Biology subjects

Murphy, Z.

Publications and source records attributed to Murphy, Z..

5 recordsLinked to original sources

bioRxiv2025

Investigating Facial Expression Processing during Fast Periodic Visual Stimulation using Highly Variable Stimuli

Facial expression recognition is a fundamental aspect of human social interaction, enabling effective communication and emotional understanding. Fast Periodic Visual Stimulation (FPVS) paradigms have recently emerged as a powerful approach for studying facial expression processing. However, previous studies often utilized identical base stimuli, making it difficult to disentangle neural responses to low-level perceptual differences from those reflecting conceptual discrimination of emotion. By introducing variability in our stimuli, we aimed to overcome these limitations and investigate neural responses to facial expressions of anger, fear, happiness, and sadness. Using EEG, robust oddball responses were observed across participants at both individual and group levels, demonstrating the paradigms sensitivity even with brief recordings and limited post-processing. Significant neural responses were detected across key regions of interest, with the right occipito-temporal region showing the strongest activity, consistent with its role in high-level facial expression processing. This study highlights the effectiveness of the FPVS paradigm for examining emotional processing using naturalistic stimuli and provides a framework for future research into neural mechanisms underlying facial emotion recognition in diverse and pathological populations.

neuroscience↗

bioRxiv2025

Reduced Fast Periodic Visual Stimulation Oddball Responses to Threatening Faces Associated with Anxiety

Facial expression processing is crucial for social communication and survival, with anxiety disorders often linked to alterations in attentional biases toward threat-related stimuli. While previous studies using event-related potentials (ERPs) have yielded conflicting findings regarding threat sensitivity in anxiety, Fast Periodic Visual Stimulation (FPVS) offers a high signal-to-noise, implicit alternative for assessing emotion processing. This study utilized FPVS to investigate neural responses to facial expressions in individuals with elevated anxiety-related characteristics (e.g., prior diagnosis or elevated symptom scores) and those without. EEG responses were recorded while participants viewed sequences of neutral faces interspersed with emotional oddball expressions (angry, fearful, happy, and sad). Results revealed robust neural discrimination responses to all facial expressions. Participants with anxiety-related characteristics showed significantly greater summed baseline-corrected amplitudes (BCA) at occipital electrodes in response to angry and sad oddball faces compared to the low-anxiety group. This was accompanied by reduced top-down interactions. Although, dimensional anxiety scores were generally low, suggesting results may reflect residual or trait-level differences rather than acute symptomatology, these findings provide preliminary evidence that FPVS may be sensitive to enduring differences in emotion processing associated with anxiety vulnerability.

neuroscience↗

bioRxiv2025

Implicit Emotional Biases in Anxiety and Depression: A Fast Periodic Visual Stimulation Study

Anxiety and depression are among the leading global causes of disability, yet their underlying neural mechanisms remain poorly understood. Traditional event-related potential (ERP) studies have shown attentional biases in anxiety and blunted responses to positive stimuli in depression, but limitations in sensitivity and interpretability hinder their clinical application. Fast Periodic Visual Stimulation (FPVS) offers an objective, high signal-to-noise ratio (SNR) approach to measuring neural responses to emotional stimuli. In this study, we applied FPVS with affective images to assess differences in emotional processing between individuals with anxiety and healthy controls across two experimental phases, optimizing stimulus presentation parameters. The results revealed that individuals with anxiety exhibited increased neural responses to negative stimuli compared to positive stimuli, as well as reduced responses to high-arousal stimuli, particularly in occipito-temporal and central-parietal regions. Additionally, individuals with comorbid depression showed blunted responses to high-arousal stimuli across multiple brain regions, consistent with reduced emotional reactivity. These findings support the feasibility of FPVS as a rapid and reliable tool for assessing emotional processing differences in clinical populations, with potential applications in translational research and psychiatric screening

neuroscience↗

bioRxiv2024

The Condensin II Complex Regulates the Expression of Essential Gene Expression Programs During Erythropoiesis

Erythropoiesis is characterized by dramatic changes in gene expression in the context of a cell that is rapidly proliferating while simultaneously condensing its nucleus in anticipation of enucleation. The mechanisms that maintain high level expression of erythroid genes and promote nuclear condensation remain poorly understood. Condensin II is a ring-like complex that promotes mitotic chromatin condensation and has roles in regulating interphase chromatin architecture and gene expression. We interrogated the role of Condensin II in erythropoiesis using an erythroid-specific deletion of the Condensin II subunit, Ncaph2. Ncaph2 loss resulted in severe embryonic anemia with lethality at embryonic day 13.5. Ncaph2 mutant erythroid cells had dysregulated maturation and disrupted cell cycle progression, but surprisingly Ncaph2 was dispensable for nuclear condensation. Genomic studies revealed that Ncaph2 occupied the promoter of key erythroid and cell cycle genes that were downregulated following Ncaph2 loss. Together, our results demonstrate an essential role for Ncaph2 in the gene expression programs that regulate cell cycle progression and erythroid differentiation, and identify a key role for the Condensin II complex in the regulation of a lineage-specific differentiation program. Summary StatementThe Condensin II complex regulates cell cycle progression and erythroid differentiation, but is dispensable for nuclear condensation during terminal erythroid maturation.

genomics↗

bioRxiv2022

Huntingtin expression influences spontaneous seizure disorder susceptibility in FVN/B mice

Huntington disease (HD) is an adult-onset neurodegenerative disorder that is caused by a trinucleotide CAG repeat expansion in the HTT gene that codes for the protein huntingtin (HTT or Htt in mice). HTT is a multi-functional, ubiquitously expressed protein that is essential for embryonic survival, normal neurodevelopment, and adult brain function. The ability of wild-type HTT to protect neurons against various forms of death raises the possibility that loss of normal HTT function may worsen disease progression in HD. Huntingtin-lowering therapeutics are being evaluated in clinical trials for HD, but concerns have been raised that decreasing wild-type HTT levels may have adverse effects. Here we show that Htt levels modulate the occurrence of an idiopathic seizure disorder that spontaneously occurs in FVB/N mice. These abnormal FVB/N mice demonstrate various cardinal features of mouse models of epilepsy including spontaneous seizures, astrocytosis, neuronal hypertrophy, upregulation of brain-derived neurotrophic factor (BDNF), and sudden seizure-related death. Interestingly, decreasing wild-type Htt levels increased the frequency of this disorder, while over-expression of HTT completely prevented it. Examination of the mechanism underlying huntingtins ability to modulate the frequency of this seizure disorder indicated that over-expression of full length HTT can promote neuronal survival following seizures. Overall, our results demonstrate a protective role for huntingtin in this form of epilepsy and provide a plausible explanation for the observation of seizures in the juvenile form of HD, Lopes-Maciel-Rodan syndrome, and Wolf-Hirschhorn syndrome. Adverse effects caused by altering huntingtin levels has ramifications related to Huntingtin-lowering therapies in development to treat HD.

neuroscience↗