Abstract
Adults with sensory impairment, such as reduced hearing acuity, have impaired ability to recall identifiable words, even when their memory is otherwise normal. We hypothesize that poorer stimulus quality causes weaker activity in neurons responsive to the stimulus and more time to elapse between stimulus onset and identification. The weaker activity and increased delay to stimulus identification reduce the necessary strengthening of connections between neurons active before stimulus presentation and neurons active at the time of stimulus identification. We test our hypothesis through a biologically motivated computational model, which performs item recognition, memory formation and memory retrieval. In our simulations, spiking neurons are distributed into pools representing either items or context, in two separate, but connected winner-takes-all (WTA) networks. We include associative, Hebbian learning, by comparing multiple forms of spike-timing-dependent plasticity (STDP), which strengthen synapses between coactive neurons during stimulus identification. Synaptic strengthening by STDP can be sufficient to reactivate neurons during recall if their activity during a prior stimulus rose strongly and rapidly. We find that a single poor quality stimulus impairs recall of neighboring stimuli as well as the weak stimulus itself. We demonstrate that within the WTA paradigm of word recognition, reactivation of separate, connected sets of non-word, context cells permits reverse recall. Also, only with such coactive context cells, does slowing the rate of stimulus presentation increase recall probability. We conclude that significant temporal overlap of neural activity patterns, absent from individual WTA networks, is necessary to match behavioral data for word recall.