Corticotropin-releasing factor (CRF) activates locus coeruleus (LC)-norepinephrine neurons during stress. Previous stress or CRF administration attenuates the magnitude of this response by decreasing postsynaptic sensitivity to CRF. Here we describe the fate of CRF receptors in LC neurons following stress. Rats were exposed to swim stress or handling and perfused one or twenty-four hours later. Sections through the LC were processed for immunogold-silver labeling of CRF receptor (CRFr). CRFr in LC dendrites was present on the plasma membrane and within the cytoplasm. In control rats, the ratio of cytoplasmic to total dendritic labeling was 0.55 ± 0.01. Swim stress increased this ratio to 0.77 ± 0.01 and 0.80 ± 0.02 at one and twenty-four hours post-stress, respectively. Internalized CRFr was associated with different organelles at different times after stress. At one hour post-stress, CRFr was often associated with early endosomes in dendrites and perikarya. By twenty-four hours, more CRFr was associated with multivesicular bodies, suggesting that some of the internalized receptor is targeted for degradation. In perikarya, more internalized CRFr was associated with Golgi apparati twenty-four hours vs. one hour post-stress. This is suggestive of changes in CRFr synthesis. Alternatively this may indicate communication between multivesicular bodies and Golgi apparati in the process of recycling. Administration of the selective CRF₁ antagonist, antalarmin, prior to swim stress attenuated CRFr internalization. The present demonstration of stress-induced internalization of CRFr in LC neurons provides evidence that CRF is released in the LC during swim stress to activate this system and initiate cellular trafficking of the receptor that determines subsequent sensitivity of LC neurons to CRF.