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Histamine potentiates N-methyl-D-aspartate receptors by interacting with an allosteric site distinct from the polyamine binding site.
J Pharmacol Exp Ther. 2010 Mar; 332(3):912-21.JP

Abstract

Histamine potentiates activation of native and recombinant N-methyl-d-aspartate receptors (NMDARs), but its mechanisms of action and physiological functions in the brain remain controversial. Using four different models, we have further investigated the histamine-induced potentiation of various NMDAR-mediated responses. In single cultured hippocampal neurons, histamine potentiated NMDA currents. It also potentiated the NMDA-induced increase in intracellular calcium in the absence, as well as with saturating concentrations, of exogenous d-serine, indicating both glycine-dependent and glycine-independent components of its effect. In rat hippocampal synaptosomes, histamine strongly potentiated NMDA-induced [(3)H]noradrenaline release. The profile of this response contained several signatures of the histamine-mediated effect at neuronal or recombinant NMDARs. It was NR2B-selective, being sensitive to micromolar concentrations of ifenprodil. It was reproduced by tele-methylhistamine, the metabolite of histamine in brain, and it was antagonized by impromidine, an antagonist/inverse agonist of histamine on NMDA currents. Up to now, histamine was generally considered to interact with the polyamine site of the NMDAR. However, spermine did not enhance NMDA-induced [(3)H]noradrenaline release from synaptosomes, and the potentiation of the same response by tele-methylhistamine was not antagonized by the polyamine antagonist arcaine. In hippocampal membranes, like spermine, tele-methylhistamine enhanced [(3)H]dl-(E)-2-amino-4-propyl-5-phosphono-3-pentenoic acid (CGP39653) binding to the glutamate site. In contrast, spermine increased nonequilibrium [(3)H]5H-dibenzo[a,d]cyclohepten-5,10-imine (dizocilpine maleate; MK-801) binding, and suppressed [(3)H]ifenprodil binding, whereas histamine and tele-methylhistamine had no effect. In conclusion, the histamine-induced potentiation of NMDARs occurs in the brain under normal conditions. Histamine does not bind to the polyamine site, but to a distinct entity, the so-called histamine site of the NMDAR.

Authors+Show Affiliations

Laboratoire de Neurobiologie et Pharmacologie Moléculaire, Centre de Psychiatrie et Neurosciences, Institut National de la Santé et de la Recherche Médicale, 2 ter rue d'Alésia, 75014 Paris, France.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20008958

Citation

Burban, A, et al. "Histamine Potentiates N-methyl-D-aspartate Receptors By Interacting With an Allosteric Site Distinct From the Polyamine Binding Site." The Journal of Pharmacology and Experimental Therapeutics, vol. 332, no. 3, 2010, pp. 912-21.
Burban A, Faucard R, Armand V, et al. Histamine potentiates N-methyl-D-aspartate receptors by interacting with an allosteric site distinct from the polyamine binding site. J Pharmacol Exp Ther. 2010;332(3):912-21.
Burban, A., Faucard, R., Armand, V., Bayard, C., Vorobjev, V., & Arrang, J. M. (2010). Histamine potentiates N-methyl-D-aspartate receptors by interacting with an allosteric site distinct from the polyamine binding site. The Journal of Pharmacology and Experimental Therapeutics, 332(3), 912-21. https://doi.org/10.1124/jpet.109.158543
Burban A, et al. Histamine Potentiates N-methyl-D-aspartate Receptors By Interacting With an Allosteric Site Distinct From the Polyamine Binding Site. J Pharmacol Exp Ther. 2010;332(3):912-21. PubMed PMID: 20008958.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Histamine potentiates N-methyl-D-aspartate receptors by interacting with an allosteric site distinct from the polyamine binding site. AU - Burban,A, AU - Faucard,R, AU - Armand,V, AU - Bayard,C, AU - Vorobjev,V, AU - Arrang,J-M, Y1 - 2009/12/15/ PY - 2009/12/17/entrez PY - 2009/12/17/pubmed PY - 2010/4/14/medline SP - 912 EP - 21 JF - The Journal of pharmacology and experimental therapeutics JO - J Pharmacol Exp Ther VL - 332 IS - 3 N2 - Histamine potentiates activation of native and recombinant N-methyl-d-aspartate receptors (NMDARs), but its mechanisms of action and physiological functions in the brain remain controversial. Using four different models, we have further investigated the histamine-induced potentiation of various NMDAR-mediated responses. In single cultured hippocampal neurons, histamine potentiated NMDA currents. It also potentiated the NMDA-induced increase in intracellular calcium in the absence, as well as with saturating concentrations, of exogenous d-serine, indicating both glycine-dependent and glycine-independent components of its effect. In rat hippocampal synaptosomes, histamine strongly potentiated NMDA-induced [(3)H]noradrenaline release. The profile of this response contained several signatures of the histamine-mediated effect at neuronal or recombinant NMDARs. It was NR2B-selective, being sensitive to micromolar concentrations of ifenprodil. It was reproduced by tele-methylhistamine, the metabolite of histamine in brain, and it was antagonized by impromidine, an antagonist/inverse agonist of histamine on NMDA currents. Up to now, histamine was generally considered to interact with the polyamine site of the NMDAR. However, spermine did not enhance NMDA-induced [(3)H]noradrenaline release from synaptosomes, and the potentiation of the same response by tele-methylhistamine was not antagonized by the polyamine antagonist arcaine. In hippocampal membranes, like spermine, tele-methylhistamine enhanced [(3)H]dl-(E)-2-amino-4-propyl-5-phosphono-3-pentenoic acid (CGP39653) binding to the glutamate site. In contrast, spermine increased nonequilibrium [(3)H]5H-dibenzo[a,d]cyclohepten-5,10-imine (dizocilpine maleate; MK-801) binding, and suppressed [(3)H]ifenprodil binding, whereas histamine and tele-methylhistamine had no effect. In conclusion, the histamine-induced potentiation of NMDARs occurs in the brain under normal conditions. Histamine does not bind to the polyamine site, but to a distinct entity, the so-called histamine site of the NMDAR. SN - 1521-0103 UR - https://www.unboundmedicine.com/medline/citation/20008958/Histamine_potentiates_N_methyl_D_aspartate_receptors_by_interacting_with_an_allosteric_site_distinct_from_the_polyamine_binding_site_ L2 - https://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=20008958 DB - PRIME DP - Unbound Medicine ER -