Disturbance of plasmalemmal astrocytic assemblies in focal and selective cerebral ischemia.

Selective cerebral ischemia was induced in the caudate nucleus of seven normothermic anesthetized cats through transorbital clamping of the anterolateral penetrating lenticulostriated arteries. The plasmalemma of astrocytic foot processes has been studied with the freeze-fracture technique and conventional electron microscopy 10, 15 and 30 min after ischemia. After 15 min of circulatory arrest, assemblies of intramembrane particles (IMPs) disappear in some areas of astroglial perivascular plasmalemma in the ischemic caudate nucleus. Interastrocytic gap junctions do not change significantly. 30 min after ischemia, the pericapillary astroglial end foot is expanded and organelles are greatly perturbed (cytotoxic edema). Although the function of astrocytic intramembrane particle assemblies is unclear, it is postulated that the disappearance of this membrane specialization may play a role in the pathophysiology of cytotoxic astroglial edema.