Clinical death was modelled on albino rats. Synapses in the molecular layer of the cerebral sensorimotor cortex were investigated 1, 2, 3, 4, 5, 6, 7, 8, and 9 months postresuscitation. The total density of synapses peaked and the number of hypertrophic and perforated contacts increased 4, 7, and 9 months after resuscitation. The role of increased number of hypertrophic and perforated contacts in the pathogenesis of postresuscitation encephalopathy is discussed.