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WIREs Cogn Sci
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Long‐term potentiation (LTP) of human sensory‐evoked potentials

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Abstract Long‐term potentiation (LTP) is the principal candidate synaptic mechanism underlying learning and memory, and has been studied extensively at the cellular and molecular level in laboratory animals. Inquiry into the functional significance of LTP has been hindered by the absence of a human model as, until recently, LTP has only been directly demonstrated in humans in isolated cortical tissue obtained from patients undergoing surgery, where it displays properties identical to those seen in non‐human preparations. In this brief review, we describe the results of paradigms recently developed in our laboratory for inducing LTP‐like changes in visual‐, and auditory‐evoked potentials. We describe how rapid, repetitive presentation of sensory stimuli leads to a persistent enhancement of components of sensory‐evoked potential in normal humans. Experiments to date, investigating the locus, stimulus specificity, and NMDA receptor dependence of these LTP‐like changes suggest that they have the essential characteristics of LTP seen in experimental animals. The ability to elicit LTP from non‐surgical patients will provide a human model system allowing the detailed examination of synaptic plasticity in normal subjects and may have future clinical applications in the assessment of cognitive disorders. Copyright © 2010 John Wiley & Sons, Ltd. This article is categorized under: Psychology > Brain Function and Dysfunction Neuroscience > Plasticity

Checkerboard visual stimulus used to induce LTP in the right hemisphere.

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LTP to an auditory stimulus and scalp distribution. Left panel: Auditory tetanus induces LTP of the N1 component. (a) Group average auditory‐evoked potentials (AEPs) to tone pip stimulation. The hatched section indicates the time window of interest. The light gray and black lines represent the two baseline blocks (pre‐tetanus) and the dark gray line indicates the post‐tetanus AEP. Note that the post‐tetanus response is substantially larger than the two baseline blocks in our time window of interest (N1). Right panel: Scalp distribution of post‐pre ‘tetanus’ N1 amplitude differences in N1 amplitude. Figure modified with permission from Ref 39 Copyright 2005 Wiley‐Blackwell..

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(a) Pre‐ and post‐tetanus average evoked potentials recorded over the occipital cortex contralateral to the visual stimulus. (b) An independent components analysis identified five components of the VEP to checkerboard stimuli. (c) Checkerboard stimuli (subtending 4 degrees visual angle with three checks per degree) to the left or right visual hemifield elicited a contralateral P100 response (c, left panel) and a bilateral N1b response (c, right panel) in occipital cortex. (d) Repetitive presentation of the checkerboard (at 9 Hz) led to a significant change in only the N1b component (d, right panel). The amplitude of the P100 (d, left panel), e.g., did not change significantly. See Figure 2(a). Figure reproduced with permission from Ref. 18 Copyright 2005 Wiley‐Blackwell.

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