rudyvdbrink/CitationDatabase huggingface dataset:
Repetition suppression for visual actions in the macaque superior temporal sulcus.
Journal of neurophysiology, 2016

In many brain areas, repetition of a stimulus usually weakens the neural response. This "adaptation" or repetition suppression effect has been observed with mass potential measures such as event-related potentials (ERPs), in fMRI BOLD responses, and locally with local field potentials (LFPs) and spiking activity. Recently, it has been reported that macaque F5 mirror neurons do not show repetition suppression of their spiking activity for single repetitions of hand actions, which disagrees with human fMRI adaptation studies. This finding also contrasts with numerous studies showing repetition suppression in macaque inferior temporal cortex, including the rostral superior temporal sulcus (STS). Since the latter studies employed static stimuli, we assessed here whether the use of dynamic action stimuli abolishes repetition suppression in the awake macaque STS. To assess adaptation effects in the STS, we employed the same hand action movies as used when examining adaptation in F5. The upper bank STS neurons showed repetition suppression during the approaching phase of the hand action, which corresponded to the phase of the action for which these neurons responded overall the strongest. The repetition suppression was present for the spiking activity measured in independent single-unit and multiunit recordings as well as for the LFP power at frequencies > 50 Hz. Together with previous data in F5, these findings suggest that adaptation effects differ between F5 mirror neurons and the STS neurons.
Embryonic transcription factor expression in mice predicts medial amygdala neuronal identity and sex-specific responses to innate behavioral cues.
eLife, 2017

The medial subnucleus of the amygdala (MeA) plays a central role in processing sensory cues required for innate behaviors. However, whether there is a link between developmental programs and the emergence of inborn behaviors remains unknown. Our previous studies revealed that the telencephalic preoptic area (POA) embryonic niche is a novel source of MeA destined progenitors. Here, we show that the POA is comprised of distinct progenitor pools complementarily marked by the transcription factors Dbx1 and Foxp2. As determined by molecular and electrophysiological criteria this embryonic parcellation predicts postnatal MeA inhibitory neuronal subtype identity. We further find that
Binge-Like Alcohol Exposure During Adolescence Disrupts Dopaminergic Neurotransmission in the Adult Prelimbic Cortex.
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2017

Repeated binge-like exposure to alcohol during adolescence has been reported to perturb prefrontal cortical development, yet the mechanisms underlying these effects are unknown. Here we report that adolescent intermittent ethanol exposure induces cellular and dopaminergic abnormalities in the adult prelimbic cortex (PrL-C). Exposing rats to alcohol during early-mid adolescence (PD28-42) increased the density of long/thin dendritic spines of layer 5 pyramidal neurons in the adult PrL-C. Interestingly, although AIE exposure did not alter the expression of glutamatergic proteins in the adult PrL-C, there was a pronounced reduction in dopamine (DA) D
Worldwide survey of neurologists on approach to autoimmune encephalitis.
Neurology. Clinical practice, 2020

To explore practice differences in the diagnosis and management of autoimmune encephalitis (AE), which is complicated by issues with sensitivity/specificity of antibody testing, nonspecific MRI/EEG/CSF findings, and competing differential diagnoses.
Enhanced regeneration and functional recovery after spinal root avulsion by manipulation of the proteoglycan receptor PTPσ.
Scientific reports, 2015

Following root avulsion, spinal nerves are physically disconnected from the spinal cord. Severe motoneuron death and inefficient axon regeneration often result in devastating motor dysfunction. Newly formed axons need to extend through inhibitory scar tissue at the CNS-PNS transitional zone before entering into a pro-regenerative peripheral nerve trajectory. CSPGs are dominant suppressors in scar tissue and exert inhibition via neuronal receptors including PTPσ. Previously, a small peptide memetic of the PTPσ wedge region named ISP (Intracellular Sigma Peptide) was generated, and its capabilities to target PTPσ and relieve CSPG inhibition were validated. Here, we demonstrate that after ventral root avulsion and immediate re-implantation, modulation of PTPσ by systemic delivery of ISP remarkably enhanced regeneration. ISP treatment reduced motoneuron death, increased the number of axons regenerating across scar tissue, rebuilt healthy neuromuscular junctions and enhanced motor functional recovery. Our study shows that modulation of PTPσ is a potential therapeutic strategy for root avulsion.
Defining "neuroinflammation".
Annals of the New York Academy of Sciences, 2008

Neuroinflammation is a hot topic in contemporary neuroscience. A relatively new open-access journal, the Journal of Neuroinflammation, focuses on this field. As another example, abstracts to the 2007 Annual Meeting of the Society for Neuroscience could be submitted in several subcategories of neuroinflammation, a strong signal of growth in this research area. While it is becoming clear that activation of microglia and astroglia and the attendant expression of proinflammatory cytokines and chemokines often are associated with disease-, trauma-, and toxicant-induced damage to the CNS, it is by no means clear that a cause-and-effect relationship exists between the presence of a neuroinflammatory process and neural damage. We have explored this issue with two models of dopaminergic neurotoxicity. We used a single low-dose regimen of MPTP or METH, a paradigm that causes selective degeneration of striatal dopaminergic nerve terminals without affecting the cell body in the substantia nigra. Both compounds increased the expression of the microglia-associated factors, Il-1alpha, Il6, Ccl2, and Tnf-alpha, and also elicited morphologic evidence of microglial activation prior to induction of astrogliosis. Pharmacologic antagonism of MPTP and METH neurotoxicity prevented these proinflammatory responses, findings suggestive of a link between neuroinflammation and the observed neurotoxic outcomes. Nevertheless, when we used minocycline to suppress the expression of all these mediators, with the exception of Tnf-alpha, we failed to see neuroprotection. Likewise, when we examined the effects of MPTP or METH in transgenic mice lacking Il6, Ccl2, or Tnfr1/2 genes, deficiency of either Il6 or Ccl2 did not alter neurotoxicity, whereas deficiency in Tnfr1/2 was neuroprotective. Although these observations pointed to a role of the proinflammatory cytokine, TNF-alpha, in the neurotoxic effects of MPTP and METH, other observations did not support this supposition. For example, activation of NF-kappaB or induction of iNOS, known components of inflammatory responses and free radical formation, were not observed. Moreover, immunosuppressive regimens of glucocorticoids failed to suppress TNF-alpha or attenuate neurotoxicity. Taken together, our observations suggest that MPTP and METH neurotoxicity are associated with the elaboration of a "neuroinflammatory" response, yet this response lacks key features of inflammation and, with the exception of TNF-alpha, neurotoxicity appears to be the cause rather than the consequence of proinflammatory signals.
Parrot Genomes and the Evolution of Heightened Longevity and Cognition.
Current biology : CB, 2018

Parrots are one of the most distinct and intriguing groups of birds, with highly expanded brains [1], highly developed cognitive [2] and vocal communication [3] skills, and a long lifespan compared to other similar-sized birds [4]. Yet the genetic basis of these traits remains largely unidentified. To address this question, we have generated a high-coverage, annotated assembly of the genome of the blue-fronted Amazon (Amazona aestiva) and carried out extensive comparative analyses with 30 other avian species, including 4 additional parrots. We identified several genomic features unique to parrots, including parrot-specific novel genes and parrot-specific modifications to coding and regulatory sequences of existing genes. We also discovered genomic features under strong selection in parrots and other long-lived birds, including genes previously associated with lifespan determination as well as several hundred new candidate genes. These genes support a range of cellular functions, including telomerase activity; DNA damage repair; control of cell proliferation, cancer, and immunity; and anti-oxidative mechanisms. We also identified brain-expressed, parrot-specific paralogs with known functions in neural development or vocal-learning brain circuits. Intriguingly, parrot-specific changes in conserved regulatory sequences were overwhelmingly associated with genes that are linked to cognitive abilities and have undergone similar selection in the human lineage, suggesting convergent evolution. These findings bring novel insights into the genetics and evolution of longevity and cognition, as well as provide novel targets for exploring the mechanistic basis of these traits.
The Speed of Visual Attention and Motor-Response Decisions in Adult Attention-Deficit/Hyperactivity Disorder.
Biological psychiatry, 2015

Adults with attention-deficit/hyperactivity disorder (ADHD) exhibit slowed reaction times (RTs) in various attention tasks. The exact origins of this slowing, however, have not been established. Potential candidates are early sensory processes mediating the deployment of focal attention, stimulus response translation processes deciding upon the appropriate motor response, and motor processes generating the response.
Differential polarization of cortical pyramidal neuron dendrites through weak extracellular fields.
PLoS computational biology, 2018

The rise of transcranial current stimulation (tCS) techniques have sparked an increasing interest in the effects of weak extracellular electric fields on neural activity. These fields modulate ongoing neural activity through polarization of the neuronal membrane. While the somatic polarization has been investigated experimentally, the frequency-dependent polarization of the dendritic trees in the presence of alternating (AC) fields has received little attention yet. Using a biophysically detailed model with experimentally constrained active conductances, we analyze the subthreshold response of cortical pyramidal cells to weak AC fields, as induced during tCS. We observe a strong frequency resonance around 10-20 Hz in the apical dendrites sensitivity to polarize in response to electric fields but not in the basal dendrites nor the soma. To disentangle the relative roles of the cell morphology and active and passive membrane properties in this resonance, we perform a thorough analysis using simplified models, e.g. a passive pyramidal neuron model, simple passive cables and reconstructed cell model with simplified ion channels. We attribute the origin of the resonance in the apical dendrites to (i) a locally increased sensitivity due to the morphology and to (ii) the high density of h-type channels. Our systematic study provides an improved understanding of the subthreshold response of cortical cells to weak electric fields and, importantly, allows for an improved design of tCS stimuli.
Characteristics of institutionalized young onset dementia patients--the BEYOnD study.
International psychogeriatrics, 2014

People with Young Onset Dementia (YOD) have specific needs for care. These people eventually require institutional care, usually delivered by institutions designed for the elderly. The Dutch network of care organizations delivering specialized YOD care offers a unique opportunity to obtain more knowledge of this special population.
Characterizing the demographics of chronic pain patients in the state of Maine using the Maine all payer claims database.
BMC public health, 2018

Chronic pain is currently a significant health problem in the United States. A comprehensive strategy is needed to increase prevention of chronic pain and to improve care for chronic pain patients. However, development of a successful strategy relies, in part, on a better understanding of the demographics and socioeconomics of patients living with chronic pain conditions. The current study was designed to understand the burden of chronic pain in the state of Maine by identifying the prevalence of chronic pain and its relationship with selected demographic and socioeconomic factors in Maine.
Understanding neurobehavioral effects of acute and chronic stress in zebrafish.
Stress (Amsterdam, Netherlands), 2021

Stress is a common cause of neuropsychiatric disorders, evoking multiple behavioral, endocrine and neuro-immune deficits. Animal models have been extensively used to understand the mechanisms of stress-related disorders and to develop novel strategies for their treatment. Complementing rodent and clinical studies, the zebrafish (
The details of structural disconnectivity in psychotic disorder: A family-based study of non-FA diffusion weighted imaging measures.
Brain research, 2017

Diffusion tensor imaging (DTI) studies in psychotic disorder have shown reduced FA, often interpreted as disturbed white matter integrity. The observed 'dysintegrity' may be of multifactorial origin, as changes in FA are thought to reflect a combination of changes in myelination, fiber organization and number of axons. Examining the structural substrate of the diffusion tensor in individuals with (risk for) psychotic disorder may provide better understanding of the underlying structural changes.
Increased phosphorylation of Ets-like transcription factor-1 in neurons of hypoxic preconditioned mice.
Neurochemical research, 2009

Ets-like transcription factor-1 (Elk-1) is a target of mitogen activated protein kinase (MAPK) which has been reported to play a key role in the induction of tolerance to ischemic and hypoxic injury, but little is known about the role of Elk-1 in the development of cerebral hypoxic preconditioning (HPC). In this study, we found that Elk-1 phosphorylation at Ser383 (p-Ser383 Elk-1), not protein expression, increased significantly (P < 0.05) in both hippocampus and frontal cortex of mice after repetitive auto-hypoxia exposures from 1 to 6 times (H1-H6, n = 6 for each group) when compared to that of the normoxic control group (H0, n = 6). The enhanced p-Ser383 Elk-1 was also found in the nuclear extract of H3 mice brain. Similarly, increased p-Ser383 Elk-1 was observed by immunostaining in the hippocampus and frontal cortex of mice from H3 and H6 groups. In addition, we found that the increased p-Ser383 Elk-1 co-localized with a neuron-specific protein, neurogranin, in the brain of H3 mice by using double immunofluorescence labeling. These results suggested that the enhanced neuron-specific phosphorylation of Elk-1 at Ser383 is involved in cerebral HPC of mice.
Validation of an integrated method for determining cognitive ability: Implications for routine assessments and clinical trials.
Cortex; a journal devoted to the study of the nervous system and behavior, 2014

Although accurate diagnosis of deficit of mild intensity is critical, various methods are used to assess, dichotomize and integrate performance, with no validated gold standard. This study described and validated a framework for the analysis of cognitive performance.
The Aging Astrocyte Transcriptome from Multiple Regions of the Mouse Brain.
Cell reports, 2018

Aging brains undergo cognitive decline, associated with decreased neuronal synapse number and function and altered metabolism. Astrocytes regulate neuronal synapse formation and function in development and adulthood, but whether these properties change during aging, contributing to neuronal dysfunction, is unknown. We addressed this by generating aged and adult astrocyte transcriptomes from multiple mouse brain regions. These data provide a comprehensive RNA-seq database of adult and aged astrocyte gene expression, available online as a resource. We identify astrocyte genes altered by aging across brain regions and regionally unique aging changes. Aging astrocytes show minimal alteration of homeostatic and neurotransmission-regulating genes. However, aging astrocytes upregulate genes that eliminate synapses and partially resemble reactive astrocytes. We further identified heterogeneous expression of synapse-regulating genes between astrocytes from different cortical regions. We find that alterations to astrocytes in aging create an environment permissive to synapse elimination and neuronal damage, potentially contributing to aging-associated cognitive decline.
Musicians and the metric structure of words.
Journal of cognitive neuroscience, 2011

The present study aimed to examine the influence of musical expertise on the metric and semantic aspects of speech processing. In two attentional conditions (metric and semantic tasks), musicians listened to short sentences ending in trisyllabic words that were semantically and/or metrically congruous or incongruous. Both ERPs and behavioral data were analyzed and the results were compared to previous nonmusicians' data. Regarding the processing of meter, results showed that musical expertise influenced the automatic detection of the syllable temporal structure (P200 effect), the integration of metric structure and its influence on word comprehension (N400 effect), as well as the reanalysis of metric violations (P600 and late positivities effects). By contrast, results showed that musical expertise did not influence the semantic level of processing. These results are discussed in terms of transfer of training effects from music to speech processing.
Drosophila semaphorin2b is required for the axon guidance of a subset of embryonic neurons.
Developmental dynamics : an official publication of the American Association of Anatomists, 2013

The process of axon guidance is important in establishing functional neural circuits. The differential expression of cell-autonomous axon guidance factors is crucial for allowing axons of different neurons to take unique trajectories in response to spatially and temporally restricted cell non-autonomous axon guidance factors. A key motivation in the field is to provide adequate explanations for axon behavior with respect to the differential expression of these factors.
Bi-allelic Mutations in ARMC2 Lead to Severe Astheno-Teratozoospermia Due to Sperm Flagellum Malformations in Humans and Mice.
American journal of human genetics, 2019

Male infertility is a major health concern. Among its different causes, multiple morphological abnormalities of the flagella (MMAF) induces asthenozoospermia and is one of the most severe forms of qualitative sperm defects. Sperm of affected men display short, coiled, absent, and/or irregular flagella. To date, six genes (DNAH1, CFAP43, CFAP44, CFAP69, FSIP2, and WDR66) have been found to be recurrently associated with MMAF, but more than half of the cases analyzed remain unresolved, suggesting that many yet-uncharacterized gene defects account for this phenotype. Here, whole-exome sequencing (WES) was performed on 168 infertile men who had a typical MMAF phenotype. Five unrelated affected individuals carried a homozygous deleterious mutation in ARMC2, a gene not previously linked to the MMAF phenotype. Using the CRISPR-Cas9 technique, we generated homozygous Armc2 mutant mice, which also presented an MMAF phenotype, thus confirming the involvement of ARMC2 in human MMAF. Immunostaining experiments in AMRC2-mutated individuals and mutant mice evidenced the absence of the axonemal central pair complex (CPC) proteins SPAG6 and SPEF2, whereas the other tested axonemal and peri-axonemal components were present, suggesting that ARMC2 is involved in CPC assembly and/or stability. Overall, we showed that bi-allelic mutations in ARMC2 cause male infertility in humans and mice by inducing a typical MMAF phenotype, indicating that this gene is necessary for sperm flagellum structure and assembly.
The Modulating Role of Self-Referential Stimuli and Processes in the Effect of Stress and Negative Emotion on Inhibition Processes in Borderline Personality Disorder: Proposition of a Model to Integrate the Self-Concept and Inhibition Processes.
Brain sciences, 2019

Impulsivity is an important clinical and diagnostic feature of borderline personality disorder (BPD). Even though it has been reported that BPD individuals' inhibition performance is significantly reduced in the context of negative emotion or stress, this literature shows mixed results, raising questions about the possible role played by other factors. Winter (2016) proposed that negative emotion stimuli can be more disruptive for BPD individuals' attention control performance because they induce higher distractibility self-referential processes. This article aimed to systematically review the literature regarding the effect of stress and negative emotions on three main inhibition processes-prepotent response inhibition, resistance to distractor interference, and resistance to proactive interference-in BPD and to verify the putative modulating role of self-referential stimuli and processes on these inhibition processes. All English and French experimental studies published until August 2018 were searched in PsychINFO and PubMED databases. The following keywords were used: "borderline* AND inhibit* OR interference* OR forget* OR task* AND emotion* OR stress* OR affect*". A total of 1215 articles were included in the study. After full text revision, twenty-six papers were selected for review. The results of this review indicate that when stimuli or procedures involve self-reference stimuli or processes, BPD individuals' performance seems to be more disrupted in all three inhibition processes. A model based on Winter's and Kernberg's models is proposed with the aim of integrating the self-concept with inhibition processes in BPD.
A distinct subtype of dopaminergic interneuron displays inverted structural plasticity at the axon initial segment.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015

The axon initial segment (AIS) is a specialized structure near the start of the axon that is a site of neuronal plasticity. Changes in activity levels in vitro and in vivo can produce structural AIS changes in excitatory cells that have been linked to alterations in excitability, but these effects have never been described in inhibitory interneurons. In the mammalian olfactory bulb (OB), dopaminergic interneurons are particularly plastic, undergoing constitutive turnover throughout life and regulating tyrosine hydroxylase expression in an activity-dependent manner. Here we used dissociated cultures of rat and mouse OB to show that a subset of bulbar dopaminergic neurons possess an AIS and that these AIS-positive cells are morphologically and functionally distinct from their AIS-negative counterparts. Under baseline conditions, OB dopaminergic AISs were short and located distally along the axon but, in response to chronic 24 h depolarization, lengthened and relocated proximally toward the soma. These activity-dependent changes were in the opposite direction to both those we saw in non-GABAergic OB neurons and those reported previously for excitatory cell types. Inverted AIS plasticity in OB dopaminergic cells was bidirectional, involved all major components of the structure, was dependent on the activity of L-type CaV1 calcium channels but not on the activity of the calcium-activated phosphatase calcineurin, and was opposed by the actions of cyclin-dependent kinase 5. Such distinct forms of AIS plasticity in inhibitory interneurons and excitatory projection neurons may allow considerable flexibility when neuronal networks must adapt to perturbations in their ongoing activity.