No abstract

Odor perception can both evoke emotional states and be shaped by emotional or hedonic states. The amygdala complex plays an important role in recognition of, and response to, hedonically valenced stimuli, and has strong, reciprocal connectivity with the primary olfactory (piriform) cortex. Here, we used differential odor-threat conditioning in rats to test the role of basolateral amygdala (BLA) input to the piriform cortex in acquisition and expression of learned olfactory threat responses. Using local field potential recordings, we demonstrated that functional connectivity (high gamma band coherence) between the BLA and posterior piriform cortex (pPCX) is enhanced after differential threat conditioning. Optogenetic suppression of activity within the BLA prevents learned threat acquisition, as do lesions of the pPCX prior to threat conditioning (without inducing anosmia), suggesting that both regions are critical for acquisition of learned odor threat responses. However, optogenetic BLA suppression during testing did not impair threat response to the CS+ , but did induce generalization to the CS−. A similar loss of stimulus control and threat generalization was induced by selective optogenetic suppression of BLA input to pPCX. These results suggest an important role for amygdala-sensory cortical connectivity in shaping responses to threatening stimuli.

In this direct replication of Mueller and Oppenheimer’s (2014) Study 1, participants watched a lecture while taking notes with a laptop ( n = 74) or longhand ( n = 68). After a brief distraction and without the opportunity to study, they took a quiz. As in the original study, laptop participants took notes containing more words spoken verbatim by the lecturer and more words overall than did longhand participants. However, laptop participants did not perform better than longhand participants on the quiz. Exploratory meta-analyses of eight similar studies echoed this pattern. In addition, in both the original study and our replication, higher word count was associated with better quiz performance, and higher verbatim overlap was associated with worse quiz performance, but the latter finding was not robust in our replication. Overall, results do not support the idea that longhand note taking improves immediate learning via better encoding of information.

Objective: To examine the relationship between depression and cognition, genetic risk, and hippocampal differences in a sample of older adults with a history of traumatic brain injury (TBI). Method: Participants were 85 males and 35 females (91 Caucasian, 29 African-American) with a mean age of 65.04 (± 8.27) years and a history of moderate, severe, or complicated mild TBI. Participants were an average of 9.33 (± 7.27) years post injury (range: 0.78-45.63). Participants underwent genetic testing, a comprehensive neuropsychological battery, surveys, and a subset underwent MRI scanning. Results: Apolipoprotein E (APOE) e4 carrier status predicted clinically significant depressive symptomatology on the Geriatric Depression Scale (GDS) with an odds ratio of 3.63, 95% CI [1.33, 9.29]. GDS was not associated with scores on measures of executive function, list learning recall, or retention. Although GDS score was initially associated with poorer confrontation naming scores and story memory recall, these effect sizes were small, and this variance was better accounted for by age and cognitive reserve. Higher GDS scores were also associated with decreased hippocampal volume. Conclusions: APOE carrier status was predictive of depression in a sample of older adults with a history of TBI. Depressive symptoms were also associated with decreased hippocampal volume but did not predict cognitive deficits in the examined domains beyond the effects of cognitive reserve. Despite the relationship between GDS and biological risks for decline, depressive symptoms in this population showed no direct relationship with cognitive decline. Key PointsQuestion: Is depression associated with cognitive decline, hippocampal volume, and APOE status in older adults with a history of moderate to severe TBI? Findings: Depression was associated with APOE genotype and decreased hippocampal volume but did not serve as a marker for cognitive decline beyond other known predictors. Importance: To date, there has been minimal research on depression in msTBI, and our research demonstrates depression's unique role in morphometric differences but not cognitive changes in older adults with TBI history and replicates more recent findings establishing an association between APOE carrier status and depression in a moderate-to-severe TBI sample. Next Steps: Given the relationship between depression and biological markers of decline in this sample, research should first replicate this finding, and if confirmed, work to identify underlying mechanisms between TBI-related depression and future health risks. This article was published Online First September 27, 2021. Samantha M. Vervoordt https://orcid.org/0000-0003-4419-5631 We have no known conflict of interest to disclose. This project is funded, in part, under a Grant from the Pennsylvania Department of Health. The Department specifically disclaims responsibility for any analyses, interpretations, or conclusions. Samantha M. Vervoord had played a lead role in formal analysis, visualization, writing of original draf...

The replication crisis poses important challenges to modern science. Central to this challenge is re-establishing ground truths, or the most fundamental theories that serve as the bedrock to a scientific community. However, the goal to identify hypotheses with the greatest support is non-trivial given the unprecedented rate of scientific publishing. In this era of high-volume science, the goal of this study is to sample from one research community within clinical neuroscience (traumatic brain injury) and track major trends that have shaped this literature over the past 50 years. To do so, we first conduct decade-wise (1980-2019) network analysis to examine the scientific communities that shape this literature. To establish the robustness of our findings, we utilized searches from separate search engines (Web of Science; Semantic Scholar). As a second goal, we sought to determine the most highly cited hypotheses influencing the literature in each decade. In a third goal, we then searched for any papers referring to “replication” or efforts to reproduce findings within our >50,000 paper dataset. From this search, 550 papers were analyzed to determine the frequency and nature of formal replication studies over time. Finally, to maximize transparency, we provide a detailed procedure for the creation and analysis of our dataset, including a discussion of each of our major decision points, to facilitate similar efforts in other areas of neuroscience. We found that the unparalleled rate of scientific publishing within the brain injury literature combined with the scarcity of clear hypotheses in individual publications are a challenge to both evaluating accepted findings and determining paths forward to accelerate science. Additionally, while the conversation about reproducibility has increased over the past decade, the rate of published replication studies continues to be a negligible proportion of the research. Meta-science and computational methods offer the critical opportunity to assess the state of the science and illuminate pathways forward, but ultimately there is structural change needed in the brain injury literature and perhaps others.