Abstract Treatment of rats with N-ethoxycarbonyl-2-ethoxy-1, 2-dihydroquinoline (EEDQ) resulted in a pronounced loss of α 2-adrenoceptor binding ([3 H] RX-781094) and a marked reduction in the ability of the α 2-agonist UK-14,304 to inhibit K+-stimulated release of both [3 H] NA and [3 H] 5-HT in cerebral cortex. Repopulation of α 2-anderoceptors was monoexponential with a t 1 2 of 4.1 days; functional recovery was also monoexponential, with t 1 2 values of 2.4 and 4.6 days for restoration of α 2-mediated inhibition of [3 H] NA and [3 H] 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.