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Experimental data and computational models suggest that blockade of muscarinic cholinergic receptors impairs paired-associate learning and increases proactive interference (E. DeRosa & M. E. Hasselmo, 2000; M. E. Hasselmo & J. M. Bower, 1993). The results presented here provide evidence in humans supporting these hypotheses. Young healthy subjects first learned baseline word pairs (A-B) and, after a delay, learned additional overlapping (A-C) and nonoverlapping (D-E) word pairs. As predicted, when compared with subjects who received the active placebo glycopyrrolate (4 microg/kg) and subjects who were not injected, those who received scopolamine (8 microg/kg) showed (a) overall impairment in new word paired-associate learning, but no impairment in cued recall of previously learned associates; and (b) greater impairment in learning overlapping (A-C) compared with nonoverlapping (D-E) paired associates.

Acute stress can impair human working memory. Little is known, however, about the effects of acute stress on working memory strategies. The goal of this research was to investigate the effects of acute stress on use of a systematic spatial working memory search strategy. Participants (28 females and 20 males per group) completed the Trier Social Stress Test (TSST) or control tasks. Use of a systematic spatial working memory search strategy was measured through performance on the spatial working memory subtest of the Cambridge Neuropsychological Test Automated Battery (CANTAB). The TSST was effective at producing subjective and cortisol stress responses, but there was no significant stress effect on use of a systematic search strategy or working memory search errors. There were also no significant relationships between subjective and cortisol stress responses and use of a systematic search strategy or working memory search errors within the stress group. These results suggest that acute stress does not impair the self-generation or execution of a systematic spatial working memory search strategy. [ABSTRACT FROM AUTHOR]

Acute stress likely impacts cognitive control. Little is known, however, about the effects that acute stress may have on specific cognitive control strategies. The goal of this research was to investigate the effects of acute stress on proactive and reactive control strategies. Participants completed the Trier Social Stress Test or control tasks. Use of proactive and reactive control strategies was measured with the AX‐Continuous Performance Test. The Trier Social Stress Test was effective at producing subjective, cortisol, and heart rate stress responses, but there was no significant effect of stress on use of proactive or reactive control strategies in between‐group analyses. However, higher subjective stress responses during performance of the AX‐Continuous Performance Test were associated with less frequent use of a proactive control strategy and more frequent use of a reactive control strategy within the stress group. [ABSTRACT FROM AUTHOR]

Background: Traumatic Brain Injury (TBI) is frequently associated with chronic, treatment-resistant memory problems, and is one of the leading causes of disability in otherwise healthy adults. Cognitive rehabilitation therapies are used with the goal of improving memory functioning; however, not all patients benefit. Prefrontal cortex (PFC) is critical for employing effective memory strategies. We hypothesized that memory improvement after a brief cognitive intervention would be associated with increases in PFC activation during a memory task., Methods: The current study used behavioral analyses and functional magnetic resonance imaging (fMRI) to examine the effects of two days of intensive semantic encoding strategy training on memory performance and brain activation patterns in patients in the post-acute stage of TBI. fMRI data were collected before and after training while participants learned word lists., Results: Post-training vs. pre-training changes in total recall and semantic clustering during recall were positively correlated with post-training vs. pre-training changes in neural activation in PFC., Conclusions: These results suggest that variability in treatment response to cognitive training after TBI may be due in part to variability in PFC function, and that some survivors of TBIs may benefit from treatments specifically targeting the PFC.