neal cavity (3). In an in vivo immunohistochemical study in gerbils with global forebrain
ischemia, chronic treatment with propentofylline ( 14 successive daily doses, of
10 mg/kg i.p. starting one day after induction of ischemia) inhibited ischemia-induced
expression of cell antigens associated with activated microglial cells (40). In addition,
immunostaining for an amyloid precursor protein, which is normally enhanced in this
model of ischemia, was strongly suppressed by the propentofylline treatment (40).
This study demonstrates that propentofylline can inhibit an ongoing and potentially
neurotoxic process of microglia activation in the postischemic brain. It also suggests a