Prefrontal cortical plasticity during learning of cognitive tasks

Training in working memory tasks is associated with lasting changes in prefrontal cortical activity. To assess the neural activity changes induced by training, we recorded single units, multi-unit activity (MUA) and local field potentials (LFP) with chronic electrode arrays implanted in the prefrontal cortex of two monkeys, throughout the period they were trained to perform cognitive tasks. Mastering different task phases was associated with distinct changes in neural activity, which included recruitment of larger numbers of neurons, increases or decreases of their firing rate, changes in the correlation structure between neurons, and redistribution of power across LFP frequency bands. In every training phase, changes induced by the actively learned task were also observed in a control task, which remained the same across the training period. Our results reveal how learning to perform cognitive tasks induces plasticity of prefrontal cortical activity, and how activity changes may generalize between tasks.

Cognitive process in high neuroticism: incompatible flexibility in frontal brain region

Objective: This study examines the difference of interference effect in high and low neuroticism. Material and Methods: Low and high groups of neuroticism performed the congruent and incongruent Stroop Colour Word task in the Event Related Potential session. The ERP P300 was extracted and analysed. Results: High neuroticism exhibited larger P300 amplitude than low neuroticism in both congruent and incongruent condition. Conclusion: High neuroticism appraises conflict and non-conflict condition under incompatibility manner driven by prefrontal cortical top–down control. Bangladesh Journal of Medical Science Vol. 21(1) 2022 Page : 129-134

Effect of Heart Rate Reserve on Prefrontal Cortical Activation While Dual-Task Walking in Older Adults

Hypertension is considered a risk factor for cardiovascular health and non-amnestic cognitive impairment in older adults. While heart rate reserve (HRR) has been shown to be a risk factor for hypertension, how impaired HRR in older adults can lead to cognitive impairment is still unclear. The objective of this study was to examine the effects of HRR on prefrontal cortical (PFC) activation under varying dual-task demands in older adults. Twenty-eight older adults (50–82 years of age) were included in this study and divided into higher (n = 14) and lower (n = 14) HRR groups. Participants engaged in the cognitive task which was the Modified Stroop Color Word Test (MSCWT) on a self-paced treadmill while walking. Participants with higher HRR demonstrated increased PFC activation in comparison to lower HRR, even after controlling for covariates in analysis. Furthermore, as cognitive task difficulty increased (from neutral to congruent to incongruent to switching), PFC activation increased. In addition, there was a significant interaction between tasks and HRR group, with older adults with higher HRR demonstrating increases in PFC activation, faster gait speed, and increased accuracy, relative to those with lower HRR, when going from neutral to switching tasks. These results provide evidence of a relationship between HRR and prefrontal cortical activation and cognitive and physical performance, suggesting that HRR may serve as a biomarker for cognitive health of an older adult with or without cardiovascular risk.

Prefrontal cortical contributions to working memory loading, maintenance and recall are parsed by hippocampal-prefrontal oscillatory assembly dynamics

Working memory enables incorporation of recent experience into subsequent decision-making. This processing recruits both prefrontal cortex and hippocampus, where neurons encode task cues, rules and outcomes. However, precisely which information is carried when, and by which neurons, remains unclear. Using population decoding of activity in rat medial prefrontal cortex (mPFC) and dorsal hippocampal CA1, we confirm that mPFC populations lead in maintaining sample information across delays of an operant non-match to sample task, despite individual neurons firing only transiently. During sample encoding, distinct mPFC subpopulations joined distributed CA1-mPFC cell assemblies hallmarked by 4-5Hz rhythmic modulation; CA1-mPFC assemblies re-emerged during choice episodes, but were not 4-5Hz modulated. Delay-dependent errors arose when attenuated rhythmic assembly activity heralded collapse of sustained mPFC encoding; pharmacological disruption of CA1-mPFC assembly rhythmicity impaired task performance. Our results map component processes of memory-guided decisions onto heterogeneous CA1-mPFC subpopulations and the dynamics of physiologically distinct, distributed cell assemblies.

Ambient Air Pollution and Increasing Depressive Symptoms in Older Women: The Mediating Role of The Prefrontal Cortex

Exposure to air pollution may accelerate brain aging and increase risk of late-life depressive symptoms (DS). Brain structures underlying these associations are unknown. Longitudinal data from 829 community-dwelling women without dementia (baseline age 81.6 ± 3.6 years old) who participated in both the Women’s Health Initiative Memory Study Magnetic Resonance Imaging study (WHIMS-MRI; 2005-06) and the WHIMS-Epidemiology of Cognitive Health Outcomes (2008-16) were analyzed to examine whether volumetric measures of brain structures mediated associations between long-term exposure to ambient air pollutants and annual increases in DS (as measured by annually assessed 15-item Geriatric Depression Scale). Annual PM2.5 (fine particulate matter of aerodynamic diameter <2.5) and NO2 were estimated at the participants’ residence using regionalized universal kriging models and aggregated to the 3-year average prior to the WHIMS-MRI. Structural equation models were constructed to estimate associations between exposure, structural brain variables, and trajectories of DS (standardized on baseline mean and SD). Living in locations with higher NO2 (standardized β = 0.023; 95% Confidence Interval (CI) = 0.004, 0.042) or PM2.5 (standardized β = 0.021; 95% CI = 0.004, 0.038) was associated with larger annual increases in DS (~60% larger annual increase in DS). Higher NO2, but not PM2.5, was associated with smaller prefrontal cortical volumes (standardized β = -0.431; 99% CI = -0.518; -0.344). Prefrontal cortical volume explained 30.4% of the total association between annual DS increase and NO2. These findings underscore the importance of the prefrontal cortex in associations between NO2 exposure and increasing DS in later-life.

A corticothalamic circuit trades off speed for safety during decision-making under motivational conflict

Decisions to act while pursuing goals in the presence of danger must be made quickly but safely. Premature decisions risk injury or death whereas postponing decisions risk goal loss. Here we show how mice resolve these competing demands. Using microstructural behavioral analyses, we identified the spatiotemporal dynamics of approach-avoidance decisions under motivational conflict. Then we used cognitive modelling to show that these dynamics reflect the speeded decision-making mechanisms used by humans and non-human primates, with mice trading off decision speed for safety of choice when danger loomed. Using calcium imaging and functional circuit analyses, we show that this speed-safety trade off occurs because increases in paraventricular thalamus (PVT) activity increase decision caution, thereby increasing approach-avoid decision times in the presence of danger. Our findings demonstrate that a discrete brain circuit involving the PVT and its prefrontal cortical input dynamically adjusts decision caution during motivational conflict, trading off decision speed for decision safety when danger is close. They identify the corticothalamic pathway as central to cognitive control during decision-making under conflict.

Glutamate Carboxypeptidase II in Aging Rat Prefrontal Cortex Impairs Working Memory Performance

Glutamate carboxypeptidase II (GCPII) expression in brain is increased by inflammation, and reduces NAAG (N-acetyl aspartyl glutamate) stimulation of mGluR3 signaling. Genetic insults in this signaling cascade are increasingly linked to cognitive disorders in humans, where increased GCPII and or decreased NAAG-mGluR3 are associated with impaired prefrontal cortical (PFC) activation and cognitive impairment. As aging is associated with increased inflammation and PFC cognitive deficits, the current study examined GCPII and mGluR3 expression in the aging rat medial PFC, and tested whether GCPII inhibition with 2-(3-mercaptopropyl) pentanedioic acid (2-MPPA) would improve working memory performance. We found that GCPII protein was expressed on astrocytes and some microglia as expected from previous studies, but was also prominently expressed on neurons, and showed increased levels with advancing age. Systemic administration of the GCPII inhibitor, 2-MPPA, improved working memory performance in young and aged rats, and also improved performance after local infusion into the medial PFC. As GCPII inhibitors are well-tolerated, they may provide an important new direction for treatment of cognitive disorders associated with aging and/or inflammation.