title: Blockade by N-methyl-D-aspartate of elevation of activator protein-1 binding after stress in rat adrenal gland.
abstract: Cold immobilization stress induced a marked elevation of expression of activator protein-1 (AP1) complex in rat hypothalamus, pituitary, adrenal, and gastric mucosa, but not in other discrete brain structures examined, when determined immediately after stress for 3 hr. Adrenal AP1 binding linearly increased with the duration of stress up to 6 hr, whereas the increase was seen in both adrenal cortex and medulla of rats stressed for 3 hr. In adrenals, the elevation exhibited decline profiles different from those of expression of cAMP response element binding protein. Western blotting revealed that stress for 3 hr induced significant increases in expression of the components of AP1 complex, c-Fos, c-Jun, and Jun-B proteins, in adrenals, without markedly affecting expression of Fos-B, Fra-2, and Jun-D proteins. The prior systemic administration of N-methyl-D-aspartate (NMDA) led to significant prevention of the elevation after stress for 3 hr in adrenals, whereas the NMDA antagonist dizocilpine alone induced a marked increase in adrenal AP1 binding, without altering the elevation by stress. These results suggest that stress may modulate de novo protein synthesis at the level of gene transcription by AP1 complex through a molecular mechanism associated with NMDA receptor channels in rat adrenal glands.
authors.affiliation: Department of Molecular Pharmacology, Kanazawa University Faculty of Pharmaceutical Sciences, Kanazawa, Ishikawa, Japan.
authors.forename: Eiichi
authors.initials: E
authors.lastname: Hinoi
authors.forename: Sayumi
authors.initials: S
authors.lastname: Fujimori
authors.forename: Masanori
authors.initials: M
authors.lastname: Yoneyama
authors.forename: Yukio
authors.initials: Y
authors.lastname: Yoneda
mesh_terms: D000311:Adrenal Glands / Q000378:metabolism*; D000818:Animals; D001667:Binding, Competitive / Q000187:drug effects*; D015153:Blotting, Western; D003080:Cold Temperature; D017362:Cyclic AMP Response Element-Binding Protein / Q000378:metabolism; D016291:Dizocilpine Maleate / Q000494:pharmacology; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005753:Gastric Mucosa / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism; D007031:Hypothalamus / Q000378:metabolism; D008297:Male; D016202:N-Methylaspartate / Q000494:pharmacology*; D009928:Organ Specificity / Q000502:physiology; D010902:Pituitary Gland / Q000378:metabolism; D011485:Protein Binding / Q000187:drug effects; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D016271:Proto-Oncogene Proteins c-myc / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D016194:Receptors, N-Methyl-D-Aspartate / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism; D012149:Restraint, Physical; D013312:Stress, Physiological / Q000378:metabolism*; D018808:Transcription Factor AP-1 / Q000378:metabolism*
chemical_list: D017362:Cyclic AMP Response Element-Binding Protein; D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D016760:Proto-Oncogene Proteins c-fos; D016271:Proto-Oncogene Proteins c-myc; D016194:Receptors, N-Methyl-D-Aspartate; D018808:Transcription Factor AP-1; D016202:N-Methylaspartate; D016291:Dizocilpine Maleate