Rats were bilaterally olfactory bulbectomized. At 15 days post-lesion, olfactory bulbectomized (OB) rats exhibited significant deficits in the acquisition of passive avoidance learning compared to sham lesioned rats. beta-Adrenoceptor binding in the amygdala, hippocampus and cerebral cortex was assayed with (-)-[125I]iodocyanopindolol (ICYP). Scatchard analyses revealed no difference between OB and sham rats in maximal binding density (Bmax) in any of the three tissues. However, in the OB rats, the affinity of the beta-adrenoceptor for the ligand was significantly increased in the amygdala and hippocampus but not in the cortex. Bulbectomy did not affect the ratio of beta 1- to beta 2-adrenoceptor subtypes in the three brain tissues. In amygdala and hippocampus but not cerebral cortex, bulbectomy resulted in an increase in the proportion and the affinity of the high-affinity beta-adrenoceptor binding sites for isoproterenol. The affinity of the low-affinity sites in the hippocampus was also increased in the OB rats. The results suggest that olfactory bulbectomy causes supersensitivity of the amygdaloid and hippocampal beta-adrenoceptor by increasing the degree of coupling of the receptor with the stimulatory guanine nucleotide binding protein (Gs protein).