Abstract

It is nearly 50 years since Bliss and Lomo first reported the long-lasting potentiation of synaptic transmission in the hippocampus (now long-term potentiation; LTP ). Subsequently, deficits in hippocampal synaptic plasticity has been implicated in various psychiatric disorders including schizophrenia, depression and Alzheimer’s Disease. Hippocampal LTP has become one of the most widely studied phenomena in neuroscience, and enormous resources have been poured into research efforts to develop treatment strategies for these disorders that target hippocampal LTP but with limited success. This failure, at least in part, reflects a lack of understanding as to the precise psychological sequelae of hippocampal LTP . The idea that hippocampal LTP provides the neural substrate for the formation of associative memories has predominated in neuroscience text books, although the empirical support for this hypothesis is limited at best. Here we provide an alternative account of the role of hippocampal synaptic plasticity in the priming of memories. This account can explain why deficits in hippocampal synaptic plasticity can lead to deficits in episodic memory retrieval in some cases, but psychosis in disorders like schizophrenia in others. It can also potentially account for the learning processes that might underpin the improvement in mood following anti-depressant treatment in patients.