It is now understood that the mechanisms leading to neuronal cell death after cardiac arrest (CA) are highly complex. A well established fact in this field is that neurons continue to die over days and months after ischemia. It has been suggested that decreases in electrophysiological activities precede the morphologic deterioration in postischemic CA1 neurons and that this deterioration may be one cause for delayed cell death. The link between synaptic dysfunction and cardiac arrest is evident by the fact that about 50% of long-term survivors of cardiac arrest exhibit impaired mental abilities, manifested as learning impairment, memory disturbance. Since PKC is known to be a key player in synaptic function and has been implicated in promoting cell death after cerebral ischemia, it is a logical candidate as a modulator of synaptic derangements after CA. In this review, we provide an overview of synaptic dysfunction following CA and the putative role of PKC on this dysfunction.