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Research ArticleCELLULAR AND MOLECULAR

Adrenal Glucocorticoids Modulate [3H]Cyclic AMP Binding to Protein Kinase A (PKA), Cyclic AMP-Dependent PKA Activity, and Protein Levels of Selective Regulatory and Catalytic Subunit Isoforms of PKA in Rat Brain

Yogesh Dwivedi and Ghanshyam N. Pandey
Journal of Pharmacology and Experimental Therapeutics July 2000, 294 (1) 103-116;
Yogesh Dwivedi
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Ghanshyam N. Pandey
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Abstract

Alterations in hypothalamic-pituitary-adrenal (HPA) function are associated with changes in mood and behavior. Protein kinase A (PKA), on activation, phosphorylates many important intracellular proteins and thereby plays a major role in mediating various physiological functions in brain. We systematically examined the relationship of altered HPA function with PKA modifications in rat brain after administering corticosterone to normal rats and by first adrenalectomizing rats and then simultaneously treating them with different doses of corticosterone. Rats were decapitated on day 1, 4, or 14. Subcutaneously implanted 50- or 100-mg corticosterone pellets in normal rats for 4 or 14 days significantly decreased PKA activity,Bmax of [3H]cyclic AMP binding, and protein levels of selective PKA regulatory (RIα, RIIβ) and catalytic (Catβ) subunit isoforms in cortex and hippocampus in a dose-dependent manner without any significant changes at day 1; these changes were more pronounced at day 14. However, adrenalectomy caused the opposite changes in these measures at day 4 or 14 in both cortex and hippocampus, and the magnitude of the changes was more pronounced at day 14. Simultaneous treatment with implanted corticosterone at 50- or 100-mg doses in adrenalectomized rats reversed the adrenalectomy-induced increases in PKA measures in a dose-dependent manner. These results suggest that endogenous glucocorticoid modifies the expression of RIα, RIIα, and Catβ subunit isoforms of PKA, as well as the catalytic and regulatory activities of PKA, and that these alterations in PKA may in part explain HPA axis-mediated changes in mood and behavior.

Footnotes

  • Send reprint requests to: Yogesh Dwivedi, Ph.D., Assistant Professor, Psychiatric Institute, Department of Psychiatry (M/C 912), University of Illinois at Chicago, 1601 West Taylor St., Chicago, IL 60612. E-mail:ydwivedi{at}psych.uic.edu

  • ↵1 This study was supported by a grant from the National Institute of Mental Health (R01-MH56528).

  • Abbreviations:
    5-HT
    serotonin (5-hydroxytryptamine)
    HPA
    hypothalamic-pituitary-adrenal
    PKA
    protein kinase A
    PKC
    protein kinase C
    AEBSF
    4-(2-aminoethyl)-benzenesulfonyl fluoride
    ECL
    enhanced chemiluminescence
    R
    regulatory
    Cat
    catalytic
    • Received November 24, 1999.
    • Accepted March 16, 2000.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 294 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 294, Issue 1
1 Jul 2000
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Research ArticleCELLULAR AND MOLECULAR

Adrenal Glucocorticoids Modulate [3H]Cyclic AMP Binding to Protein Kinase A (PKA), Cyclic AMP-Dependent PKA Activity, and Protein Levels of Selective Regulatory and Catalytic Subunit Isoforms of PKA in Rat Brain

Yogesh Dwivedi and Ghanshyam N. Pandey
Journal of Pharmacology and Experimental Therapeutics July 1, 2000, 294 (1) 103-116;

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Research ArticleCELLULAR AND MOLECULAR

Adrenal Glucocorticoids Modulate [3H]Cyclic AMP Binding to Protein Kinase A (PKA), Cyclic AMP-Dependent PKA Activity, and Protein Levels of Selective Regulatory and Catalytic Subunit Isoforms of PKA in Rat Brain

Yogesh Dwivedi and Ghanshyam N. Pandey
Journal of Pharmacology and Experimental Therapeutics July 1, 2000, 294 (1) 103-116;
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