“…Hitherto, although the direct actions of cal cium antagonists such as nimodipine on the cerebral vasculature have been investigated comprehen sively (Allen and Bahr, 1979;Allen and Banghart, 1979;Edvinsson et aI., 1979;To wart andKazda, 1980, 1982;McCalden and Bevan, 1982;White et aI., 1982;Andersson et aI., 1983;Auer et aI., 1983;Brandt et aI., 1983) and smooth muscle), and there is good evidence to believe that these highly specific binding sites, at least in peripheral tissue, represent the locus of ac tion of calcium antagonists Glossmann et aI., 1982;Bellemann et aI., 1983;Fairhurst et aI., 1983;Glossmann and Ferry, 1983;Holck et aI., 1983;Quirion, 1983). Second, the administration of calcium antagonists can effect overt, though subtle, alterations in behaviour (Hoff meister et aI., 1982), and changes in cerebral func tion are generally manifested as local alterations in cerebral metabolic activity (Sokoloff, 1981(Sokoloff, , 1982McCulloch, 1982). However, nimodipine at an in fusion concentration with marked cerebrovascular effects did not alter the rate of glucose utilisation in any CNS region.…”