Abstract
The efficacy of β 1-adrenoceptor—G protein coupling was studied in postmortem temporal cortex synaptic membranes from a series of control and Alzheimer's disease subjects. For the control cases, the non-hydrolysable GTP analogue 5′-guanylylimidodiphosphate (Gpp[NH]p) gave a significant reduction in the affinity of the agonist isoprenaline to displace binding of the radiolabelled antagonist (±)-4-(3- t-butylamino-2-hydroxypropoxy)-[5,7- 3H]benzimidazol-2-one ([ 3H]CGP-12177). This effect was attributed to the conversion of high agonist-affinity sites to a lower-affinity state and was not found for the Alzheimer's disease cases. These data indicate that a disruption of β 1-adrenoceptor—G protein coupling occurs in the temporal cortex of Alzheimer's disease patients.
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