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Palmitic acid methyl ester directly induces hippocampal neuroprotection against oxygen and glucose deprivation
Author(s) -
Neumann Jacob,
Van Allen Joshua,
Azizbayeva Rinata,
Lin Hung Wen
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.500.11
Subject(s) - neuroprotection , neuroscience , cortical spreading depression , pharmacology , hippocampal formation , hippocampus , medicine , chemistry , anesthesia , biology , migraine
Cardiopulmonary arrest (CA) is one of the leading causes of death and disability in the USA. The prevalent quandary in this field is the multi‐factorial nature of CA (i.e., whole body ischemia), which compromises systemic blood parameters and cerebral, renal and cardiac functions. This disruption of cerebral blood flow (CBF) also results in severe and selective brain damage (i.e., neuronal cell death) in the hippocampus, especially in the cornu Ammonis 1 (CA1) region. While previous research has indicated PAME (a vasodilator) as a neuroprotective agent, the specific mechanism(s) of neuroprotection is/are currently unknown and it is currently unknown if PAME‐induced neuroprotection is from direct modulation of CBF or due to direct activation of neuroprotective pathways. Here, we tested the hypothesis that PAME induces neuroprotection independent of CBF, and that PAME alters additional signaling pathways to induce neuroprotection in the hippocampus. Our studies used an in vitro hippocampal model (hippocampal organotypic slices) to determine the requirement of CBF for PAME‐induced neuroprotection and if specific modulation of alpha‐7 nicotinic acetylcholine receptors (a potential target of PAME) can induce neuroprotection following oxygen and glucose deprivation (OGD) using propidium iodide staining. All of the protocols were approved by the West Virginia School of Osteopathic Medicine Institutional Animal Care and Use Committee. Our results suggest that the direct application of PAME or inhibition of alpha‐7 nicotinic acetylcholine receptors induced neuroprotection following OGD in the CA1 region of the hippocampus. These data suggest that PAME‐induced neuroprotection occurs independent of CBF and identifies alpha‐7 nicotinic acetylcholine receptors as a potential mechanism for PAME‐induced neuroprotection. Support or Funding Information This study was supported by a West Virginia School of Osteopathic Medicine intramural grant and a grant from the American Heart Association 17GRNT33660336 . This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .