The human brain anticipates the sensory consequences of an action and generates a prediction error (PE) signal when the intended action effect does not occur. This study investigated auditory event-related potential PE markers based on whether participants intended to perform a specific action or produce a specific action effect. Participants were instructed to press a left or right button to produce low- or high-pitched tones, following a visual pattern. The instructions, actions and tone sequences were identical for all participants. The visual patterns differed in two groups: In the action-effect intention group, the visual pattern consisted of 'notes' (indicating low/high pitch). In the action intention group, the visual pattern consisted of 'letters' (indicating left/right button-press). In both groups, a button-press occasionally failed to produce the associated tone (incongruent sounds). The key finding was that these incongruent sounds elicited an enhanced auditory N1 component compared to congruent sounds only in the 'notes' group. We propose that participants in the 'notes' group selected their actions based on the intended action effect, which induced a predictive sensory representation of the expected tone. A violation of this prediction resulted in the early PE, reflected in the auditory N1. Later PE responses, specifically the N2b and P3 components, were observed in both groups. This suggests that action-effect associations were represented, and their violation was processed at a conceptual level even in the 'letters' group. These results support theories postulating that event representations integrate features of stimuli, actions and their associated outcomes.
Chronic stress is increasingly acknowledged as a pivotal precipitating factor in the pathogenesis of neuropsychiatric and neurodegenerative disorders, notably including depression and Alzheimer's disease (AD). Astrocytes, which constitute the predominant population of glial cells involved in the maintenance of synaptic homeostasis, the recycling of neurotransmitters, and the provision of metabolic support, display a pronounced susceptibility to sustained exposure to stress. The deleterious effects of astrocytic dysfunction instigate a series of neuroinflammatory and synaptic modifications that undermine both cognitive and emotional resilience. This review articulates the mechanistic interactions between stress-induced astrocyte dysfunction, neuroinflammatory signaling, and compromised neuroplasticity, underscoring the converging pathways that are implicated in both depression and AD. A thorough synthesis of the literature from 2020 to 2025 was conducted utilizing databases such as PubMed, Scopus, and Web of Science, with an emphasis on molecular, in vitro, in vivo, and translational studies that examine the modulation of astrocytic function under conditions of chronic stress and its pertinence to depression and AD. The chronic activation of the hypothalamic-pituitary-adrenal (HPA) axis precipitates morphological alterations, diminished expression of glutamate transporters (GLT-1/EAAT2), disrupted brain-derived neurotrophic factor (BDNF) signaling, and an augmented release of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) from astrocytes. These biochemical alterations exacerbate excitotoxicity, disturb monoaminergic and glutamatergic neurotransmission, and hasten synaptic degeneration. In the context of depression, this phenomenon is manifested as impaired mood regulation and a decline in neurogenesis. In AD, it synergistically interacts with amyloid-beta and tau pathologies to facilitate progressive cognitive impairment. Both conditions exhibit a common feature of diminished neurosignaling plasticity, which limits the brain's capacity for adaptation and repair. Astrocyte dysfunction constitutes a central mechanistic nexus wherein chronic stress, neuroinflammation, and synaptic pathology intersect to promote the progression of depression and AD. The targeting of astrocytic health via the modulation of reactive astrocyte phenotypes, the restoration of glutamate homeostasis, and the enhancement of neurotrophic signaling emerges as a promising therapeutic avenue for alleviating stress-related neurodegeneration and mood disorders.
Presynaptic inhibition (PSI) at the spinal cord level is crucial for coordinating postural preparation with step initiation. People with freezing of gait and Parkinson's disease (PD + FOG) show loss of PSI of the soleus muscle during step initiation that is associated with abnormal anticipatory postural adjustments (APA). Here, we hypothesize that increasing PSI of the soleus muscle during step initiation via wrist vibration in PD + FOG would decrease abnormally large APA. Fifteen PD + FOG performed self-initiated steps on a force platform without electrical stimulation and with test or conditioned Hoffman reflexes (H-reflex) to measure PSI of the soleus muscle under three conditions: OFF medication, OFF medication with vibration, and ON medication without vibration. Soleus H-reflexes were recorded during quiet stance (a control task) and when the amplitude of the APA under the same leg exceeded 10%-20% of the mean baseline mediolateral displacement. Vibration consisted of 200-300 Hz applied to the wrist when the ipsilateral leg during APA (same leg where H-reflexes were evoked) was on the ground. PD + FOG showed decreased PSI during APA in OFF and ON medication, but PSI was increased during vibration (p < 0.05). Increased PSI was associated with smaller APA during vibration (p < 0.05). Smaller APAs were associated with lower subjective freezing of gait severity (p < 0.05). These preliminary results show that wrist vibration decreases abnormal APA during step initiation by increasing ipsilateral PSI levels of the soleus muscle. Because PSI is modulated by cortical and brainstem areas related to FOG and APA, proprioceptive drive during vibration may reorganize these brain circuits.
Although some forms of epilepsy directly result from mutations in nicotinic acetylcholine receptors, none of the currently available antiepileptic drugs (AEDs) is specifically designed to target the cholinergic system. However, there is growing evidence that some established AEDs, which were primarily designed to modulate excitatory glutamatergic and/or inhibitory GABAergic currents, may also influence cholinergic signalling. This study therefore investigated whether topiramate (TPM), a second-generation AED, directly affects calcium signals and whether the deacetylase sirtuin-1 (Sirt-1) contributes to this effect. Calcium imaging in the human neuroblastoma cell line SH-SY5Y was used to quantify acetylcholine- and nicotine-induced calcium signals following TPM treatment. To evaluate the role of protein deacetylases, TPM effects were further analysed in the presence of the deacetylase inhibitors trichostatin A (TSA) and inauhzin. TPM treatment significantly enhanced acetylcholine- and nicotine-induced calcium signals. This effect of TPM was completely abolished in the presence of TSA. However, the presence of inauhzin resulted in an inhibitory effect of TPM on acetylcholine-induced calcium signals. These findings reveal a previously uninvestigated modulatory effect of TPM on cholinergic calcium signalling that is directly dependent on the activity of deacetylases, like Sirt-1. The results may contribute to a better understanding of TPM's anticonvulsive mechanisms of action.
Transcranial magnetic stimulation (TMS) can modulate corticospinal excitability during stretch-evoked long-latency responses (LLRs). It has been previously established that suprathreshold TMS intensities can partially inhibit the cortical contribution to LLRs by relying on a cortical silent period occurring after TMS. However, it is unknown whether the TMS-induced inhibition of stretch-evoked LLRs that relies on the cortical silent period can also be achieved via subthreshold stimulation. In this study, 12 healthy participants performed a protocol combining surface electromyography (EMG), robot-evoked wrist perturbations, and single pulse TMS applied to the motor cortex to study the effect of TMS intensity on the LLR amplitude in the flexor carpi radialis. We tested two TMS intensities of subthreshold (90%) and suprathreshold (130%) of the active motor threshold applied such that the motor-evoked potential (MEP) peak would arrive 50 ms prior to perturbation onset. In suprathreshold TMS trials, TMS significantly reduced the cortical contribution to a LLR when applied prior to perturbation onset. When comparing the effects measured in the presence and absence of robot-applied muscle stretch, we observed that only suprathreshold conditions achieved inhibition of LLR, while subthreshold conditions did not result in LLR-specific inhibition. Overall, our findings establish a clear distinction between the effect of subthreshold and suprathreshold TMS on the LLR inhibition via the cortical silent period. These findings highlight the application of TMS to induce cortical inhibition of LLRs.
Successfully learned motor skills can generalize or transfer to the untrained arm. The neural substrate underlying such intermanual/interlimb generalization of newly acquired skill memory is unclear. Here, we focused on contralateral primary motor cortex (cM1), which is considered a key brain area for skill learning and memory consolidation. We probed the causal role of cM1 in intermanual skill generalization in a 2-day study involving right-handed young individuals (n = 31) who learned a novel motor skill reaching task. Immediately following (right-arm) learning, we delivered low-frequency (1 Hz, 1800 pulses) repetitive transcranial magnetic stimulation (rTMS) to target left cM1 in one group of individuals (n = 15), whereas another group (n = 16) served as an active control in which ipsilateral M1 (iM1) was targeted. On the same day, we measured corticospinal excitability (CSE) to assess learning-induced and rTMS-induced neuroplastic changes occurring in the targeted M1s. Next day after 24-h, both groups were tested for intermanual skill generalization (left arm), followed by a brief test of intralimb retention (right arm). Our results show that stimulating cM1, versus iM1, reduced the amount of generalization to the untrained arm on the next day, without affecting its (re)learning ability or the follow-up retention performance of the trained arm. Further, low frequency rTMS stimulation in our study surprisingly induced a net facilitation in CSE-with higher facilitation tending to correlate to lower generalization in a subset of high learners in the cM1 group. Taken together, this study highlights the role of cM1 in skill generalization such that it seems to mediate the early transfer of learning to the untrained arm.
The presence of another human in our immediate or distant environment is a crucial factor for survival and social behavior. Our actions vary depending on the other person's relative proximity, involving integration of brain functions subserved by neural oscillations, to generate the most appropriate behavior. This study highlights the alpha EEG role and its neural generators in interpersonal space sensitivity (IPSS). To investigate this, participants stood face-to-face, gazing into each other's eyes, while wearing a mask preventing them from staring at each other. An auditory order instructed them to alternately close and open their eyes. It was observed that alpha power of the occipito-parietal region increased as the distance decreased, transitioning from extrapersonal space (4 m) to peripersonal space (< 40 cm) when the eyes were closed. Conversely, alpha power decreased for the same distances when the eyes were open. These significant event-related synchronization (ERS) and desynchronization (ERD) effects were absent when participants' heads were masked. Beta oscillations were not significantly involved in IPSS. The number of spontaneous blinks was not significantly influenced by IPSS. Source modeling identified alpha ERS and ERD in cortical and subcortical generators significantly involved in IPSS with independent components localized in: the parietal cortex bilaterally (BA7), the left limbic gyrus (BA23), the anterior cingulate cortex (ACC) (right BA31, left and right BA24, right BA32), the right premotor cortex (BA6, including the supplementary motor area [SMA]), and the right frontal eye fields (BA8). These cortical areas were accompanied by the recruitment of the thalamus and cerebellum.
The human auditory system rapidly distinguishes between novel and familiar sounds, a process reflected in mismatch negativity (MMN), an electroencephalogram (EEG)-based biomarker of auditory novelty detection. MMN is impaired in psychiatric conditions, most notably schizophrenia (SCZ), yet the neuronal mechanisms underlying this deficit remain unclear. Here, we combined computational modelling and genetic analyses to investigate how SCZ-associated cellular abnormalities affect auditory novelty detection. We developed an integrate-and-fire spiking network model capable of detecting four types of auditory novelty, including stimulus omission. Based on assumptions of short-term depressing synapses between the subpopulations of the network and the existence of neuronal inputs that are phase-locked to the rhythm of the recently experienced stimulus sequence, we showed that the model reliably reproduced MMN-like novelty detection and allowed systematic testing of SCZ-related cellular alterations. We also demonstrated that the required phase locking can theoretically be achieved in a synfire chain network exhibiting spike-timing dependent plasticity (STDP) in its feedback synapses that becomes entrained to the rhythmic stimulus. Simulations of our novelty-detecting network revealed that both reduced pyramidal cell excitability, linked to ion channel dysfunction, and decreased spine density impaired novelty detection, with the latter producing stronger deficits. Our work provides a flexible spiking network model of auditory novelty detection that can link cellular-level abnormalities to measurable MMN deficits, improving their mechanistic interpretation and helping to explain the heterogeneity of SCZ.
Visual search is extremely critical in the real world and is modulated by contextual guidance. Extensive research highlights the role of contextual manipulation in enhancing visual search performance. However, the neural timeline underlying contextual guidance during ecologically valid visual search tasks remains largely unresolved. The current study uses heterogeneous targets in naturalistic visual search to explore the role of contextual facilitation of spatial attention in visual search under varying task difficulty. We hypothesized that contextual guidance-based deployment of attention to the expected location of the target will emerge in visual search tasks even in the absence of the target and investigated the neural timeline of attentional deployment, modulated by task difficulty. We used multivariate pattern classifiers to predict coarse contextual locations from single trial electroencephalogram (EEG) signals during naturalistic visual search in the absence of targets. Participants searched for heterogeneous targets in natural images, and the target-absent images carrying information for possible target locations provided by scene context were considered for analysis. Our results demonstrate that task consistent contextual locations in natural scenes can be predicted reliably pointing to the role of contextual information guiding early deployment of spatial attention in visual search. Multivariate pattern analysis (MVPA) failed to predict the expected location using the same stimuli in a separate control EEG study when contextual information was made inconsequential. Finally, we demonstrated that for easy tasks, contextual guidance facilitation starts as early as 130-170 ms poststimulus onset, alluding to the role of task difficulty in mediating the early neural timeline of contextual guidance.
Brain reserve capacity has recently gained an increasing interest in stroke recovery research to provide a deeper understanding of outcome variability. For instance, global and focal parameters of brain health, such as white matter hyperintensity burden or the structural reserve of the cerebellum, have been linked to recovery. Recently, it was shown that the pre-stroke structural state of key areas of the dopaminergic network might influence outcomes after stroke. We reanalyzed resting-state functional MRI data of 19 severely impaired acute stroke patients and 19 healthy controls and computed amplitudes of low-frequency fluctuations (ALFF) and functional connectivity (FC) in and between eight subcortical and cortical areas of the nigrostriatal and mesocorticolimbic dopaminergic network of the contralesional hemisphere. Linear regression modeling was used to compare patients and controls and combine patients' ALFF and FC data with clinical follow-up data obtained after 3-6 months. The group comparison revealed a significant upregulation of ALFF in the prefrontal cortices, the ventral tegmental area, the nucleus accumbens, and the caudate nucleus. Additionally, for some regions and connections within the nigrostriatal and mesocorticolimbic network, ALFF and FC estimates were significantly linked to global disability and symptom burden at follow-up. These data indicate a link between the pre-stroke functional state of key areas and pathways of the contralesional dopaminergic system and recovery from a severe stroke, thereby adding novel functional insights to recent structural data and promoting the emerging concepts of brain reserve capacity after stroke.
Number sense is the intuitive, non-verbal ability to perceive and process numerical quantities without formal counting. This evolutionarily conserved trait, shared by different animal species, is supported by two mechanisms: the object tracking system (OTS) for small sets and the approximate number system (ANS) for larger quantities. Although historically viewed as distinct, these systems interact dynamically; their disruption is implicated in developmental dyscalculia and disorders such as Williams-Beuren syndrome (WBS), a chromosome microdeletion characterised by marked numerical and visuospatial deficits. Here, we synthesise neurobiological advances to provide an integrative perspective on the neural substrates of number sense. Field studies provide ecological validity, while laboratory procedures offer tighter precision; together, they illuminate the biological foundations of numerical cognition. Although number sense is conserved, human studies indicate only moderate heritability likely reflecting directional selection. Nonetheless, genetic findings converge on neurodevelopmental and synaptic mechanisms. Zebrafish (Danio rerio) offer a powerful platform to bridge genes, circuits and behaviour. For instance, manipulating zebrafish genes linked to WBS reveals gene-specific effects on quantity processing. At the neural level, numerical cognition is largely supported by specialised number-selective neurons. Whole-brain calcium imaging in larval zebrafish demonstrates that these neurons emerge by 3 days postfertilisation and follow a trajectory where representations of small numerosities precede larger ones. Altogether, integrating genetic, behavioural and circuit-level approaches provides a powerful framework for uncovering conserved mechanisms of numerosity supporting higher-level cognitive functions, including mathematics.
Mismatch negativity arises from the construction of a memory trace encoding regularities extracted from auditory stimuli in an oddball paradigm. A previous study argued that when phonetic standards are varied within the limits of a phoneme category (i.e., the mental representation of speech sounds), the auditory cortex retrieves a discrete phoneme representation from long-term memory and uses it as the memory trace for deviance detection. This claim has motivated a body of work using varying-standards paradigms to probe phonological underspecification. A strong version of this claim predicts that varying standards should eliminate mismatch negativity when both standards and deviants belong to the same phoneme category, because the memory trace is purely phonemic and lacks acoustic detail. We tested this prediction in three electroencephalography experiments using English /t/ varying in voice onset time. In Experiment 1, a within-category deviant with a long voice onset time elicited a robust mismatch negativity even when standards varied across shorter values, contrary to the prediction of an exclusively symbolic phoneme-based memory trace. Experiments 2 and 3 further examined whether the within-category mismatch response reflects long-term memory representations of phonetic realizations associated with the evoked phoneme category or listeners' ad hoc representation of the stimulus distribution. The weight of the evidence suggests that the within-category mismatch negativity in the varying-standards paradigm reflects sensitivity to the statistical structure of the stimulus physical properties, rather than exclusive access to abstract phonological categories. Findings invite reinterpretation of studies using varying-standards paradigm in light of encoding of stimulus statistics.
Mllt11 (myeloid/lymphoid or mixed-lineage leukemia translocated to chromosome 11; also known as Af1q/TcF7c) has been identified as a novel regulator of neural development, playing a role in the migration and outgrowth of cortical projection neurons. We previously reported that the conditional inactivation of the Mllt11 gene in the mouse superficial cortex resulted in reduced connectivity of the corpus callosum and white matter fiber tracts, resulting in reduced cortical thickness. However, the behavioral consequences of Mllt11 loss are unknown. Callosal abnormalities are thought to be present in 3%-5% of all neurodevelopmental disorders and reduced corpus callosum volume correlates with core symptoms of autism spectrum disorder (ASD) in humans. Cortical thickness dysregulation is likewise shared among various neurodevelopmental disorders including ASD. We therefore investigated the behavioral consequences of conditional knockout of Mllt11 using transgenic Cux2iresCre/+ mice. Utilizing tasks designed to reflect core ASD symptoms, we examined the behaviors of both male and female conditional knockout animals. These tests included olfaction habituation/dishabituation, three-chambered social approach, marble burying, and nestlet shredding. We found sex-dependent disruptions in social preference and nestlet shredding in animals lacking Mllt11, with the female mice presenting with more disruptions than the males. Understanding the behavioral phenotype associated with genes of interest, specifically in the context of sex differences, is crucial to individualized treatment for neurodevelopmental disorders.
Electroconvulsive therapy (ECT) is the most effective treatment for severe depression but uptake is hindered due to effects on memory and a poor understanding of its mechanisms of action. Hippocampal plasticity is one consequence of ECT that may be related to both the therapeutic and amnestic effects. In animals, electroconvulsive shock (ECS) dramatically increases adult neurogenesis in the dentate gyrus (DG). However, little is known about how ECS impacts the morphology of adult-born neurons. Moreover, it is unknown whether ECS differentially impacts DG neurons that are born in development versus adulthood. To address these questions, here, we subjected male and female mice to a clinically relevant schedule of chronic ECS and examined effects on DG neuron populations. As predicted, ECS dramatically increased the survival of adult-born DG neurons generated shortly before treatment and the number of immature neurons present after treatment. Adult-born neurons from ECS-treated mice also had longer dendrites and larger presynaptic terminals, suggesting enhanced circuit integration. In contrast, ECS did not affect the survival of neurons born in early postnatal development and it did not alter the structure of their dendrites or presynaptic terminals. Instead, ECS reduced spine density on developmentally born neurons in the dorsal DG and, in the ventral DG, it increased mushroom spine density. Thus, adult-born neurons generally display greater ECS-induced plasticity than developmentally born neurons, which may be relevant for the effects of ECS/ECT on cognition and mood.
Consonance/dissonance (C/D) is an important feature in music; it mainly arises from the relation of fundamental frequencies (f0) within chords or dyads. The current magnetoencephalography study investigated early cortical and subcortical C/D correlates and their robustness against (1) the physical presence of f0 and listener's propensity for f0-based pitch processing, (2) active vs. passive listening, and (3) the listener's musical expertise. A sample of N = 39 normal-hearing adults underwent psychometric testing for individual pitch perception preference and musical aptitude. They also listened to consonant and dissonant dyads with and without physically present f0 while their cortical auditory evoked fields and brainstem-level frequency-following responses (FFRs) were simultaneously recorded, in a paradigm comprising both active- and passive-listening conditions. Consonant dyads elicited earlier transient cortical activity than dissonant dyads and stronger FFRs to the f0 of the high dyad component. Moreover, the C/D-related transient responses evolved comparably for dyads with vs. without f0 and were unchanged by active listening, musical aptitude, or individual pitch perception preference. Active listening, in turn, went with larger amplitudes in the continuous subcortical and cortical activity, reflecting top-down attentional gain. Listeners with more f0-based pitch perception showed worse behavioral performance in dyads with missing f0. Both active listening and the processing of missing f0 information were unrelated to the listener's musical aptitude. Together, our results show how active listening and missing f0 processing are reflected in psychophysiological responses; however, early neural C/D correlates appear largely robust against these variables.
How the brain signals prediction errors for non-rewarding, yet significant, sensory events remains a central question. Although the cortical mismatch negativity provides a well-known signature for deviance detection, the contribution of subcortical dopamine remains unclear. This study tested the hypothesis that phasic dopamine in the nucleus accumbens encodes the salience associated with the violation of an ongoing statistical regularity. Using fiber photometry in freely moving rats, we contrasted an auditory oddball paradigm with a many-standards control. Deviant stimuli elicited a significantly amplified dopamine response compared with standard stimuli. Crucially, this dopamine response enhancement was absent in the control condition, demonstrating that the nucleus accumbens dopamine responds specifically to rule violation rather than mere stimulus rarity. The long latency of this signal (~500 ms) relative to the cortical mismatch negativity argues against a direct role in the initial detection of deviance. Instead, our findings support a model in which subcortical dopamine acts as a distinct salience signal, operating in parallel with cortical deviance detection, to evaluate unexpected events and guide subsequent behavioral adjustments.
Controllability analysis provides a useful framework for assessing the ability of specific brain regions to modulate states in the other regions and is often applied to structural and functional magnetic resonance imaging data. Here, I explored frequency-dependent characteristics of oscillation-based controllability from resting-state magnetoencephalography (MEG) data, along with their associations with cross-frequency coupling and molecular systems. Resting-state MEG data were measured in 27 healthy participants. Whole-brain source activities were reconstructed, and functional connectivities among source points in several frequency bands were estimated using the phase-lag index (PLI). PLI-based average/modal controllability (AC/MC) and phase-amplitude coupling (PAC) were calculated at each source location. Spatial correlations were also examined: (1) between each pair of frequency bands of AC/MCs, (2) between controllability and PAC, and (3) between AC/MCs and public positron emission tomography maps for various neurotransmission receptors. Results showed that low-frequency (delta, theta, and alpha-band) AC/MCs were spatially correlated with each other and with PACs when the frequency band of AC/MCs and PAC phase were the same. Beta- and gamma-band AC/MCs also exhibited significant spatial correlations. Low-frequency ACs were elevated in the temporal and occipital areas, whereas beta- and gamma-band ACs were mainly located in the medial part of the frontal and parietal areas. Molecular-informed analysis indicated frequency-specific associations of AC/MCs with distinct neurotransmitter systems. Taken together, the present study is the first to show that frequency-dependent spatial patterns of oscillation-based controllability are linked to cross-frequency coupling and molecular systems in local circuits.
Developmental language disorder (DLD) is a persistent difficulty in the acquisition and use of expressive and/or receptive language, which negatively impacts academic and social development. The present study evaluated the validity of the statistical learning model proposed to account for language difficulties in children with DLD. To this end, two auditory paradigms of varying complexity, framed within predictive coding theory, were passively presented to children diagnosed with DLD and to typically developing children without neurological impairments. The paradigms consisted of stimulus sequences with decreasing or increasing frequencies, interspersed with the sporadic occurrence of unexpected tone endings. The psychophysiological response was recorded using EEG, focusing on the P1, mismatch negativity (MMN), postimperative negative variation (PINV), and contingent negative variation (CNV) components. Results showed an absent MMN and a higher P1 response to deviant tones in children with DLD, suggesting an impaired development of frontal MMN generators, potentially compensated by activity in the primary auditory cortex. DLD participants also showed increased PINV and CNV responses during the most complex paradigm, which could imply greater cognitive effort and resource allocation for reassessment of stimulus patterns. Finally, incomplete maturation of frontal areas in children within this age range (3-11 years) was proposed as a possible explanation for the absence of differences between groups in P1 and N1/MMN responses elicited by simple and complex conditions. These findings support statistical learning as a valid model for understanding the possible neural basis of DLD and highlight this predictive EEG design as a potential protocol for early detection.
This study presents the relative authorship index (RAI), a novel metric designed to address the limitations of traditional bibliometric indicators, such as publication counts, citation numbers, and the h-index, by correcting for authorship inflation. Conventional metrics can overestimate productivity by failing to account for the number of co-authors or the possibility of inflated authorship. To detect such inflation, this index evaluates the number of co-authors on a paper relative to the number of authors in the references cited within the same paper, which are assumed to reflect the researcher's specific field of study. By using this field-specific baseline, the index identifies whether a publication involves an unusually high number of co-authors compared to field standards, thus flagging potential authorship inflation. Applied to neuroscience articles authored by researchers affiliated with Italian universities, the index revealed significant regional and university differences, with higher values in southern regions and private universities. A case study of a single department also revealed high variability among individual researchers, indicating that the index can capture consistent patterns in authorship practices. In addition, we propose an authorship correction formula to adjust bibliometric indicators. The formula introduces parameters that penalize authorship inflation based on the RAI and also penalize large co-author counts, with the latter scaled according to whether the researcher occupies key authorship positions (first, last, and/or corresponding author).
We have recently shown that occluding retronasal pathways with a nose clip reduces both the subjective and neural responses to sucrose, suggesting the involvement of retronasal pathways in sucrose perception. However, how other sweet tastes such as stevia might also be affected by retronasal occlusion at the subjective and neural level is unknown. We examined the neural activity to stevia with a nose clip on (blocking retronasal pathways) and nose clip off, in a robust sample of healthy adults (N = 34, mean 25 years). Neural activity to stevia was reduced with the nose clip on in the olfactory cortex, hypothalamus, the subgenual and pregenual anterior cingulate and the nucleus accumbens. Stevia pleasantness was tracked by the posterior insula, but this was not apparent with the nose clip on. In conclusion, our findings are the first to demonstrate that blocking retronasal pathways significantly reduces neural responses to stevia taste, supporting the proposal that retronasal pathways play a role in the perception of tastes like stevia, and that stevia-sweetened products could be made more palatable via retronasal pathways.