Preclinical studies indicate that endogenous or exogenous glucocorticoids acting during the pre- or postnatal periods produce a significant Purkinje cell dendritic atrophy, especially during late postnatal ages. The present authors hypothesized that the underlying substrate that may contribute in part to this morphological change is the under-expression of the metabotropic glutamate 1a receptor (mGluR1a) because its expression is correlated with Purkinje cell dendritic outgrowth. Therefore, in the current study, they analyzed the impact of antenatal betamethasone on the immunoreactive expression of the mGluR1a and on anxiety-like behavior in the elevated plus maze (EPM). Pregnant rats were randomly divided into two experimental groups: control (CONT) and betamethasone-treated (BET). At gestational day 20 (G20), BET rats were subcutaneously injected with a solution of 170 μg.kg^-1 of betamethasone, and CONT animals received a similar volume of saline. At postnatal days 22 (P22) and P52, BET and CONT offspring were evaluated behaviorally in the EPM, and their cerebella were immunohistochemically processed. Contrary to the uthors’ expected results, animals that were prenatally treated with a single course of betamethasone did not exhibit under-expression of mGluR1a or behavioral changes consistent with anxiety-like behaviors.