1. Department of Biology, Åbo Akademi University, Turku, Finland
2. ^*Laboratoire d'Immunopharmacologie Moléculaire, UPR 415 CNRS, Institut Cochin de Génétique Moléculaire, Paris, France
3. ^‡Laboratory of Molecular Neurobiology, Institute of Biophysics, Biological Research Center, Szeged, Hungary

Correspondence: Pertti Panula, Department of Biology, Åbo Akademi University, Biocity 2nd fl., Artillerigatan 6A, FIN-20520 Turku, Finland.

^†Dr. F. Joó is deceased.

Received 27 January 1998; Revised 9 June 1998; Accepted 9 June 1998.

Abstract

The purpose of this work was to determine whether cerebral endothelial cells have the capacity to synthesize histamine or to express mRNA of receptors that specifically respond to available free histamine. The histamine concentrations and the expression of L-histidine decarboxylase (HDC) and histamine H₁ and H₂ receptor mRNA, both in adult rat brain and in cultured immortalized RBE4 cerebral endothelial cells, were investigated. In this study endothelial cells were devoid of any kind of detectable histamine production, both in vivo and in the immortalized RBE4 cells in culture. Both the immunostainings for histamine and the in situ hybridizations for HDC were negative, as well as histamine determinations by HPLC, indicating that endothelial cells do not possess the capacity to produce histamine. Also, glucocorticoid (dexamethasone) treatment failed to induce histamine production in the cultured cells. Although the cerebral endothelial cells lack histamine production, a nonsaturable uptake in RBE4 cells is demonstrated. The internalized histamine is detected both in the cytoplasm and in the nucleus, which could indicate a role for histamine as an intracellular messenger. Histamine H₁ and H₂ receptor mRNA was expressed in RBE4 cells, and glucocorticoid treatment down-regulated the mRNA levels of both H₁ and H₂ receptors. This mechanism may be involved in glucocorticoid-mediated effects on cerebrovascular permeability and brain edema.