Remote areas connected to cortical infarcts, such as the thalamus, are affected by stroke due to delayed retrograde degeneration of afferent connections. This is temporally associated with the accumulation of β-amyloid (Aβ) and calcium. Here we tested a hypothesis that prevention of excessive Ca 2+ influx into the axoplasm via the reverse Na + /Ca 2+ exchanger (NCX) would provide axonal protection and eventually lessen the Aβ and calcium load in the thalamus. We found that chronic treatment with a specific inhibitor of the reverse NCX, KB-R7943 (30mg/kg once daily, 27 days) after middle cerebral artery occlusion did not prevent atypical secondary pathology in the thalamus or improve functional outcome. The present data do not support a role for reverse NCX activity in the complex pathology within the thalamus after cerebral ischemia.