European Journal of Neuroscience最新文献

The reproducibility crisis highlights several unresolved issues in science, including the need to develop measures that gauge both the consistency and convergence of data sets. While existing meta-analytic methods quantify the consistency of evidence, they do not quantify its convergence: the extent to which different types of empirical methods have provided evidence to support a hypothesis. To address this gap in meta-analysis, we and colleagues developed a summary metric—the cumulative evidence index (CEI)—which uses Bayesian statistics to quantify the degree of both consistency and convergence of evidence regarding causal hypotheses between two phenomena. Here, we outline the CEI's underlying model, which quantifies the extent to which studies of four types—positive intervention, negative intervention, positive non-intervention and negative non-intervention—lend credence to any of three types of causal relations: excitatory, inhibitory or no-connection. Along with p-values and other measures, the CEI can provide a more holistic perspective on a set of evidence by quantitatively expressing epistemic principles that scientists regularly employ qualitatively. The CEI can thus address the reproducibility crisis by formally demonstrating how convergent evidence across multiple study types can yield progress toward scientific consensus, even when an individual type of study fails to yield reproducible results.

Depression is a heterogeneous syndrome that impacts an individual's emotional, social, cognitive and bodily functioning. Depression is associated with biases in emotional processing, but alterations in basic sensory processing have received less attention in depression research. Here, we measured event-related potentials (ERPs) in response to changes in the intensity of auditory stimuli and the location of somatosensory stimuli in participants with depression and in non-depressed control participants. We tested whether auditory mismatch negativity, P3a or N1 intensity dependence response or somatosensory mismatch response, P3a, P50 or N80 can dissociate depressed participants and non-depressed controls, and we also analysed the effects of depression medication and age in this sample. N1 intensity dependence response was increased in unmedicated depressed participants relative to non-depressed controls. When age was controlled for in the analysis, the effect of depression was only at a trend level. N1 intensity dependence response correlated with depression severity at the whole sample level. We did not observe any depression-related alterations in auditory mismatch negativity or P3a or somatosensory ERPs. Our results may reflect an association between the N1 intensity dependence response and altered neurotransmitter activity in depression, but this should be confirmed in future studies.

Flash sequences appear as steady emission of light if the frequency is above the flicker-fusion threshold. One can display flicker-fused letters against a background, and using the Talbot-Plateau law, vary the average luminance of the letters to control degree of match to background luminance. We have previously reported that the visual system can identify letters that have an average luminance that equals background luminance, which can be described as an anomalous contrast discrimination. The present work confirms the earlier report, and provides additional evidence that the phenomenon is not based on a shift in luminance balance. We discuss the possible role of ON and OFF retinal channels in registering the anomalous contrast.

Despite predictions that neuroscientific discoveries would revolutionize psychiatry, decades of research have not yet led to clinically significant advances in psychiatric care. For this reason, an increasing number of researchers are recognizing the limitations of a purely biomedical approach in psychiatric research. These researchers call for reevaluating the conceptualization of mental disorders and argue for a non-reductionist approach to mental health. The aim of this paper is to discuss philosophical assumptions that underly neuroscientific research in psychiatry and offer practical tools to researchers for overcoming potential conceptual problems that are derived from those assumptions. Specifically, we will discuss: the analogy problem, questioning whether mental health problems are equivalent to brain disorders, the normativity problem, addressing the value-laden nature of psychiatric categories and the priority problem, which describes the level of analysis (e.g., biological, psychological, social, etc.) that should be prioritized when studying psychiatric conditions. In addition, we will explore potential strategies to mitigate practical problems that might arise due to these implicit assumptions. Overall, the aim of this paper is to suggest philosophical tools of practical use for neuroscientists, demonstrating the benefits of a closer collaboration between neuroscience and philosophy.

Gilles de la Tourette syndrome (GTS) and dystonia (DYS) are both hyperkinetic movement disorders effectively treated by deep brain stimulation (DBS) of the internal part of the globus pallidus (GPi). In this study, we compared single-neuron activity in the GPi between 18 GTS patients (with an average of 41 cells per patient) and 17 DYS patients (with an average of 54 cells per patient), all of whom underwent bilateral pallidal stimulation surgery, under general anesthesia or while awake at rest. We found no significant differences in GPi neuronal activity characteristics between patients operated on under general anesthesia versus those who were awake, irrespective of their diagnosis (GTS or DYS). We found higher firing rates, firing rate in bursts, pause duration and interspike interval coefficient of variation in GTS patients compared to DYS patients. On the opposite, we found higher number of pauses and bursts frequency in DYS patients. Lastly, we found a higher proportion of GPi oscillatory activities in DYS compared to GTS patients, with predominant activity within the low-frequency band (theta/alpha) in both patient groups. These findings underscore the complex relationship between the different neuronal discharge characteristic such as oscillatory or bursting activity within the GPi in shaping the clinical phenotypes of hyperkinetic disorders. Further research is warranted to deepen our understanding of how neuronal patterns are transmitted within deep brain structures and to develop strategies aimed at normalizing these pathological activities, by refining DBS techniques to enhance treatment efficacy and individual outcomes.

Ohgomori, T., Yamasaki, R., Takeuchi, H., Kadomatsu, K., Kira, J.-i. and Jinno, S. Differential activation of neuronal and glial STAT3 in the spinal cord of the SOD1^G93A mouse model of amyotrophic lateral sclerosis. European Journal of Neuroscience 2024; 46(4): 2001–2014. https://doi.org/10.1111/ejn.13650

In Figure 2, the magenta image of Figure 2E₂ (STAT3 immunofluorescence) was incorrect. We mistakenly used the magenta image of Figure 2C₃ for 2E₂. In the revised Figure 2, we have replaced the magenta image of 2E₂ with the correct image.

We apologize for this error.

The sleep homeostatic process in adults is moderately stable over time and unique to an individual. Work in transgenic mice has suggested a role of genes in sleep homeostasis. The current study quantified the genetic contribution to sleep homeostasis in adolescence. We use slow wave energy (SWE) as a metric for sleep pressure dissipation during sleep. This measure reflects both sleep intensity and duration. High-density (58 derivations) sleep electroencephalogram (EEG) was recorded in 14 monozygotic and 12 dizygotic adolescent twin pairs (mean age = 13.2 years; standard deviation [SD] = 1.1; 20 females). SWE at the end of sleep was quantified as the cumulative delta power (1–4.6 Hz) over the night. We also examined the time constant of the decay and the level of slow wave activity (SWA) at the beginning of the sleep episode. Structural equation modelling was used to quantify the amount of variance in SWE and the dissipation of sleep pressure due to genes. We found that most (mean = 76% across EEG derivations) of the variance in SWE was due to genes. In contrast, genes had a small (mean = 33%) influence on the rate of dissipation of sleep pressure, and this measure was largely (mean = 67%) driven by environmental factors unique to each twin. Our results show that the amount of dissipated sleep pressure is largely under genetic control; however, the rate of sleep pressure dissipation is largely due to unique environmental factors. Our findings are in line with research in animals and suggest that the heritability of the rate of sleep pressure dissipation is limited.

Carey, SD, Conant, K, Maguire-Zeiss, KA. Short-term exposure to HIV Tat induces glial activation and changes in perineuronal nets. European Journal of Neuroscience 2024; 60(3): 4303–4316. https://doi.org/10.1111/ejn.16427.

In the text describing Figure 4, the **p = 0.0062 was incorrect. The correct p value is **p = 0.0058.

We apologize for this error.

In Figure 4, the incorrect figure was used. The correct figure is shown here. The statistical values and interpretation do not change.

We apologize for this error.

In Figure 7g, the incorrect figure was used. The correct figure is shown below. The statistical values and interpretation do not change.

We apologize for this error.

Area 8A has traditionally been considered to be the frontal eye field (FEF), i.e. the area for the motor production of eye movements. However, recent research has shown that the FEF lies posteriorly in premotor area 6. Research in macaque monkeys has demonstrated that, in contrast to premotor area 6, which is involved in the production of motor actions, area 8A is implicated in the cognitive allocation of attention to stimuli based on instruction cues. The aim of the present study was to elucidate the specific cognitive role of area 8A by examining a unique patient with a lesion restricted to area 8A, i.e. sparing the premotor cortex. This right-handed male patient underwent neuropsychological assessment and testing on two conditional associative-learning tasks: the motor hand conditional associative-learning task (MCALT) assessing the selection of motor actions based on instruction cues and the visual conditional associative-learning task (VCALT) assessing the selection of visual stimuli based on instruction cues. The patient's performance on the VCALT was significantly impaired compared to control subjects, but performance on the MCALT and on an Eye Movement Control Task was preserved. The present study provides evidence that area 8A is critical for the cognitive process regulating the allocation of attention to different stimuli in the environment, but not in the production of eye movements. These findings enhance understanding of the functional organization of the posterior dorsolateral frontal region in the human brain and suggest a specialized role of area 8A in high-level cognitive processes.

Eveningness has been associated with both disturbed sleep and depression. It is unclear, however, if deprived sleep explains evening types' vulnerability to depression. The role of pre-sleep rumination in these associations also remains understudied. The present study assessed the relationship between eveningness and sleep quality, as well as the possible mediating effect of pre-sleep rumination and the moderating effect of a history of depression, under naturalistic conditions. Eighty-eight Dutch-speaking participants (87.5% females, 21.4 ± 3.7 years) were selected on the basis of their non-intermediate chronotype using the Morningness Eveningness Questionnaire (evening types (n = 53); morning types (n = 35)). Depression status was assessed through a diagnostic interview (healthy (n = 61); remitted depressed (n = 27)). Participants' sleep characteristics were monitored via actigraphy and sleep diaries for seven consecutive days and nights. Pre-sleep rumination was measured via a self-report questionnaire. Evening types had longer subjective and actigraphic sleep onset latency than morning types. Pre-sleep rumination did not mediate the former associations but predicted longer subjective sleep onset latency. Furthermore, the relationship between chronotype and subjective sleep onset latency was moderated by depression history. Remitted depressed evening types reported longer sleep onset latency than healthy evening and morning types, possibly posing the former at a higher risk for depressive relapse. Overall, the current findings address the need to further investigate the physiological signature of circadian rhythms and sleep latency. This could serve as a foundation for the development of prevention and early intervention programs, tailored for mood and sleep disorders.