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@ARTICLE{Arboit:162924,
      author       = {Arboit, Alberto and Krautwald, Karla and Angenstein, Frank},
      title        = {{T}he cholinergic system modulates negative {BOLD}
                      responses in the prefrontal cortex once electrical perforant
                      pathway stimulation triggers neuronal afterdischarges in the
                      hippocampus.},
      journal      = {Journal of cerebral blood flow $\&$ metabolism},
      volume       = {42},
      number       = {2},
      issn         = {1559-7016},
      address      = {London},
      publisher    = {Sage},
      reportid     = {DZNE-2021-01576},
      pages        = {364-380},
      year         = {2022},
      note         = {(CC BY)},
      abstract     = {Repeated high-frequency pulse-burst stimulations of the rat
                      perforant pathway elicited positive BOLD responses in the
                      right hippocampus, septum and prefrontal cortex. However,
                      when the first stimulation period also triggered neuronal
                      afterdischarges in the hippocampus, then a delayed negative
                      BOLD response in the prefrontal cortex was generated. While
                      neuronal activity and cerebral blood volume (CBV) increased
                      in the hippocampus during the period of hippocampal neuronal
                      afterdischarges (h-nAD), CBV decreased in the prefrontal
                      cortex, although neuronal activity did not decrease. Only
                      after termination of h-nAD did CBV in the prefrontal cortex
                      increase again. Thus, h-nAD triggered neuronal activity in
                      the prefrontal cortex that counteracted the usual neuronal
                      activity-related functional hyperemia. This process was
                      significantly enhanced by pilocarpine, a mACh receptor
                      agonist, and completely blocked when pilocarpine was
                      co-administered with scopolamine, a mACh receptor
                      antagonist. Scopolamine did not prevent the formation of the
                      negative BOLD response, thus mACh receptors modulate the
                      strength of the negative BOLD response.},
      keywords     = {Animals / Cerebrovascular Circulation / Hippocampus: blood
                      supply / Hippocampus: metabolism / Hyperemia: metabolism /
                      Male / Muscarinic Agonists: pharmacology / Muscarinic
                      Antagonists: pharmacology / Neurons: metabolism / Perforant
                      Pathway: blood supply / Perforant Pathway: metabolism /
                      Pilocarpine: pharmacology / Prefrontal Cortex: blood supply
                      / Prefrontal Cortex: metabolism / Rats / Rats, Wistar /
                      Scopolamine: pharmacology / Cerebral blood volume (CBV)
                      (Other) / electrophysiology (Other) / negative BOLD response
                      (Other) / pilocarpine (Other) / scopolamine (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},
      pmc          = {pmc:PMC8795231},
      pubmed       = {pmid:34590894},
      doi          = {10.1177/0271678X211049820},
      url          = {https://pub.dzne.de/record/162924},
}