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Biology subjects

Fang, F.

Publications and source records attributed to Fang, F..

At least 19 recordsLinked to original sources

Evidence Accumulation in Synaptic Efficacy: Activity-Silent Decision-Making with Short-Term Plasticity

Decision-making requires accumulation of evidence over time, yet exactly how neural circuits implement this computation remains debated. Classical models posit that evidence accumulation is realized by ramping neural activity, whereas recent experimental findings suggest an alternative mechanism in which neural activity remains largely silent before abruptly transitioning into an active decision state. This mechanism leaves a fundamental question unanswered: how is evidence accumulated during the neural activity-silent period? To address this question, we trained excitatory-inhibitory recurrent neural networks (RNNs) with short-term synaptic plasticity (STP) on a reaction-time decision task. We found that after training, the networks learned to leverage STP to make decisions in an activity-silent manner. Choice-tuning analysis revealed a clear functional organization of the network, and connection-pruning analysis uncovered the coupling between choice-selective excitatory and inhibitory neural groups. Guided by the architecture of trained RNNs, we constructed a minimal neural circuit model, in which evidence accumulates in facilitated synaptic efficacy that progressively reshapes the circuit's phase portrait, eventually driving the network state across the stability boundary and triggering a rapid transition to a choice state. We further compared activity before a choice between the theoretical STP and Static models to examine the potential energy benefit of activity-silent decision-making. Together, our results suggest STP as a mechanism for evidence accumulation in activity-silent decision-making and offer insights into the design of energy-efficient artificial neural networks.

neuroscience↗

Advancing Neurological Liquid Biopsy via Six-Base Sequencing of Cerebrospinal Fluid Cell-Free DNA

Real-time molecular insights into the human brain are crucial for understanding neurological conditions and development of soluble biomarkers but challenged by the limited access to target tissue. Here we utilize 6-base sequencing to profile DNA modifications of cell-free DNA released from neural cells into cerebrospinal fluid. This strategy provides molecular, quantitative and qualitative insights into the ongoing neurodegenerative biology, which paves the way for liquid biopsy approaches to study neurological conditions.

neuroscience↗

Metagenomic and metabolomic analysis of a bryozoan-associated microbial complex from the Hanjiang River, China

Background Bryozoans are ancient colonial animals that have existed for over 470 million years and are widely distributed across aquatic environments. Recently, many spherical colloids (average diameter{approx}1 meter in diameter), containing bryozoans and diverse microorganisms, were found in the Hanjiang river in China. In this study, we investigated these bryozoan-dominated microbial complexes using metagenomic sequencing, metabolomic profiling, and complementary approaches. Results The results revealed that the microbial structure dominated by bryophytes included eukaryotes such as fungi, microalgae, and small parasites etc., as well as prokaryotes such as bacteria and viruses. All members form a highly integrated consortium that collaboratively maintains community function and stability, which displayed the shape and structure of a regular microbial complex and increased in size. Additionally, the results suggested the predominately presence of Proteobacteria were particularly abundant and are known to produce bryostatins in response to bryozoan signals. Interesting, it was implied that a decrease or even a loss in virulence occurs when pathogenic microorganisms become members of the complex. This is the first study focusing on the composition and metabolites of the unusual microorganism complex. The results discovered the close and intriguing connections within the microbial communities dominated by the ancient organism bryozoan through multi-omics technologies. It showed that both eukaryotes and prokaryotes can coordinate or compete, thereby forming a stable composite structure.

zoology↗

Proteoform Barcode: An Intuitive Visualization Framework for Top-Down Proteomics

Top-down proteomics (TDP) advances biomedical research by providing a birds-eye view of proteoforms in cells, tissues, and biofluids. Thousands of proteoforms can be characterized using well-established TDP technologies, and potential proteoform biomarkers of diseases have been discovered. However, there is a lack of an easy and biologically informative approach to present the quantitative global TDP data. Here, we present proteoform barcode as a straightforward visualization approach that simultaneously displays proteoform abundance and their associated Gene Ontology (GO) biological processes, converting a list of proteoforms to a biologically informative image. The proteoform barcode allows 1) a global view of proteoforms (i.e., relative abundance and functional information) in complex biological systems (i.e., bacteria, yeast, human cells, and human plasma) and 2) the accurate distinction of samples in diverse biological conditions (i.e., control and disease) assisted by machine learning approaches. The proteoform barcode, assisted by the random forest model, accurately separated the human plasma samples of healthy controls and early-stage breast cancer. The data demonstrates the high potential of the proteoform barcode-based approach for early diagnosis of diseases in an easy and biologically informative manner.

systems biology↗

Differences in microbial community structure and soil nutrients between healthy and diseased soils of Zingiber officinale

To investigate the differences in soil nutrients and microbial community structure in the rhizosphere between healthy and diseased Zingiber officinale plants, soil samples were collected from healthy root-zone soil (ZSH), healthy rhizosphere soil (RSH), diseased root-zone soil (ZSD), and diseased rhizosphere soil (RSD). Diseased soils had significantly higher pH values, whereas RSH showed the strongest acidity. Moreover, pH, AN, and AK contents in diseased soils were significantly higher than those in healthy soils, while SOM and AP were significantly lower. The -diversity of microbial communities in diseased soils was significantly reduced, and the community structure was distinctly differentiated from that of healthy soils. In diseased soils, the abundance of potential pathogenic taxa such as Ralstonia solanacearum increased significantly, while beneficial genera such as Bradyrhizobium decreased. Redundancy analysis and correlation analysis indicated that soil pH, AN, SOM, and AP were the major environmental factors driving changes in microbial community structure. The occurrence of soil-borne diseases in Zingiber officinale is closely associated with soil nutrient imbalance and disruption of microbial community structure. The study identified candidate microbial taxa (e.g., beneficial Sphingomonas, Streptomyces) and key soil properties (pH, available nitrogen) that differentiate healthy from diseased ginger soils. Together, these findings provide a theoretical basis for improving diseased soils through microecological regulation strategies, and also serve as a foundation for generating testable hypotheses in future hypothesis-driven research on ginger soil-borne disease suppression.

microbiology↗

Human-like sequential sound-to-meaning transfer drives artificial speech comprehension

Artificial intelligence has reached a pivotal threshold. Multimodal large models can approach human-level speech comprehension by rapidly transforming sound into meaning. However, whether this process relies on human-like mechanisms remains unknown. Here, we compared the human brain with twelve speech language models (SLMs) using a phonology-semantics confusion paradigm. Stereo-electroencephalography revealed two mechanisms of phonology-to-semantics (P2S) transfer in the human brain: a local sequential transformation within specific neuronal populations, and a global cross-regional hierarchy of P2S representations. Only brain-model alignment in the local sequential manner predicted model performance. Correspondingly, targeted lesioning of local sequential P2S-transfer model units markedly impaired comprehension performance, while activation steering of these units improved performance. In addition, such local sequential P2S-transfer model units were identified across languages. Together, this study establishes local sequential P2S transformation as a fundamental computational principle shared across biological and artificial intelligence, offering a mechanistic bridge for future brain-inspired speech systems.

neuroscience↗

From Representation to Action: A Unified Laplacian Framework for Spatial Representation and Path Planning

Navigation in complex environments relies on internal spatial representations that guide action. While the brain employs a diverse repertoire of spatial tuning cells--including grid, place, and head-direction cells--a normative theory linking these static neural codes to the dynamic process of navigation remains elusive. In this work, we propose a Unified Laplacian Framework derived from first principles of representational smoothness and efficiency. We first demonstrate that diverse spatial codes emerge naturally as spectral decompositions of the Laplace operator. Crucially, bridging the gap from representation to action, we derive a biologically plausible navigation policy based on the Greens function potential. We show that this potential encodes the environments intrinsic geometry to enable simple, trap-free gradient ascent, achieving improved sample efficiency and generalization in goal-reaching tasks. Furthermore, we demonstrate that these spectral representations can be learned directly from high-dimensional visual inputs, confirming their plausibility in realistic environments. Our results suggest that the "cognitive map" can be viewed as a spectral embedding of the Laplacian, providing a rigorous foundation for spatial cognition in both biological and artificial agents.

neuroscience↗

Primary cilia regulate mechanical adaptation of tendon and enthesis via hedgehog signaling

BackgroundPhysical loading mediates postnatal growth, homeostasis, and healing of the tendon and its attachment to bone, which is critical for rotator cuff functional integrity. Our prior studies have highlighted the mechano-sensing role of primary cilia; However, the mechanisms through which cilia convert mechanical stimuli into structural functional adaptation under altered loading conditions remain unanswered. MethodsPublicly available scRNA-seq datasets of mechanically loaded human patellar tendon cells were re-analyzed to identify cilia-related transcriptional changes. Tendon-specific cilia knockout mice (ScxCre;Ift88fl/fl) and wild-type controls (Ift88fl/fl) underwent mechanical unloading induced by botulinum toxin A injection, followed by micro-computed tomography, biomechanical testing, histology, qPCR, and immunohistochemistry to evaluate structural, mechanical, and Hedgehog (Hh) signaling responses. Primary tendon fibroblasts from wild-type and cilia-deletion mice were treated with Hh agonist or antagonist to assess Hh signaling responsiveness in vitro. Students t-test for two groups and two-way ANOVA for two groups with two treatments were performed for our statistical analysis. ResultsHere, we find that mechanical force causes changes in cilia- and hedgehog (Hh)-related gene expression in human tendon fibroblasts. Cilia ablation in the enthesis blunts force-driven remodeling of tissue structure and mechanical strength. Cilia deletion also leads to impaired Hh signaling in tendon cells and decreased responsiveness to activation and inactivation of hedgehog signaling. ConclusionsOur results demonstrate loading-regulated ciliary Hh signaling during postnatal growth of the tendon and enthesis and provide proof-of-concept for developing new cilia-targeted mechanical and biological therapies for enthesis repair.

developmental biology↗

Celastrol alleviates SGLT2 inhibitor-induced diabetic hyperketonemia by inhibiting hepatic ketogenesis

SGLT2 inhibitor (SGLT2i)-induced diabetic hyperketonemia is a life-threatening acute complication of diabetes. While Celastrol has been reported to exert beneficial effects on obesity; its potential role in ketogenesis remains unclear. In this study, Celastrol administration significantly attenuates the fasting-induced elevation of blood {beta}-hydroxybutyrate. Moreover, a 7-day course of Celastrol (1 mg/kg/day) leads to reductions in body weight and fat mass. Mechanistically, Celastrol specifically downregulates HMGCS2 expression and suppressess hepatic ketogenesis through inhibiting PPAR expression in the short term ([≤] 2 days). However, after prolonged treatment for 7 days, Celastrol modulates both PPARand serum free fatty acids (FFAs) levels. Furthermore, anti-ketogenic effect of Celastrol is abolished in Ppar{square} /{square} mice. Importantly, Celastrol effectively ameliorates SGLT2i-induced hyperketonemia. In summary, Celastrol curbs hepatic ketone overproduction in a PPAR-dependent manner, indicating its protective potential against SGLT2i-induced hyperketonemia.

molecular biology↗

Uncovering zebrafish embryonic proteome dynamics across 16 time points during the first 24 hours of development

Defining how proteins change over developmental time is amenable to studies deciphering regulatory genetic networks in vertebrate development, biology, and pharmacology. In an approach toward such quantitative studies of dynamic network behavior, we produced an atlas using the mass spectrometry-based method to investigate protein expression changes across 16 time points from the zygote to the early pharyngula stage zebrafish embryos. We systematically summarize 8 clusters for interrogating changes in protein expression associated with the development of zebrafish embryos. Specifically, we identified a class of zinc finger-related transcription factors primarily located on the long arm of chromosome 4, which are highly expressed during zygotic genome activation. Furthermore, we highlight the power of this analysis to assign developmental stage-specific expression information to chromosomes and tissues. Time-resolved analyses reveal significant discordance between differential transcript and protein expression, whereas no time lag is observed for proteins involved in stable and fundamental biological processes, such as metabolism (e.g., Ppt2a and Gatm), cytoskeletal organization (e.g., Col18a1), and the translation machinery (e.g., Eif4enif1). This atlas offers high-resolution and in-depth molecular insights into zebrafish development, providing a resource for developmental biologists to generate hypotheses for functional analysis of proteins during early vertebrate embryogenesis. HighlightsO_LIA global protein expression database with high time resolution is created for zebrafish embryos. C_LIO_LIDistinct patterns of protein expression correlate with biological processes. C_LIO_LITranscription factors have a burst of expression from the gastrulation stage. C_LIO_LIDevelopmental stage-specific protein expressions were assigned to chromosomes and tissues. C_LIO_LIHigh-resolution embryonic transcriptome and proteome datasets were compared and connected. C_LI

developmental biology↗

A population-scale red blood cell proteome reveals genetically encoded aging clocks predictive of hemolysis and blood donor activity

As the most abundant human cell and the foundation of transfusion medicine, red blood cells (RBCs) offer a unique readout of systemic health, yet they have never been characterized at population scale. We generated a proteome atlas of 13,091 blood donors with multi-omics longitudinal phenotyping, characterizing the influence of demographics and genetic variation on the reproducibility of RBC proteomes across donations. Elastic-net aging clocks captured biological aging with high accuracy and uncovered genetic regulators of {Delta}Age at FN1, C4/IKZF1, CRAT, PFAS, TRIM58. Across independent cohorts, {Delta}Age was accelerated in G6PD deficiency, sickle cell trait/disease, and iron deficiency, reversed by iron repletion, and slowed in high-frequency donors, linking molecular aging to brain iron/myelin and cognitive performance. Molecular aging signatures predicted storage, osmotic, and oxidative hemolysis, hemoglobin increments after transfusion, and long-term donor activity over 12-years. These results establish RBC proteomics as a scalable biomarker of aging, donor healthspan, and transfusion outcomes. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=200 SRC="FIGDIR/small/710284v1_ufig1.gif" ALT="Figure 1"> View larger version (96K): org.highwire.dtl.DTLVardef@15bd46eorg.highwire.dtl.DTLVardef@1d7c107org.highwire.dtl.DTLVardef@1c1d870org.highwire.dtl.DTLVardef@168dc6f_HPS_FORMAT_FIGEXP M_FIG Dzieciatkowska et al. generate the first population-scale atlas of the RBC proteome across 13,000 donors and develop proteomic and metabolomic aging clocks that quantify biological age. Molecular {Delta}Age is reproducible across donations, genetically encoded and accelerated in G6PD deficiency, sickle cell trait/disease, and iron deficiency - yet reset by iron repletion, tracking with cognitive function and brain iron/myelin. RBC aging clocks predict hemolytic fragility, transfusion efficacy, and donor activity 12 years later. C_FIG HighlightsO_LIRBC proteome atlas of 13,091 donors reveals demographic and genetic programs C_LIO_LIGenetically encoded RBC aging clocks identify regulators of molecular {Delta}age C_LIO_LIMolecular aging features predict hemolysis and transfusion response across cohorts C_LIO_LIRBC molecular age forecasts long-term donor activity over a 12-year follow-up C_LI

biochemistry↗

Global Proteomic Analysis of Colorectal Cancers Stratified by Microsatellite Instability Subtype Reveals Protein Differences

Lynch syndrome, historically known as hereditary nonpolyposis colorectal cancer, is caused by germline mutations in the DNA mismatch repair (MMR) genes, MLH1, MSH2 (EPCAM), MSH6, and PMS2. While the genetic changes associated with Lynch Syndrome have previously been characterized, there have not been studies of the associated proteomic alterations, in part because of the limited availability of primary samples and the absence of in vitro model systems. In this study, the first large-scale tissue proteomic assessment of Lynch Syndrome samples as well as three other subtypes of colorectal cancer was completed with specimens from the Ohio Colorectal Cancer Prevention Initiative. The cohort contained three groups of microsatellite unstable (MSI-high) CRC patients (Lynch syndrome, double somatic MMR mutation, and MLH1 hypermethylation) and a group of microsatellite stable (MSS) CRC patients. A total of 122 tumor and complimentary normal mucosa samples from 61 patients were evaluated using label-free bottom-up proteomic analysis. Hierarchical clustering analysis of the global proteome showed that the MSS group was significantly different than the three MSI-high groups. Of the 1,084 proteins found to be dysregulated across all four colorectal cancer subtypes, there were age at diagnosis associated shifts in proteins correlated with tumor proliferation and immune regulation for the Lynch syndrome and Double Somatic samples. The proteins TPD52, GMDS, and DSP showed increased protein abundance correlated with older age at diagnosis. In addition, the Lynch syndrome samples showed substantial sex-based differences in immune and inflammatory pathways, for example, downregulation of ZG16, DIS3, and WDR43. This study fills a critical gap as the first proteomic characterization of Lynch syndrome samples to date. Data are available via ProteomeXchange with identifier PXD073693. TeaserThis is the first study of the global proteomic differences between Lynch Syndrome and other forms of colorectal cancer.

cancer biology↗

Lipid nanoparticle protein coronas form via lipoprotein fusion rather than shell-like adsorption

The protein corona influences the in vivo biodistribution of ionizable lipid nanoparticles (LNPs) in nucleic acid delivery, yet its structural architecture remains poorly defined. Using cryo-transmission electron microscopy, we visualized LNP-protein interactions in their native state. We show that, unlike the discrete "fuzzy" shells observed on hard nanoparticles, LNPs displayed no peripheral protein shell. Instead, controlled incubation and competitive "dual-particle" assays, supported by molecular dynamics simulations, indicate that LNP membranes undergo localized thickening and electron-dense remodeling consistent with lipoprotein integration rather than surface adsorption. Similar features were observed in extracellular vesicles, suggesting this behavior is shared among lipid-based carriers, and proteomic analysis identified apolipoproteins as the dominant associated proteins. Together, these findings support a model in which the biological identity of LNPs arises through membrane remodeling rather than shell-like adsorption, and provide a framework for the rational design of targeted nanomedicines. TOC Graphic O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=138 SRC="FIGDIR/small/695162v2_ufig1.gif" ALT="Figure 1"> View larger version (79K): org.highwire.dtl.DTLVardef@a6f2b2org.highwire.dtl.DTLVardef@879d12org.highwire.dtl.DTLVardef@159196dorg.highwire.dtl.DTLVardef@945749_HPS_FORMAT_FIGEXP M_FIG C_FIG

bioengineering↗

Acetylcholine Enhances Deviance Detection in Hodgkin-Huxley Neuronal Networks

The brains ability to detect unexpected events, deviance detection (DD), is critical for survival. While DD has been computationally explained by synaptic plasticity, the role of neuromodulators like acetylcholine (ACh) remains less understood. Here, we examine how ACh modulates DD without invoking additional plasticity mechanisms. Using a cholinergic-sensitive Hodgkin-Huxley network of 200 neurons arranged in 2D space and stimulated via five spatially distinct inputs (A-E), we implemented an oddball paradigm with three conditions: standard (80% A, 20% B), deviant (20% A, 80% B), and a multi-standard control (20% each of A-E). ACh levels were controlled by the conductance of the slow K+ current. In the absence of ACh, the network already exhibited DD, responding more strongly to deviant A compared to control A. Notably, introducing a small amount of ACh amplified DD, while further increases suppressed it. Maximal DD occurred when strong spike frequency adaptation to standard B reduced competition, and enhanced phase-locking synchronized the networks response to deviant A. These findings reveal how neuromodulation can shape context-sensitive neural computation, optimizing detection of salient events through a dynamic balance of suppression and synchronization.

neuroscience↗

Neural Correlates of Trial Outcome Monitoring during Long-term Learning in Primate Posterior Parietal Cortex

Monitoring behavioral outcomes is crucial for optimizing behavior and learning new tasks. However, how the brain monitors outcome information during long-term learning remains largely unknown. Using two-photon calcium imaging in behaving monkeys, we tracked neuronal activity in area 7a of the posterior parietal cortex (PPC), an important associative cortex that has not been typically implicated in associative learning (AL), while the macaque monkeys learned new visual-motor associations over multiple days. We found robust neuronal representation of salient behavioral outcomes (correct vs. incorrect) which closely correlated with the monkeys learning behavior. Furthermore, outcome representation significantly reorganized when monkeys transitioned to learn novel associations, followed by gradual evolution over subsequent learning days, a process constrained by the functional connectivity among neurons within local network. These suggest a substantive role for primate PPC in long-term AL through monitoring trial outcome, and indicate a principle for long-term learning: network connectivity constrains the evolution of neural encodings.

neuroscience↗

Spleen-derived Small Extracellular Vesicles Protect against Myocardial Infarction via Mediating Spleen-heart Crosstalk

Background and AimsAcute myocardial infarction (AMI) triggers systemic responses that influence cardiac injury and repair, but protective mediators within the cardiosplenic axis remain incompletely understood. This study aimed to investigate whether spleen-derived small extracellular vesicles (sEVs) exert cardioprotection after AMI, identify critical cargo, and evaluate their clinical relevance. MethodsThe effects of splenectomy, spleen-derived sEVs and pharmacological inhibition of sEVs biogenesis on cardiac injury were evaluated in mice with AMI. Parabiosis, donor splenectomy, and fluorescent labelling traced the origin and myocardial recruitment of circulating sEVs. 4D-proteomics profiled sEVs cargo with a focus on pyruvate carrier-1 (MPC1). ResultsSplenectomy worsened survival, ventricular function, infarct size, and fibrosis in mice with AMI. AMI upregulated splenic extracellular-vesicle pathways, with sEVs release peaking at day 3 (M3D-sEVs). Labelled splenic sEVs preferentially accumulated in ischemic myocardium, confirmed by parabiosis experiments. M3D-sEVs improved survival and cardiac function and reduced infarct size, fibrosis, apoptosis, inflammation, and hypertrophy. In addition, anti-apoptotic effects were reproduced in vitro. Inhibition of sEVs biogenesis decreased circulating sEVs, aggravated injury, and was rescued by M3D-sEVs. M3D-sEVs were enriched in MPC1, and MPC1 neutralization or pharmacological blockade abrogated sEVs-mediated restoration of respiration, ATP generation, and reduction of reactive oxygen species. Plasma sEVs-associated MPC1 was highest in patients with AMI, intermediate in coronary heart disease, and lowest in controls. ConclusionsThe spleen responds adaptively to AMI by releasing MPC1lenriched sEVs that travel to injured myocardium, preserve mitochondrial energetics, and reduce damage, supporting cargolspecific sEVs augmentation and sEVslMPC1 as a potential therapeutic target and biomarker in ischemic heart disease. Structured graphical abstractAcute myocardial infarction activates a spleen-heart axis in which the spleen releases mitochondrial pyruvate carrier 1 (MPC1) enriched small extracellular vesicles that home to the infarcted myocardium, preserve mitochondrial oxidative phosphorylation, reduce ROS, and limit infarct size, apoptosis, fibrosis, and hypertrophy. Circulating sEVs-associated MPC1 might serve as a potential biomarker for estimating risk of ischemic heart disease. Translational perspectiveO_LIOur findings reveal a novel heart-spleen communication axis mediated by splenic small extracellular vesicles (sEVs) following AMI. These vesicular messengers predominantly deliver mitochondrial pyruvate carrier 1 (MPC1), enhancing cardiac mitochondrial energy metabolism in the injured myocardium, ultimately improving post-AMI functional recovery in experimental models. C_LIO_LIA higher plasma sEVs-associated MPC1 level was observed in AMI patients when compared with non-AMI patients. These findings support the clinical relevance of the spleen-heart axis, introduce sEVs-associated MPC1 as a potential circulating biomarker for early myocardial injury and therapeutic target. C_LI

molecular biology↗

Active and predictive adjustment of pupil size for accommodating visual regularity

The visual system efficiently encodes information by summarizing visual regularities that could be quantified by summary statistics. While summary statistics are thought to be processed in several cortical and subcortical areas, we investigated whether the earliest stage of visual processing, the pupil, is involved in this process. In three experiments, participants either performed ensemble orientation estimation with or passively viewed bar arrays with different bar orientation distributions while their pupil size was recorded. We found that pupil size increased when the orientation distribution became more dispersed and was closely linked to participants estimation performance. Furthermore, pupillary responses occurred automatically during passive viewing and could even predict ensemble orientation estimation performance. Moreover, when anticipating a dispersed distribution, the pupil dilated in advance. Our findings reveal a new cognitive role of the pupil - it actively and predictively adjusts its size to facilitate the extraction of visual regularity.

neuroscience↗

Independent regulation of memory and emotion by selective retrieval

Selective retrieval of a target memory often triggers inhibitory control to reduce competition from related traces, a process that induces forgetting of the competing content. It is unknown, however, whether inhibition during selective retrieval specifically targets a competitors episodic representation or instead extends to its affective components. Here we report evidence in humans that selective retrieval of a neutral memory not only diminishes access to the mnemonic content of unpleasant competing memories, but also alters their emotional character. Memory and emotion suppression effects were accompanied by reduced neural activation and weakened representational patterns unique to competing memories in the VTC and amygdala respectively, in an independent fashion. Selective retrieval engaged the left VLPFC, which decreased in activity over repeated retrievals of the same memory, as competition from the unpleasant scene was resolved. This left VLPFC region colocalizes with key prefrontal regions engaged during cognitive reappraisal, suggesting that selective retrievals impact on affective responses may contribute to reappraisals benefits. These findings indicate that inhibitory control during selective retrieval affects both mnemonic and affective representations, providing a novel mechanistic basis for a well-known emotion regulation practice.

neuroscience↗