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Kirk, I. J.

Publications and source records attributed to Kirk, I. J..

6 recordsLinked to original sources

Investigating the Influence of the Brain-Derived Neurotrophic Factor Val66Met Single Nucleotide Polymorphism on Familiarity and Recollection Event-Related Potentials

The Val66Met single nucleotide polymorphism (SNP) has previously been reported to impact performance on recognition memory tasks. Whether the two subprocesses of recognition--familiarity and recollection--are differentially impacted by the Val66Met SNP remains unknown. Using event-related potentials (ERPs) recorded during a source memory task, we attempted to dissociate these two subprocesses. Behaviourally, we used participants scores on an item-recognition subtask as a measure of familiarity, and participants scores on a source-recognition subtask as a measure of recollection. Our findings reveal that Val/Val individuals outperform Met allele carriers on the item-but not the source-recognition task. Electrophysiologically, we were interested in the N400, an early frontal component previously linked to familiarity, and the late positive complex (LPC), a posterior component linked to recollection. We found evidence for Val/Val individuals having larger amplitudes of the LPC compared to Met allele carriers, and evidence for no difference in the N400 amplitudes of these groups. Based on the lack of dissociation between familiarity- and recollection-specific ERPs at the LPC time window, we argue that our behavioural and ERP results might reflect better item-recognition for Val/Val individuals compared to Met allele carriers. We further suggest that both these results reflect differences related to familiarity, rather than recollection.

neuroscience↗

Increased sensorimotor activity during categorisation of ambiguous emotional expressions

Actions are rarely devoid of emotional content. Thus, a more complete picture of the neural mechanisms underlying mental simulation of observed actions requires more research using emotion information. The present study used electroencephalography (EEG) to investigate mental simulation associated with facial emotion categorisation. Mu rhythm modulation was measured to infer the degree of sensorimotor simulation. Categorising static images of neutral faces as happy or sad was associated with stronger mu suppression than categorising clearly happy or sad faces. Results suggest the sensitivity of the sensorimotor activity to emotional information rather than visual attentional engagement, because further control analyses revealed (1) no effect of emotion type on occipital alpha modulation, and (2) no difference in mu modulation between the conditions of a control task, which required categorising images with the head oriented right, left, or forward as right or left. This finding provides evidence for the role of the sensorimotor activity in a higher form of mental simulation. Consistent with a predictive coding account of action perception, stronger mu suppression during attempted emotion categorisation of neutral faces may involve minimising the mismatch between predicted kinematics of a happy/sad face and the observed stationarity of neutral faces.

neuroscience↗

The Brain-Derived Neurotrophic Factor Val66Met Genotype Does Not Influence the Grey or White Matter Structures Underlying Recognition Memory

A single nucleotide polymorphism (SNP) in the gene coding for brain-derived neurotrophic factor (BDNF) has previously been associated with a reduction in recognition memory performance. While previous findings have highlighted that this SNP contributes to recognition memory, little is known about its influence on subprocesses of recognition, familiarity and recollection. Previous research has reported reduced hippocampal volume and decreased fractional anisotropy in carriers of the Met allele across a range of white matter tracts, including those networks that may support recognition memory. Here, we used a source memory task to measure accuracy on each recognition subprocess, in order to determine whether the Val66Met SNP influences these equally. Additionally, we compared grey matter volume between these groups for structures that underpin familiarity and recollection separately. Finally, we used probabilistic tractography to reconstruct tracts that subserve each of these two recognition systems. Behaviourally, we found group differences on the familiarity measure, but not on recollection. However, we did not find any group difference on grey- or white-matter structures. Together, these results suggest a functional influence of the Val66Met SNP that is independent of coarse structural changes, and nuance previous research highlighting the relationship between BDNF, brain structure, and behaviour.

neuroscience↗

Mental simulation of facial expressions: Mu suppression to the viewing of dynamic neutral face videos

The mirror neuron network (MNN) has been proposed as a neural substrate of action understanding. Electroencephalography (EEG) mu suppression has commonly been studied as an index of MNN activity during execution and observation of hand and finger movements. However, in order to establish its role in higher order processes, such as recognising and sharing emotions, more research using social emotional stimuli is needed. The current study aims to contribute to our understanding of the sensitivity of mu suppression to facial expressions. Modulation of the mu and occipital alpha (8 - 13 Hz) rhythms was calculated in 22 participants while they observed dynamic video stimuli, including emotional (happy and sad) and neutral (mouth opening) facial expressions, and non-biological stimulus (kaleidoscope pattern). Across the four types of stimuli, only the neutral face was associated with a significantly stronger mu suppression than the non-biological stimulus. Occipital alpha suppression was significantly greater in the non-biological stimulus than all the face conditions. Source estimation (sLORETA) analysis comparing the neural sources of mu/alpha modulation between neutral face and non-biological stimulus showed more suppression in the central regions, including the supplementary motor and somatosensory areas, than the more posterior regions. EEG and source estimation results may indicate that reduced availability of emotional information in the neutral face condition requires more sensorimotor engagement in deciphering emotion-related information than the full-blown happy or sad expressions that are more readily recognised.

neuroscience↗

Human sensory Long-Term Potentiation (LTP) predicts visual memory performance and is modulated by the brain-derived neurotrophic factor (BDNF) Val66Met polymorphism

BackgroundLong-Term Potentiation (LTP) is recognised as a core neuronal process underlying long-term memory. However, a direct relationship between LTP and human memory performance is yet to be demonstrated. The first aim of the current study was thus to assess the relationship between LTP and human long-term memory performance. With this also comes an opportunity to explore factors thought to mediate the relationship between LTP and long-term memory, and to gain additional insight into variations in memory function and memory decline. The second aim of the current study was to explore the relationship between LTP and memory in groups differing with respect to BDNF Val66Met; a single nucleotide polymorphism implicated in memory function.\n\nMethods28 participants (15 female) were split into three genotype groups (Val/Val, Val/Met, Met/Met) and were presented with both an EEG paradigm for inducing LTP-like enhancements of the visually-evoked response, and a test of visual memory.\n\nResultsThe magnitude of LTP 40 minutes after induction was predictive of long-term memory performance. Additionally, the BDNF Met allele was associated with both reduced LTP and reduced memory performance.\n\nConclusionsThe current study not only presents the first evidence for a relationship between sensory LTP and human memory performance, but also demonstrates how targeting this relationship can provide insight into factors implicated in variation in human memory performance. It is anticipated that this will be of utility to future clinical studies of disrupted memory function.

neuroscience↗

Indexing sensory plasticity: Evidence for distinct Predictive Coding and Hebbian Learning mechanisms in the cerebral cortex

HighlightsO_LIERP and DCM study of two sensory plasticity paradigms: roving MMN and visual LTP\nC_LIO_LIFirst demonstration of multiple learning mechanisms under different task demands\nC_LIO_LIEvidence for both Predictive Coding and Hebbian learning mechanisms\nC_LIO_LIThe BDNF Val66Met polymorphism modulates ERPs for both paradigms\nC_LIO_LIHowever, the polymorphism only modulates MMN network connectivity\nC_LI\n\nThe Roving Mismatch Negativity (MMN), and Visual LTP paradigms are widely used as independent measures of sensory plasticity. However, the paradigms are built upon fundamentally different (and seemingly opposing) models of perceptual learning; namely, Predictive Coding (MMN) and Hebbian plasticity (LTP). The aims of the current study were to 1) compare the generative mechanisms of the MMN and visual LTP, therefore assessing whether Predictive Coding and Hebbian mechanisms co-occur in the brain, and 2) assess whether the paradigms identify similar group differences in plasticity. Forty participants were split into two groups based on the BDNF Val66Met polymorphism and were presented with both paradigms. Consistent with Predictive Coding and Hebbian predictions, Dynamic Causal Modelling revealed that the generation of the MMN modulates forward and backward connections in the underlying network, while visual LTP only modulates forward connections. Genetic differences were identified in the ERPs for both paradigms, but were only apparent in backward connections of the MMN network. These results suggest that both Predictive Coding and Hebbian mechanisms are utilized by the brain under different task demands. Additionally, both tasks provide unique insight into plasticity mechanisms, which has important implications for future studies of aberrant plasticity in clinical populations.

neuroscience↗