1989/06/01 by John Bamford, J M Bamford, Peter Sandercock +4 · 1 citation
Medicine · Biochemistry, Genetics and Molecular Biology · #Acute Ischemic Stroke Management #Traumatic Brain Injury and Neurovascular Disturbances #S100 Proteins and Annexins
paper · doi:10.1161/01.str.20.6.828
stantia nigra lesion, abolished the massive release of dopamine 2 and markedly attenuated the degree of ischemic neuronal damage in the ipsilateral striatum. 3 These results clearly establish the participatory role of dopamine in ischemia and suggest that excessive release of dopamine mediates an injurious effect in the postischemic striatum.The mechanism by which dopamine endangers striatal neurons in the aftermath of ischemia is not clear.We have previously demonstrated that marked postischemic elevation of the metabolism/flow ratio in the striatum correlated with morphological evidence of selective striatal injury. 4 The degree of postischemic metabolism/flow uncoupling was significantly suppressed by prior substantia nigra lesion. 5These results suggest that excessive release of dopamine may be detrimental by accentuating postischemic metabolism/flow uncoupling in the striatum.