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Recent research has suggested that cortical long-term potentiation can be induced non-invasively in humans by using rapid visual stimulation. The present study extends these findings by investigating the specificity of this long-term potentiation effect to the inducing stimulus. One group of study participants were tetanized using a one cycle-per-degree sine grating, while a second group was tetanized using a five cycles-per-degree sine grating. Using electroencephalography, we found that an increase in the N1b potential was specific to sine gratings of the same frequency as the tetanus. No effect was observed in the N1b for sine gratings of a different spatial frequency. These results suggest that the long-term potentiation effect induced by the sensory tetanus is isolated to a discrete neural population in the visual cortex.

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. For further resources related to this article, please visit the WIREs website.

Dysfunction in FHD is widespread in both complexity and hand networks, and impairments are demonstrated even when performing tasks that do not evoke dystonic symptoms. These results suggest that such impairments are inherent to, rather than symptomatic of, the disorder.