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@ARTICLE{Sergeeva:908294,
      author       = {Sergeeva, Olga A. and Mazur, Karolina and Reiner-Link,
                      David and Lutsenko, Kiril and Haas, Helmut L. and
                      Alfonso-Prieto, Mercedes and Stark, Holger},
      title        = {{OLHA} ({N}-oleoylhistamine) modulates activity of mouse
                      brain histaminergic neurons},
      journal      = {Neuropharmacology},
      volume       = {215},
      issn         = {0028-3908},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {FZJ-2022-02517},
      pages        = {109167},
      year         = {2022},
      abstract     = {Histaminergic (HA) neurons are located in the
                      tuberomamillary nucleus (TMN) of the posterior hypothalamus,
                      from where they project throughout the whole brain to
                      control wakefulness. We examined the effects of
                      Nα-oleoylhistamine (OLHA), a non-enzymatic condensation
                      product of oleic acid (OLA) and histamine, on activity of
                      mouse HA neurons in brain slices. OLHA bidirectionally
                      modulated the firing of HA neurons. At 10 nM OLHA inhibited
                      or had no action, whereas at 1 μM it evoked excitatory and
                      inhibitory responses. Inhibition was not seen in presence of
                      the histamine receptor H3 (H3R) antagonist clobenpropit and
                      in calcium-free medium. Pre-incubation with a
                      histamine-reuptake blocker prevented the decrease in firing
                      by OLHA. OLHA-evoked increase in firing (EC50 ∼44 nM) was
                      insensitive to blockers of cannabinoid 1 and 2 receptors and
                      of the capsaicin receptor, but was significantly impaired by
                      the peroxisome proliferator-activated receptor-alpha
                      (PPAR-alpha) antagonist MK886, which suppressed also the
                      rise in intracellular calcium level caused by OLHA. The
                      OLHA-evoked excitation was mimicked by synthetic PPAR-alpha
                      agonists (gemfibrozil and GW7647) and was abolished by the
                      PKA inhibitor H-89. The H3R affinity (Ki) for histamine,
                      measured in HEK293 cells with stable expression of human
                      H3R, was higher than for OLHA (Ki: 42 vs 310 nM,
                      respectively). Expression of PPAR-alpha was not different
                      between TMN regions of males and females, responses to OLHA
                      did not differ. Molecular modelling of PPAR-alpha bound to
                      either OLHA or OEA showed similar binding energies. These
                      findings shed light on a novel biotransformation product of
                      histamine which may play a role in health and disease.},
      cin          = {IAS-5 / INM-9},
      ddc          = {610},
      cid          = {I:(DE-Juel1)IAS-5-20120330 / I:(DE-Juel1)INM-9-20140121},
      pnm          = {5241 - Molecular Information Processing in Cellular Systems
                      (POF4-524) / 5252 - Brain Dysfunction and Plasticity
                      (POF4-525)},
      pid          = {G:(DE-HGF)POF4-5241 / G:(DE-HGF)POF4-5252},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {35750238},
      UT           = {WOS:000826851500002},
      doi          = {10.1016/j.neuropharm.2022.109167},
      url          = {https://juser.fz-juelich.de/record/908294},
}