European Journal of Neuroscience最新文献

The human brain tracks regularities in the environment and extrapolates these to predict future events. Prior work on music cognition suggests that low-frequency (1-8 Hz) brain activity encodes melodic predictions beyond the stimulus acoustics. Building on this work, we aimed to disentangle the frequency-specific neural dynamics linked to melodic prediction uncertainty (modelled as entropy) and prediction error (modelled as surprisal) for temporal (note onset) and content (note pitch) information. By using multivariate temporal response function (TRF) models, we re-analysed the electroencephalogram (EEG) from 20 subjects (10 musicians) who listened to Western tonal music. Our results show that melodic expectation metrics improve the EEG reconstruction accuracy in all frequency bands below the gamma range (< 30 Hz). Crucially, we found that entropy contributed more strongly to the reconstruction accuracy enhancement compared to surprisal in all frequency bands. Additionally, we found that the encoding of temporal, but not content, information metrics was not limited to low frequencies, rather it extended to higher frequencies (> 8 Hz). An analysis of the TRF weights revealed that the temporal predictability of a note (entropy of note onset) may be encoded in the delta- (1-4 Hz) and beta-band (12-30 Hz) brain activity prior to the stimulus, suggesting that these frequency bands associate with temporal predictions. Strikingly, we also revealed that melodic expectations selectively enhanced EEG reconstruction accuracy in the beta band for musicians, and in the alpha band (8-12 Hz) for non-musicians, suggesting that musical expertise influences the neural dynamics underlying predictive processing in music cognition.

The integration of visual letters and speech sounds is a crucial part of learning to read. Previous studies investigating this integration have revealed a modulation by audiovisual (AV) congruency, commonly known as the congruency effect. To investigate the cortical oscillations of the congruency effects across different oscillatory frequency bands, we conducted a Japanese priming task in which a visual letter was followed by a speech sound. We analyzed the power and phase properties of oscillatory activities in the theta and beta bands between congruent and incongruent letter-speech sound (L-SS) pairs. Our results revealed stronger theta-band (5-7 Hz) power in the congruent condition and cross-modal phase resetting within the auditory cortex, accompanied by enhanced inter-trial phase coherence (ITPC) in the auditory-related areas in response to the congruent condition. The observed congruency effect of theta-band power may reflect increased neural activities in the left auditory region during L-SS integration. Additionally, theta ITPC findings suggest that visual letters amplify neuronal responses to the following corresponding auditory stimulus, which may reflect the differential cross-modal influences in the primary auditory cortex. In contrast, decreased beta-band (20-35 Hz) oscillatory power was observed in the right centroparietal regions for the congruent condition. The reduced beta power seems to be unrelated to the processing of AV integration, but may be interpreted as the brain response to predicting auditory sounds during language processing. Our data provide valuable insights by indicating that oscillations in different frequency bands contribute to the disparate aspects of L-SS integration.

RETRACTION: H. Guo, I. Singh, Y. Wang, R. Deane, T. Barrett, J. A. Fernández, N. Chow, J. H. Griffin and B. V. Zlokovic, “Neuroprotective Activities of Activated Protein C Mutant With Reduced Anticoagulant Activity,” European Journal of Neuroscience 29, no. 6 (2009): 1119–1130, https://doi.org/10.1111/j.1460-9568.2009.06664.x.

The above article, published online on 16 March 2009 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editors-in-Chief, John Foxe and Yoland Smith; the Federation of European Neuroscience Societies; and John Wiley & Sons Ltd. The retraction has been agreed as the corresponding author contacted the editors of European Journal of Neuroscience reporting that similarities were observed between Figure 1a of this article and another figure published elsewhere. The latter figure was published five years earlier by some of the same authors and represents a different experiment.

Following an investigation, it was found that the duplicated images showed signs of cropping and digital manipulation. The authors provided some raw data but were unable to provide the original micrographs for figure 1a; instead, they shared results from recently repeated experiments. However, questions remain regarding the rigor devoted to the collection and analysis of data presented in this article; as a result, the journal retracts this article. The authors disagree with the retraction.

Initial symptoms of neurodegenerative diseases are often defined by the loss of the most vulnerable neural populations specific to each disorder. In the early stages of Alzheimer's disease, vulnerable circuits in the temporal lobe exhibit diminished activity prior to overt degeneration. It remains unclear whether these functional changes contribute to regional vulnerability or are simply a consequence of pathology. We previously found that entorhinal neurons in the temporal cortex undergo cell death following transient suppression of electrical activity, suggesting a causal role for activity disruption in neurodegeneration. Here we demonstrate that electrical arrest of this circuit stimulates the injury-response transcription factor c-Jun. Entorhinal silencing induces transcriptional changes consistent with c-Jun activation that share characteristics of gene signatures in other neuronal populations vulnerable to Alzheimer's disease. Despite its established role in the neuronal injury response, inhibiting c-Jun failed to ameliorate entorhinal degeneration following activity disruption. Finally, we present preliminary evidence of integrated stress response activity that may serve as an alternative hypothesis to what drives entorhinal degeneration after silencing. Our data demonstrate that c-Jun is activated in response to neuronal silencing in the entorhinal cortex but is decoupled from subsequent neurodegeneration.

Aging is often associated with changes in social, sexual, emotional and pain functioning, as well as with the increased prevalence of certain psychopathologies. However, the neurodevelopmental basis underpinning these age-related changes remains to be determined. Considering the key roles of oxytocin (OTR) and μ-opioid (MOPr) receptor systems in regulating social, sexual, pain, reward and emotional processing, it seems plausible that they are also implicated in age-related behavioural alterations. Although the ontogeny of both receptors has been well characterized in rodent brains from early development till adulthood, little is known concerning the neuroadaptations occurring from middle age to old age. Therefore, we mapped the neuroadaptations in OTR and MOPr in the brains of mice at those developmental endpoints. Quantitative OTR and MOPr autoradiographic binding was carried out in the brains of male mice at 2, 6, 9, 12 and 18 months of age. A significant whole brain decline in OTR density was detected between 2 and 6 months of age, with no additional decline thereafter. Interestingly, for MOPrs, the decline in density was not detected until 9 months of age. Region-specific age-related decline in OTR density was concentrated in the lateral anterior olfactory nuclei (AOL) and, for MOPr, in the AOL and the nucleus accumbens for MOPr. Identifying the tipping point of these age-related variations in both receptors may assist with our understanding of the neurobiology underlining age-related changes in social, pain and emotional functioning/processing. It may also help us target interventions to specific developmental windows to abrogate certain age-related psychopathologies.

Technological tools, like electroencephalography and functional near-infrared spectroscopy, have deepened our understanding of cortical regions involved in balance control. In this systematic literature review, we aimed to identify the prevalent cortical areas activated during balance tasks with specific motor or cognitive demands. Our search strategy encompassed terms related to balance control and cortical activity, yielding 2250 results across five databases. After screening, 67 relevant articles were included in the review. Results indicated that manipulations of visual and/or somatosensory information led to prevalent activity in the parietal, frontal and temporal regions; manipulations of the support base led to prevalent activity of the parietal and frontal regions; both balance-cognitive dual-tasking and reactive responses to extrinsic perturbations led to prevalent activity in the frontal and central regions. These findings deepen our comprehension of the cortical regions activated to manage the complex demands of maintaining body balance in the performance of tasks posing specific requirements. By understanding these cortical activation patterns, researchers and clinicians can develop targeted interventions for balance-related disorders.

Anxiety is a prominent non-motor symptom of Parkinson's disease (PD). Changes in the B-spectrum recordings in PD patients of the prefrontal cortex correlate with increased anxiety. Using a rodent model of PD, we reported alterations in glutamate synapses in the striatum and substantia nigra following dopamine (DA) loss. We hypothesize that DA loss will result in increased anxiety-related behaviours and that this will be associated with alterations in glutamate synapses and transporters within the medial prefrontal cortex (mPFC). Following 4 weeks of progressive 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration, there was an increase in anxiety-related behaviours and a 78% decrease in plasma corticosterone levels versus the vehicle (VEH)-treated mice. This was associated with a 30% decrease in the density of dendritic spines in Layers Il/Ill, and a 53% decrease in the density of glutamate immuno-gold labelling within vesicular glutamate transporter 1 (Vglut1)-labelled nerve terminals and spines, with no change within vesicular glutamate transporter 2 (Vglut2) positive terminals/spines in the MPTP versus VEH groups. Our prior work determined that a decrease in striatal glutamate terminal density was associated with an increase in extracellular glutamate levels. There was an increase in protein expression of Vglut1 (40%), Vglut2 (37%) and glutamate aspartate transporter (GLAST) (225%), and a decrease in glutamate transporter 1 (GLT-1) (50%) and excitatory amino acid carrier 1 (EAAC1) (51%), in the MPTP versus VEH groups within the mPFC. These data suggest that the decrease in dendritic spines within the mPFC following nigrostriatal DA loss may be due to increased extracellular glutamate levels (decrease in glutamate transporters), leading to an increase in anxiety-related behaviours.

Inconsistent results are observed in the effects of transcranial direct current stimulation (tDCS) with different montages on motor learning. This study aimed to compare the effects of anodal and cathodal tDCS (c-tDCS) over primary motor cortex (M1) at different intensities on motor learning in healthy young adults. The participants were randomly divided into: (1) 1 mA M1 c-tDCS, (2) 1 mA M1 anodal tDCS (a-tDCS), (3) 2 mA M1 c-tDCS, (4) 2 mA M1 a-tDCS and (5) M1 sham tDCS groups. The groups received 20-min stimulation with serial reaction time task (SRTT) incidentally, while the tDCS was turned off after 30 s in the sham tDCS group. Response time (RT) and error rate (ER) during SRTT were assessed prior, during and 72 h after the intervention. The results of the paired t-test indicated that online learning occurred in all groups (p < 0.05), except in M1 c-tDCS (1 mA) (p > 0.05). One-way ANOVA analysis also indicated that there were differences in offline learning (RT (F(DF) = 5.19(4); p < 0.001; and ER (F(DF) = 9(4), p < 0.0001) among groups, with more offline learning in 1 mA M1 a-tDCS, 2 mA M1 c-tDCS and 2 mA M1 a-tDCS groups (p < 0.05). On the other hand, the 1 mA M1 c-tDCS group did not indicate any consolidation effect or even a trend toward negative offline learning. M1 a-tDCS with different intensities and also 2 mA M1 c-tDCS may be helpful for the enhancement of motor learning in young healthy adults. This study enhances our understanding of tDCS intensity and polarity effects on motor learning, with potential for optimizing therapeutic protocols.

Attention is one of the basic cognitive functions sensitive to high altitude, and most studies have focussed on exposure times of approximately 3 years; however, it is unclear how attention changes in migrants who have lived and worked at high altitude for nearly 20 years. We explored the dynamics of attentional networks and neurophysiological mechanisms in migrants over 3–20 years using the Attentional Network Test combined with Electrocardiograph and Electroencephalography and found a consistent quadratic correlation between exposure and executive control efficiency, P3 amplitude and heart rate variability (HRV), with a decrease followed by an increase/relative stability, with approximately 10 years being the breakpoint. However, neither linear nor quadratic trajectories were observed for the alerting and orienting network. Mediation analysis revealed that the P3 amplitude mediated the decrease and increase in executive control efficiency with exposure time depends on the breakpoint. Correlations between HRV and executive control efficiency and P3 amplitude suggest that U-shaped changes in executive control in migrants may be related to body homeostasis maintained by the autonomic nervous system, and that P3 amplitude may serve as a neurophysiological marker of migrants' adaptation/recovery from high-altitude exposure.

Emerging evidence suggests that autobiographical memory (ABM) is altered in Huntington's disease (HD). While these impairments are typically attributed to frontostriatal dysfunction, the neural substrates of ABM impairment in HD remain unexplored. To this end, we assessed ABM in 30 participants with genetically confirmed HD (18 premanifest, 12 manifest) and 24 age-matched healthy controls. Participants completed the Autobiographical Interview to assess free and probed ABM recall and underwent structural brain imaging. Whole-brain voxel-based morphometry (VBM) was used to explore voxel-wise associations between ABM performance and grey matter intensity (False Discovery Rate corrected at q = 0.05). Relative to controls, HD participants displayed significantly less detailed ABM retrieval across free and probed recall conditions, irrespective of disease stage. Recall performance did not differ significantly between manifest and premanifest HD groups. VBM analyses indicated that poorer ABM performance was associated with atrophy of a distributed cortico-subcortical network. Key regions implicated irrespective of ABM condition included the bilateral occipital cortex, left precuneus, right parahippocampal gyrus and right caudate nucleus. In addition, probed ABM recall was associated with the superior and inferior frontal gyri, frontal pole, right hippocampus, nucleus accumbens, paracingulate gyrus and cerebellum. Overall, our findings indicate that ABM impairments in HD reflect the progressive degeneration of a distributed cortico-subcortical brain network comprising medial temporal, frontal, striatal and posterior parietal cortices. Our findings advance our understanding of the neurocognitive profile of HD, providing an important foundation for future interventions to support memory function in this population.