At the acute symptomatic stage, extracellular glutamate by concentration as determined microdialysis was found to be elevated in the thalamus but within normal limits in the non-vulnerable parietal cortex. This result suggests an involvement of glutamate in the pathogenesis of thiamine deficiency lesions. An in vivo examination of L-type voltage-sensitive calcium channel activity using quantitative autoradiography and ($ sp3$H) -nimodipine at the same stage of PTD revealed that increased activity was present in and localized to the thalamus, but was absent in areas resistant to histological damage. The finding indicates a likelihood of regional depolarization. Finally, induction of the proto-oncogene c-fos was detected in the thalamus and inferior colliculus with quantitative in situ hybridization analysis at the acute symptomatic stage, thereby confirming the association of PTD with depolarization-related events occurring in advance of the appearance of frank infarction.