Synaptic runaway denotes the formationof erroneous synapses and premature functional decline accompanying activity-dependent learning in neural networks. This work studies synaptic runaway both analytically and numerically in binary- ring associative memory networks. It turns out that synaptic runaway is of fairly moderate magnitude in these networks under normal, baseline, conditions. However, it may become extensive if the threshold for Hebbian learning is reduced. These ndings are combined with recent evidence for arrested N-methyl-D-aspartate (NMDA) maturation in schizophrenics, to formulate a new hypothesis concerning the pathogenesis of schizophrenic psychotic symptoms, in neural terms. Supported by an Alon Fellowship, and to whom correspondence should be addressed. 0