rudyvdbrink/CitationDatabase huggingface dataset:
Associations of acute and chronic stress hormones with cognitive functions in autism spectrum disorder.
Neuroscience, 2017

Extensive studies have reported cognitive abnormalities in neurodevelopmental disorders, such as autism spectrum disorder (ASD). Another line of evidence suggests that stress also affects cognitive functions. In this study, we investigated whether there were associations between stress hormones and cognitive functions in ASD and typically developing (TD) children. Cognitive functions in ASD and TD children were evaluated with a battery of psychological tests for working memory, behavioral flexibility, and social cognition for emotional assessments of others. ASD children exhibited higher hair and salivary cortisol, which reflects chronic and acute stress hormone levels of subjects, respectively, than TD children. Autism-spectrum quotient (AQ) was positively correlated with hair cortisol and the scores of Spence Children's Anxiety Scale in ASD children. In addition, a negative correlation was present between spatial working memory performance and hair cortisol in ASD, but not in TD, children. These results suggest that chronic stress hormone elevation may have relationships with some aspects of cognitive dysfunction in ASD subjects.
Atrial fibrillation detected after stroke is related to a low risk of ischemic stroke recurrence.
Neurology, 2018

To compare the risk of 1-year ischemic stroke recurrence between atrial fibrillation (AF) diagnosed after stroke (AFDAS) and sinus rhythm (SR) and investigate whether underlying heart disease is as frequent in AFDAS as it is in AF known before stroke (KAF).
Nimodipine attenuates the parkinsonian neurotoxin, MPTP-induced changes in the calcium binding proteins, calpain and calbindin.
Journal of chemical neuroanatomy, 2019

We have recently demonstrated neuroprotective abilities of nimodipine, an L-type voltage dependent calcium channel (VDCC) blocker in cellular and animal models of Parkinson's disease (PD). To understand the calcium regulatory mechanisms in the disease pathogenesis, the present study examined calcium regulatory proteins calbindin and calpain mRNA and protein levels employing quantitative PCR and western blot in 1-methyl-4-phenyl pyridinium ion (MPP
NF-Y inactivation causes atypical neurodegeneration characterized by ubiquitin and p62 accumulation and endoplasmic reticulum disorganization.
Nature communications, 2014

Nuclear transcription factor-Y (NF-Y), a key regulator of cell-cycle progression, often loses its activity during differentiation into nonproliferative cells. In contrast, NF-Y is still active in mature, differentiated neurons, although its neuronal significance remains obscure. Here we show that conditional deletion of the subunit NF-YA in postmitotic mouse neurons induces progressive neurodegeneration with distinctive ubiquitin/p62 pathology; these proteins are not incorporated into filamentous inclusion but co-accumulated with insoluble membrane proteins broadly on endoplasmic reticulum (ER). The degeneration also accompanies drastic ER disorganization, that is, an aberrant increase in ribosome-free ER in the perinuclear region, without inducing ER stress response. We further perform chromatin immunoprecipitation and identify several NF-Y physiological targets including Grp94 potentially involved in ER disorganization. We propose that NF-Y is involved in a unique regulation mechanism of ER organization in mature neurons and its disruption causes previously undescribed novel neuropathology accompanying abnormal ubiquitin/p62 accumulation.
Dissociating between the N2pc and attentional shifting: An attentional blink study.
Neuropsychologia, 2018

The N2pc is routinely used as an electrophysiological index of attentional shifting. Its absence is thus taken as evidence that no shift of attention occurred. We provide evidence in contrast to this notion using a variant of the attentional blink (AB) paradigm. Two target letters, embedded in two streams of distractor letters and defined by their color, were separated by either 300 or 800 ms. The second target was preceded by a distractor frame of the same color (cue). As expected, identification of the second target was poorer at the short than at the long lag (the AB effect). The AB did not affect attentional capture by the cue, but suppressed and delayed the N2pc associated with it. This result suggests that the N2pc does not reflect attentional shifting. Instead, we conclude that the N2pc indexes the transient enhancement that occurs at the spatial focus of attention and promotes high-level processing such as identification. This conclusion calls for a reinterpretation of findings from the attentional capture literature that relied on the N2pc as an index of attentional shifting. Our results also inform contemporary models of the AB.
"As long as that is my hand, that willed action is mine": Timing of agency triggered by body ownership.
Consciousness and cognition, 2018

We investigated whether agency triggered by body ownership shares similar temporal constraints with agency induced by actual movements. We compared agency over the movements of the own hand, a fake hand and an embodied fake hand when they pressed a button delivering a stimulus to the participant's body after 500, 1000 or 2000 ms. In the first two delays, the movement of the embodied fake hand was misattributed to the participant's own will and the stimulus intensity was attenuated, as it happened when the own hand delivered the stimulus. With the longest delay, the movement of the embodied fake hand was neither misattributed to the participant's will nor the stimulus intensity was attenuated, as it happened when the fake non-embodied hand delivered the stimulus. By showing that illusory and veridical agency arise under similar temporal constraints, we further demonstrated that body ownership per se acts upon agency attribution.
Predictive and reactive tuning of the locomotor CPG.
Integrative and comparative biology, 2007

The neural control of locomotion involves a constant interplay between the actions of a central pattern generator (CPG) and sensory input elicited by bodily movement. With respect to the CPG, recent analysis of fictive locomotion has shown that durations of flexion and extension tend to covary along specific lines in plots of phase duration versus cycle duration. The slopes of these lines evidently depend on internal states that vary among preparations, but, within a preparation, remain rather steady from one sequence to the next. These relationships can be reproduced in a simple oscillator model having two pairs of preset parameters, suggesting that steady internal drives to flexor and extensor half-centers determine how phase durations covary. Regarding the role of sensory inputs, previous experiments have revealed state-dependent rules that govern phase-switching independently of the CPG rhythm. In addition, sensory input is known to modulate motoneuronal activation through stretch reflexes. To explore how sensory input combines with the locomotor CPG, we used a neuromechanical model with muscle actuators, proprioceptive feedback, sensory phase-switching rules, and a CPG. Interestingly, sequences of stable locomotion were always associated with phase durations that conformed to an extensor-dominated phase-duration characteristic (where extension durations vary more than flexion durations). This is the characteristic seen in normal animals, but not necessarily in fictive locomotion, where movement and associated sensory input are absent. This suggests that to produce the biomechanical events required for stability, an extensor-dominated phase-duration characteristic is required. In the model, when the preset CPG phase durations were well matched to coincide the biomechanical requirements, CPG-mediated phase switching produced stable cycles. When CPG phase durations were too short, phases switched prematurely and the model soon fell. When CPG phase durations were too long, sensory rules fired and overrode the CPG, maintaining stability. We posit that under normal circumstances, descending input from higher centers continually adjusts the operating point of the CPG on the preset phase-duration characteristic according to anticipated biomechanical requirements. When the predictions are good, CPG-generated phase durations closely match those required by the kinetics and kinematics, and little or no sensory adjustment occurs. We propose the term "neuromechanical tuning" to describe this process of matching the CPG to the biomechanical requirements.
Elucidation of the Impact of P-glycoprotein and Breast Cancer Resistance Protein on the Brain Distribution of Catechol-
Drug metabolism and disposition: the biological fate of chemicals, 2017

P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) are clinically important efflux transporters that act cooperatively at the blood-brain barrier, limiting the entry of several drugs into the central nervous system (CNS) and affecting their pharmacokinetics, therapeutic efficacy, and safety. In the present study, the interactions of catechol-
Topographic organization of V1 projections through the corpus callosum in humans.
NeuroImage, 2010

The visual cortex in each hemisphere is linked to the opposite hemisphere by axonal projections that pass through the splenium of the corpus callosum. Visual-callosal connections in humans and macaques are found along the V1/V2 border where the vertical meridian is represented. Here we identify the topography of V1 vertical midline projections through the splenium within six human subjects with normal vision using diffusion-weighted MR imaging and probabilistic diffusion tractography. Tractography seed points within the splenium were classified according to their estimated connectivity profiles to topographic subregions of V1, as defined by functional retinotopic mapping. First, we report a ventral-dorsal mapping within the splenium with fibers from ventral V1 (representing the upper visual field) projecting to the inferior-anterior corner of the splenium and fibers from dorsal V1 (representing the lower visual field) projecting to the superior-posterior end. Second, we also report an eccentricity gradient of projections from foveal-to-peripheral V1 subregions running in the anterior-superior to posterior-inferior direction, orthogonal to the dorsal-ventral mapping. These results confirm and add to a previous diffusion MRI study (Dougherty et al., 2005) which identified a dorsal/ventral mapping of human splenial fibers. These findings yield a more detailed view of the structural organization of the splenium than previously reported and offer new opportunities to study structural plasticity in the visual system.
American Clinical Neurophysiology Society Guideline 3: A Proposal for Standard Montages to Be Used in Clinical EEG.
Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society, 2016

This revision to the EEG Guidelines is an update incorporating current electroencephalography technology and practice and was previously published as Guideline 6. A discussion of methodology for the appropriate selection of reference electrodes is added. In addition, montages are added to assist with localization of abnormal activity in mesial frontal and anterior temporal regions.
Differential neuronal susceptibility and apoptosis in congenital Zika virus infection.
Annals of neurology, 2017

To characterize the mechanism of Zika virus (ZIKV)-associated microcephaly, we performed immunolabeling on brain tissue from a 20-week fetus with intrauterine ZIKV infection. Although ZIKV demonstrated a wide range of neuronal and non-neuronal tropism, the infection rate was highest in intermediate progenitor cells and immature neurons. Apoptosis was observed in both infected and uninfected bystander cortical neurons, suggesting a role for paracrine factors in induction of neuronal apoptosis. Our results highlight differential neuronal susceptibility and neuronal apoptosis as potential mechanisms in the development of ZIKV-associated microcephaly, and may provide insights into the design and best timing of future therapy. Ann Neurol 2017;82:121-127.
Neuropeptide orphanin FQ inhibits dendritic morphogenesis through activation of RhoA.
Developmental neurobiology, 2013

Brain-derived neurotrophic factor (BDNF) plays a facilitatory role in neuronal development and promotion of differentiation. Mechanisms that oppose BDNF's stimulatory effects create balance and regulate dendritic growth. However, these mechanisms have not been studied. We have focused our studies on the BDNF-induced neuropeptide OrphaninFQ/ Nociceptin (OFQ); while BDNF is known to enhance synaptic activity, OFQ has opposite effects on activity, learning, and memory. We have now examined whether OFQ provides a balance to the stimulatory effects of BDNF on neuronal differentiation in the hippocampus. Golgi staining in OFQ knockout (KO) mice revealed an increase in primary dendrite length as well as spine density, suggesting that endogenous OFQ inhibits dendritic morphology. We have also used cultured hippocampal neurons to demonstrate that exogenous OFQ has an inhibitory effect on dendritic growth and that the neuropeptide alters the response to BDNF when pre-administered. To determine if BDNF and OFQ act in a feedback loop, we inhibited the actions of the BDNF and OFQ receptors, TrkB and NOP using ANA-12 and NOP KO mice respectively but our data suggest that the two factors do not act in a negative feedback loop. We found that the inhibition of dendritic morphology induced by OFQ is via enhanced RhoA activity. Finally, we have evidence that RhoA activation is required for the inhibitory effects of OFQ on dendritic morphology. Our results reveal basic mechanisms by which neurons not only regulate the formation of proper dendritic growth during development but also control plasticity in the mature nervous system.
Strength and Diversity of Inhibitory Signaling Differentiates Primate Anterior Cingulate from Lateral Prefrontal Cortex.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017

The lateral prefrontal cortex (LPFC) and anterior cingulate cortex (ACC) of the primate play distinctive roles in the mediation of complex cognitive tasks. Compared with the LPFC, integration of information by the ACC can span longer timescales and requires stronger engagement of inhibitory processes. Here, we reveal the synaptic mechanism likely to underlie these differences using
Type 1 adenylyl cyclase is essential for maintenance of remote contextual fear memory.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008

Although molecular mechanisms for hippocampus-dependent memory have been extensively studied, much less is known about signaling events important for remote memory. Here we report that mice lacking type 1 adenylyl cyclase (AC1) are able to establish and retrieve remote contextual memory but unable to sustain it as long as wild-type mice. Interestingly, mice overexpressing AC1 show superior remote contextual memory even though they exhibit normal hippocampus-dependent contextual memory. These data illustrate that calcium coupling to cAMP contributes to the stability of remote memory and identifies AC1 as a potential drug target site to improve long-term remote memory.
Emotional modulation of alpha asymmetry in dysphoria: results from an emotional imagery task.
International journal of psychophysiology : official journal of the International Organization of Psychophysiology, 2015

Studies on electroencephalographic (EEG) alpha band asymmetry at rest have reported that, compared to healthy controls, dysphoric and clinically depressed individuals often display relatively less left- than right-sided cortical activity at anterior scalp sites, and the opposite pattern at posterior scalp sites. It has also been shown that depression-related differences in alpha lateralization at anterior and posterior sites are more likely to emerge during emotional tasks and during visuospatial tasks, respectively, rather than during resting conditions. However, although it is the well-established that posterior cortical activity plays a key role also in emotional processing in healthy individuals, the influence of dysphoria on posterior alpha asymmetry sites during an emotional task has yet to be examined. To this end, dysphoric (n=23) and nondysphoric (n=24) individuals performed an emotional imagery task including pleasant, neutral, and unpleasant narratives. The group with, but not without, dysphoria showed reduced left relative to right cortical activity at anterior sites, irrespective of emotional condition. By contrast, at posterior sites, individuals with dysphoria showed reduced right relative to left parietal activity during unpleasant, but not pleasant and neutral, imagery condition compared to nondysphoric individuals. Results at anterior scalp sites provide further evidence for the presence of a stable pattern of reduced approach motivation in dysphoric individuals. The association between dysphoria and right relative to left parietal hypoactivation in response to unpleasant imagery suggests that dysphoric individuals are more likely to use state-dependent dysfunctional strategies to regulate negative emotions compared to nondysphoric individuals.
Functional Imaging of Audio-Visual Selective Attention in Monkeys and Humans: How do Lapses in Monkey Performance Affect Cross-Species Correspondences?
Cerebral cortex (New York, N.Y. : 1991), 2017

The cross-species correspondences and differences in how attention modulates brain responses in humans and animal models are poorly understood. We trained 2 monkeys to perform an audio-visual selective attention task during functional magnetic resonance imaging (fMRI), rewarding them to attend to stimuli in one modality while ignoring those in the other. Monkey fMRI identified regions strongly modulated by auditory or visual attention. Surprisingly, auditory attention-related modulations were much more restricted in monkeys than humans performing the same tasks during fMRI. Further analyses ruled out trivial explanations, suggesting that labile selective-attention performance was associated with inhomogeneous modulations in wide cortical regions in the monkeys. The findings provide initial insights into how audio-visual selective attention modulates the primate brain, identify sources for "lost" attention effects in monkeys, and carry implications for modeling the neurobiology of human cognition with nonhuman animals.
Drosophila CaV2 channels harboring human migraine mutations cause synapse hyperexcitability that can be suppressed by inhibition of a Ca2+ store release pathway.
PLoS genetics, 2018

Gain-of-function mutations in the human CaV2.1 gene CACNA1A cause familial hemiplegic migraine type 1 (FHM1). To characterize cellular problems potentially triggered by CaV2.1 gains of function, we engineered mutations encoding FHM1 amino-acid substitutions S218L (SL) and R192Q (RQ) into transgenes of Drosophila melanogaster CaV2/cacophony. We expressed the transgenes pan-neuronally. Phenotypes were mild for RQ-expressing animals. By contrast, single mutant SL- and complex allele RQ,SL-expressing animals showed overt phenotypes, including sharply decreased viability. By electrophysiology, SL- and RQ,SL-expressing neuromuscular junctions (NMJs) exhibited enhanced evoked discharges, supernumerary discharges, and an increase in the amplitudes and frequencies of spontaneous events. Some spontaneous events were gigantic (10-40 mV), multi-quantal events. Gigantic spontaneous events were eliminated by application of TTX-or by lowered or chelated Ca2+-suggesting that gigantic events were elicited by spontaneous nerve firing. A follow-up genetic approach revealed that some neuronal hyperexcitability phenotypes were reversed after knockdown or mutation of Drosophila homologs of phospholipase Cβ (PLCβ), IP3 receptor, or ryanodine receptor (RyR)-all factors known to mediate Ca2+ release from intracellular stores. Pharmacological inhibitors of intracellular Ca2+ store release produced similar effects. Interestingly, however, the decreased viability phenotype was not reversed by genetic impairment of intracellular Ca2+ release factors. On a cellular level, our data suggest inhibition of signaling that triggers intracellular Ca2+ release could counteract hyperexcitability induced by gains of CaV2.1 function.
Delineating neural structures of developmental human brains with diffusion tensor imaging.
TheScientificWorldJournal, 2010

The human brain anatomy is characterized by dramatic structural changes during fetal development. It is extraordinarily complex and yet its origin is a simple tubular structure. Revealing detailed anatomy at different stages of brain development not only aids in understanding this highly ordered process, but also provides clues to detect abnormalities caused by genetic or environmental factors. However, anatomical studies of human brain development during the fetal period are surprisingly scarce and histology-based atlases have become available only recently. Diffusion tensor imaging (DTI) measures water diffusion to delineate the underlying neural structures. The high contrasts derived from DTI can be used to establish the brain atlas. With DTI tractography, coherent neural structures, such as white matter tracts, can be three-dimensionally reconstructed. The primary eigenvector of the diffusion tensor can be further explored to characterize microstructures in the cerebral wall of the developmental brains. In this mini-review, the application of DTI in order to reveal the structures of developmental fetal brains has been reviewed in the above-mentioned aspects. The fetal brain DTI provides a unique insight for delineating the neural structures in both macroscopic and microscopic levels. The resultant DTI database will provide structural guidance for the developmental study of human fetal brains in basic neuroscience, and reference standards for diagnostic radiology of premature newborns.
Hippocampal Spike-Timing Correlations Lead to Hexagonal Grid Fields.
Physical review letters, 2017

Space is represented in the mammalian brain by the activity of hippocampal place cells, as well as in their spike-timing correlations. Here, we propose a theory for how this temporal code is transformed to spatial firing rate patterns via spike-timing-dependent synaptic plasticity. The resulting dynamics of synaptic weights resembles well-known pattern formation models in which a lateral inhibition mechanism gives rise to a Turing instability. We identify parameter regimes in which hexagonal firing patterns develop as they have been found in medial entorhinal cortex.
Sertad1 plays an essential role in developmental and pathological neuron death.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010

Developmental and pathological death of neurons requires activation of a defined pathway of cell cycle proteins. However, it is unclear how this pathway is regulated and whether it is relevant in vivo. A screen for transcripts robustly induced in cultured neurons by DNA damage identified Sertad1, a Cdk4 (cyclin-dependent kinase 4) activator. Sertad1 is also induced in neurons by nerve growth factor (NGF) deprivation and Abeta (beta-amyloid). RNA interference-mediated downregulation of Sertad1 protects neurons in all three death models. Studies of NGF withdrawal indicate that Sertad1 is required to initiate the apoptotic cell cycle pathway since its knockdown blocks subsequent pathway events. Finally, we find that Sertad1 expression is required for developmental neuronal death in the cerebral cortex. Sertad1 thus appears to be essential for neuron death in trophic support deprivation in vitro and in vivo and in models of DNA damage and Alzheimer's disease. It may therefore be a suitable target for therapeutic intervention.