Neurodegeneration Revealed By Histology Studies

that involves permanent structural damage of the brain. Instead, it is more likely associated with dysfunctions of certain neuroanatomical structures. Because the malfunctions of these circuitries result from hypoxia-induced injury, if this animal faithfully mimics cerebral hypoxia in humans, there should be some similarities in the brain structures that show injuries in this model compared with human cases. Studies using computerized tomography imaging showed both diffuse cortical and subcortical damage as well as myoclonic jerking movements in patients who had suffered severe cerebral hypoxia.

Histological studies have been performed in this animal model. Using Nissl staining and Fluoro-Jade histochemistry, a profound neuronal degeneration in the motor cortex and the primary and secondary somatosensory cortices of both hemispheres was found. Extensive neurodegeneration was also found in the thalamic reticular nucleus and in the hippocampus, including the CA1, CA2, and CA3 regions in rats with 8-minute, but not 4-minute, cardiac arrest. In addition, a severe loss of the Purkinje neurons in the cerebellum was also observed. Using monoclonal antibody targeting EAAC-1, the presynaptic neuronal glutamate transporter, in rat cerebellar brain sections, revealed a profound loss of the EAAC-1 expression in Purkinje cell layer of the cerebellum in 8-minute hypoxic rats (Truong et al., 2002). This indicates an impairment of function in the regions involved in motor coordination in this animal model of movement disorder.

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