Table 2. Measures of dendritic neurons expressed as the mean length (µm) of basilar crossings and basilar branches in chronic corticosterone treated MRL+/+ mice.

Neuromorphological measures in the CA1 region of the hippocampus following corticosterone treatment. By inducing a state of hypercortisolemia in MRL +/+ mice, similar to the innate condition documented in autoimmune diseased MRL-lpr animals (Shanks et al., 1999), an exacerbated deterioration of neuronal dendrites was observed. However, the overall mean lengths of CA1 dendrites in both corticosterone and control groups were notably reduced in comparison to the first cohort of MRL +/+ mice (seen in Table 1). This can likely be attributed to the well-known effects of chronic ethanol consumption (i.e. drinking water contained 1.2% ethanol) on hippocampal fields (Pawlak et al., 2002). Regardless of the adverse effects of ethanol, the present results demonstrate that early neuronal damage can be caused by sustained upregulation of glucocorticoids in MRL mice. While corticosterone-induced atrophy of neurons may be reversible, it is also indicative of an early stage of neurodegeneration (McEwen, 1999).

Hippocampus	MRL +/+ CORT	MRL +/+ VEH
Crossings	81.15 ± 1.89*	90.88 ± 1.75
Branches	34.22 ± 0.78†	39.32 ± 0.39

^*In comparison to MRL +/+ VEH treated mice mean total length of dendritic crossings (t₁₉ = 52.033, p < 0.001)

^†The mean total length of dendritic branches was significantly lower in MRL +/+ CORT animals relative to VEH (t₁₉ = 54.294, p < 0.001).

Note: N = 14 areas per mouse for total number of crossings; N = 6 areas per mouse for total number of branches.