title: The involvement of glutamate in recall of the conditioned NK cell response.
abstract: The molecular mechanisms responsible for the conditioned enhancement of natural killer (NK) cell activity were investigated. The primary goal of the study was to examine the roles of glutamate and gamma-aminobutyric acid (GABA) in recall of the conditioned NK cell response. Both neurochemical blocking assay and high performance liquid chromatography (HPLC) technique were used in the study. Results from the neurochemical blocking assay demonstrated that glutamate but not GABA was required in recall of the conditioned NK cell response. NMDA but not the kainate/AMPA receptors, are believed to be involved. The levels of glutamate that were released and/or taken up also appeared to be critical in that interruption of glutamate release and/or uptake blocked the conditioned NK cell response. Results from the HPLC analysis, however, did not show any significant difference in the glutamate content between the conditioned and control brains.
authors.affiliation: Department of Education and Research, Taichung Veterans General Hospital, Taichung, Taiwan.
authors.forename: J S
authors.initials: JS
authors.lastname: Kuo
authors.forename: S F
authors.initials: SF
authors.lastname: Chen
authors.forename: H J
authors.initials: HJ
authors.lastname: Huang
authors.forename: C S
authors.initials: CS
authors.lastname: Yang
authors.forename: P J
authors.initials: PJ
authors.lastname: Tsai
authors.forename: C M
authors.initials: CM
authors.lastname: Hsueh
mesh_terms: D000280:Administration, Inhalation; D000818:Animals; D001921:Brain / Q000378:metabolism; D002164:Camphor / Q000008:administration & dosage; D002478:Cells, Cultured; D002851:Chromatography, High Pressure Liquid; D003214:Conditioning, Classical / Q000187:drug effects / Q000502:physiology*; D004334:Drug Administration Schedule; D018691:Excitatory Amino Acid Antagonists / Q000008:administration & dosage; D005260:Female; D018756:GABA Antagonists / Q000008:administration & dosage; D018698:Glutamic Acid / Q000378:metabolism*; D007111:Immunity, Cellular / Q000187:drug effects / Q000502:physiology; D007156:Immunologic Memory / Q000187:drug effects / Q000502:physiology*; D007274:Injections, Intraperitoneal; D007276:Injections, Intraventricular; D007694:Killer Cells, Natural / Q000166:cytology / Q000187:drug effects / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008845:Microinjections; D011070:Poly I-C / Q000008:administration & dosage / Q000276:immunology; D018091:Receptors, AMPA / Q000037:antagonists & inhibitors; D018092:Kainic Acid Receptors / Q000037:antagonists & inhibitors; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
chemical_list: D002164:Camphor; D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D018698:Glutamic Acid; D011070:Poly I-C; D018091:Receptors, AMPA; D018092:Kainic Acid Receptors; D016194:Receptors, N-Methyl-D-Aspartate; D005680:gamma-Aminobutyric Acid