Calbindin-D28K expression increases in the dorsolateral hippocampus following corticosterone treatment in female zebra finches (Taeniopygia guttata).

The hippocampus (HP) in zebra finches (Taeniopygia guttata) is important in the consolidation of spatial memories. Chronic, elevated levels of steroid hormones, like the glucocorticoids, can decrease this type of memory function in birds and mammals; neuronal atrophy, loss, and a decrease in synaptic contacts in the mammalian HP are observed as the underlying cause. Calbindin-D28k is constitutively expressed in cells of the nervous system but increases in concentration following a neurotoxic insult, protecting neurons against apoptotic cell death. We hypothesized that treatment of female zebra finches with a glucocorticoid (corticosterone) would increase calbindin expression in the HP and the caudomedial nidopallium (NCM), a region important for perceptual (song) memories, relative to "blank" controls. Additionally, because the HP in zebra finches appears similar to that in mammals, based on a variety of structural and functional factors, and as particular regions of the HP in mammals are more vulnerable to glucocorticoid-induced damage, we also hypothesized that expression of calbindin would vary among the HP subdivisions. Overall levels of calbindin were higher in the HP of corticosterone-treated birds, due almost entirely to elevated calbindin expression in the dorsolateral subdivision of the HP only. In contrast, the dorsomedial HP, ventral HP, and NCM appear less affected by glucocorticoid exposure. These results suggest a role for glucocorticoids in the modulation of HP- but not NCM-dependent memories as well as a further functional differentiation among the HP subdivisions.