Blockade by N‐methyl‐D‐aspartate of elevation of activator protein‐1 binding after stress in rat adrenal gland

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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.