Learning interference occurs when learning something new causes forgetting of an older memory (retrograde interference) or when learning a new task disrupts learning of a second subsequent task (anterograde interference). This phenomenon, described in cognitive, sensory and motor domains, limits our ability to learn multiple tasks in close succession. It has been suggested that the source of interference is competition of neural resources, although the neuronal mechanisms are unknown. Learning induces long-term potentiation (LTP) that can ultimately limit the ability to induce further LTP, a phenomenon known as occlusion. In humans we quantified the magnitude of occlusion of anodal transcranial direct current stimulation (A-tDCS)-induced increased excitability after learning a skill task as an index of the amount of LTP-like plasticity used. We found that retention of a newly acquired skill, as reflected by performance in the second day of practice, is proportional to the magnitude of occlusion. Moreover, the degree of behavioral interference was correlated with the magnitude of occlusion. Individuals with larger occlusion after learning the first skill were (1) more resilient to retrograde interference and (2) experienced larger anterograde interference when training a second task, as expressed by decreased performance of the learned skill in the second day of practice. This effect was not observed if sufficient time elapsed between training the 2 skills and LTP-like occlusion was not present. These findings suggest competition of LTP-like plasticity is a factor that limits the ability to remember multiple tasks trained in close succession.

The current study found a significant decrease in DAT BP in two independent studies. These results when viewed along with prior RLS SPECT and autopsy studies of DAT, and cell culture studies with iron deficiency and DAT, suggest that membrane-bound striatal DAT, but not total cellular DAT, may be decreased in RLS.

BACKGROUND: Poor sleep has adverse affects on heath, yet few studies have addressed the goal of improving sleep among hospitalized patients. We evaluated the effectiveness of a sleep-promoting intervention on the quality and quantity of sleep among inpatients.

Study Objectives: To evaluate the validity of an ambulatory electroencephalographic (EEG) monitor for the estimation of sleep continuity and architecture in healthy adults. Methods: Healthy, good sleeping participants (n = 14) were fit with both an ambulatory EEG monitor (Sleep Profiler) and a full polysomnography (PSG) montage. EEG recordings were gathered from both devices on the same night, during which sleep was permitted uninterrupted for eight hours. The study was set in an inpatient clinical research suite. PSG and Sleep Profiler records were scored by a neurologist board certified in sleep medicine, blinded to record identification. Agreement between the scored PSG record, the physician-scored Sleep Profiler record, and the Sleep Profiler record scored by an automatic algorithm was evaluated for each sleep stage, with the PSG record serving as the reference. Results: Results indicated strong percent agreement across stages. Kappa was strongest for Stage N3 and REM. Specificity was high for all stages; sensitivity was low for Wake and Stage N1, and high for Stage N2, Stage N3, and REM. Agreement indices improved for the manually scored Sleep Profiler record relative to the autoscore record. Conclusions: Overall, the Sleep Profiler yields an EEG record with comparable sleep architecture estimates to PSG. Future studies should evaluate agreement between devices with a clinical sample that has greater periods of wake in order to better understand utility of this device for estimating sleep continuity indices, such as sleep onset latency and wake after sleep onset.