The prefrontal cortex is also a target for the glucocorticoids in stress (dexamethasone binds to receptors in frontal and prefrontal cortex at about 75% of concentration of hippocampus). Endogenous regulation of corticosteroid receptors is indicated by altered binding of the previously mentioned compound in the prefrontal cortex with administration of corticosteroids. Furthermore, regulation of stress activities involves the prefrontal cortex. Lesions in rat prefrontal cortices impair spontaneous alternation, radial maze performance, and passive avoidance. In primates these impair inhibition of line-of-sight responses. Chronic administration of corticosteroids decreases 5-HT1A receptor binding, 5-HT2 receptor binding, serotonin levels, and expression of neural cell adhesion molecule (a cell-surface macromolecule involved in regulating aspects of synapse stabilization). These changes indicate structural change follows stress hormone elevation.