Human EEG and the mechanisms of memory: investigating long-term potentiation (LTP) in sensory-evoked potentials

Long-term potentiation (LTP) at synapses within neural networks is the most likely candidate mechanism for learning and memory. LTP has been extensively studied in laboratory animals, but inquiry into the functional significance of LTP had, until the mid-2000s, been compromised by the lack of a human model. In this brief review, we describe the results of paradigms developed in our laboratory for inducing 'LTP-like' changes in human EEG-derived visual-, and auditory-evoked potentials. We describe how rapid, repetitive presentation of sensory stimuli leads to a long-lasting amplitude increase in some components of sensory-evoked potentials in neurotypical humans. Subsequent experiments, by us and others, investigating the locus, stimulus specificity, NMDA receptor dependence, and genetics of these 'LTP-like' effects suggest that they have the essential characteristics of LTP seen in experimental animals. We suggest therefore, that the increased amplitudes of components of sensory-evoked potentials are due to LTP at synapses in the neural networks generating the scalp-level EEG-derived evoked potentials. Thus, the ability to elicit and measure LTP from people other than those undergoing surgery provides a human model system allowing the detailed examination of synaptic plasticity in neurotypical subjects, and has been shown to have clinical applications in a number of disorders.

Automated summary

Long-term potentiation (LTP) is a likely mechanism for learning and memory, and can be studied in humans through paradigms inducing "LTP-like" changes in sensory-evoked potentials, revealing an increase in synaptic LTP in the neural networks generating these potentials. By eliciting and measuring LTP effects, further research on synaptic plasticity can be conducted with clinical applications in various disorders.