AUTORADIOGRAPHIC ANALYSIS OF L-TYPE AND N-TYPE VOLTAGE-DEPENDENT CALCIUM-CHANNEL BINDING IN CANINE BRAIN AFTER GLOBAL CEREBRAL ISCHEMIA REPERFUSION/

Binding of antagonists to L- and N-type voltage-dependent calcium chan nels (VDCC) was measured in canine brain following global ischemia and reperfusion. Ischemia was induced by 10 min cardiac arrest, followed by restoration of spontaneous circulation for periods of up to 24 h. B inding of [H-3]PN200-110 and [I-125]omega-conotoxin GVIA to frozen sec tions from hippocampus, striatum, parietal cortex and temporal cortex was analyzed using quantitative receptor autoradiography. The binding patterns of the two radioligands were similar in cortex and striatum, but differed in hippocampus. In the latter tissue, [I-125]omega-conoto xin GVIA binding was dense over synaptic regions, especially the presy naptic polymorph layer of the dentate gyrus, but was virtually absent over cell body layers. In contrast, [H-3]PN200-110 binding was more ho mogenously distributed, with highest binding in the molecular layer of the dentate gyrus. The binding of [I-125]omega-conotoxin GVIA was not different from sham controls at any time point following cardiac arre st. [H-3]PN200-110 binding was decreased in each region immediately fo llowing ischemia, recovering within 30 min of recirculation. These fin dings are in contrast to earlier findings of rapid increases in L-type VDCC binding to membrane fractions obtained from cortex and striatum in this model, and suggest that the previously detected increases may be due to a redistribution of channels from subcellular compartments t o the plasma membrane during ischemia.