Treatment of rats with N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) resulted in a pronounced loss of alpha 2-adrenoceptor binding ( [3H]RX-781094) and a marked reduction in the ability of the alpha 2-agonist UK-14,304 to inhibit K+-stimulated release of both [3H]NA and [3H]5-HT in cerebral cortex. Repopulation of alpha 2-adrenoceptors was monoexponential with a t1/2 of 4.1 days; functional recovery was also monoexponential, with t1/2 values of 2.4 and 4.6 days for restoration of alpha 2-mediated inhibition of [3H]NA and [3H]5-HT release, respectively. Other studies suggest the difference in functional recovery rate may reflect the presence of a large receptor reserve for autoreceptors relative to heteroreceptors.