.neuroimage.2021.118769},
      url          = {https://pub.dzne.de/record/163678},
}