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Parallel decrease of adenylyl cyclase activity and beta1-adrenoceptor density in brain cortex of aging mice.

C Viticchi1, L Piantanelli

  • 1Center of Biochemistry, Gerontologic Research Department, INRCA I-60121, Ancona, via Birarelli, 8, Italy.

Archives of Gerontology and Geriatrics
|March 1, 1993
PubMed
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Aging impairs brain cortex beta1-adrenergic receptors (beta1ARs) and adenylyl cyclase (AC) activity. These changes suggest both receptor-dependent and independent alterations contribute to age-related AC dysfunction.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Aging Research

Background:

  • Progressive alterations in beta-adrenergic receptors (betaARs) and adenylyl cyclase (AC) activity occur in the aging mouse brain cortex.
  • Specifically, beta1-adrenergic receptors (beta1ARs) show age-related changes, while beta2-adrenoceptors (beta2ARs) remain unaffected.

Purpose of the Study:

  • To investigate whether age-related AC alterations are solely due to beta1AR changes or if receptor-independent modifications also play a role.
  • To differentiate between beta1AR-dependent and independent contributions to AC activity changes in aging.

Main Methods:

  • Experiments were conducted on brain cortex membranes from young and old mice.
  • Assayed beta1AR and beta2AR characteristics and AC activity stimulated by isoproterenol (IPR) and forskolin.

Related Experiment Videos

  • Utilized dithiothreitol (DTT) treatment to specifically abolish beta1AR binding capacity.

    • Main Results:

    • No significant differences in basal AC activity were observed between young and old mice.
    • IPR-stimulated AC activity was impaired in old mice compared to young mice.
    • Forskolin-stimulated AC activity was also impaired in aged mice, indicating post-receptor alterations.

    Conclusions:

    • Age-related AC alterations in the brain cortex involve both beta1AR-dependent and post-receptor mechanisms.
    • The findings suggest a complex interplay of factors contributing to impaired AC function during aging.