Rabies has been an enigmatic disease because microscopic findings in central nervous system tissues do not always correlate well with the severity of the clinical illness. Immunohistochemical staining of the calcium-binding protein calbindin (specifically CbD28k) seems to be the technique most used to identify Purkinje neurons under normal and pathological conditions. In the present work, we evaluated CbD28k immunoreactivity in the cerebellar cortex of normal and natural Rabies virus (RABV)-infected cattle. We examined brains from 3 normal cows and from 6 crossbreed cattle with a histologic diagnosis of rabies. Samples were taken from the cerebral cortex, cerebellum, hippocampus, and brainstem. Immunohistochemistry was carried out using the following primary antibodies: anti-RABV, anti-GFAP, and anti-CbD28k. In the cerebellar cortex, RABV infection caused the loss of CbD28k immunostaining in Purkinje cells; some large interneurons in the granular layer maintained their positive CbD28k immunoreaction. The identification of this loss of CbD28k reactivity in cerebellar Purkinje cells of RABV-infected cattle presents a potentially valuable tool to explore the impairment of Ca2+ homeostasis. In addition, this may become a useful method to identify specific molecular alterations associated with the higher prevalence of Negri bodies in Purkinje cells of cattle. Furthermore, we detected the presence of rabies viral antigens in different regions of the central nervous system, accompanied by microglial proliferation and mild reactive astrogliosis.
Solanum bonariense intoxication is characterized by cerebellar neuronal vacuolation, degeneration, and necrosis. Cerebellar Purkinje cells seem especially susceptible, but more research is needed to determine the pathogenesis of neuronal necrosis and the mechanism of Purkinje cell susceptibility. Calbindin D28k (CbD28k) is highly expressed in Purkinje cells and has been used as a marker for normal and degenerative Purkinje cells. The goal of this study was to describe S bonariense-induced disease by ascertaining Purkinje cell-specific degenerative changes using CbD28k expression and to correlate this with apoptosis in Purkinje cells, as determined using TUNEL (transferase-mediated dUTP-biotin nick end-labeling) and ultrastructural changes. In all cases, an increase in both dose and duration of S bonariense intoxication resulted in a decrease in the number of Purkinje cells. CbD28k immunohistochemistry was an excellent marker for Purkinje cells because immunoreactivity did not change in normal or degenerative tissues. This finding suggests that excessive calcium excitatory stimulation does not induce rapid neuronal degeneration and death. As found in previous studies, TUNEL tests and electron microscopy suggest that Purkinje cell degeneration and death are not occurring via an apoptotic process. These findings suggest that S bonariense poisoning induces progressive Purkinje cell death that is not mediated by excitotoxicity or apoptotic activation.
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