rudyvdbrink/CitationDatabase huggingface dataset:
Learning to be inflexible: Enhanced attentional biases in Parkinson's disease.
Cortex; a journal devoted to the study of the nervous system and behavior, 2016

Impaired attentional flexibility is considered to be one of the core cognitive deficits in Parkinson's disease (PD). However, the mechanisms that underlie this impairment are contested. Progress in resolving this dispute has also been hindered by the fact that cognitive deficits in PD are heterogeneous; therefore, it is unclear whether attentional impairments are only present in a subgroup of patients. Here, we demonstrate that what differentiates PD patients from age-matched controls is an inability to shift attention away from previously relevant information (perseveration) and an inability to shift attention towards previously irrelevant information (learned irrelevance). In contrast, there was no evidence that PD patients, compared to controls, were impaired in being able to appropriately attend to, or ignore, novel information. Furthermore, when patients were stratified according to their level of executive impairment, the executively impaired group showed a selective deficit in set formation compared to the unimpaired group, a behavioural pattern reminiscent of cortical dopamine depletion. Cumulatively, these results suggest that cognitive inflexibility in PD relates to a specific form of attentional dysfunction, in which learned attentional biases cannot be overcome.
Neuromuscular Adaptations to Short-Term High-Intensity Interval Training in Female Ice-Hockey Players.
Journal of strength and conditioning research, 2019

Kinnunen, J-V, Piitulainen, H, and Piirainen, JM. Neuromuscular adaptations to short-term high-intensity interval training in female ice-hockey players. J Strength Cond Res 33(2): 479-485, 2019-High-intensity interval training (HIIT)-related neuromuscular adaptations, changes in force production, and on-ice performance were investigated in female ice-hockey players during preseason. Fourteen Finnish championship level ice-hockey players (average age 22 ± 3 years) participated in 2½-week HIIT. Both spinal (H-reflex) and supraspinal (V-wave) neuromuscular responses of the soleus muscle were recorded before and after the training period. Static jump (SJ) and countermovement jump heights, plantarflexor maximum voluntary contraction (MVC), and rate of force development (RFD) were measured. In addition, soleus and tibialis anterior muscle activations (electromyography) were measured during MVC and RFD tests. During on-ice training, skating speed and acceleration tests were performed. Subjects significantly improved their plantarflexion MVC force (11.6 ± 11.2%, p < 0.001), RFD (15.2 ± 15.9%, p < 0.01), and SJ (4.8 ± 7.6%, p ≤ 0.05). Voluntary motor drive to the soleus muscle (V-wave amplitude) increased by 16.0 ± 15.4% (p < 0.01), and coactivation of the tibialis anterior muscle during the plantarflexion RFD test was reduced by -18.9 ± 22.2% (p ≤ 0.05). No change was observed in spinal α-motoneuron excitability (H-reflex) during MVC or in on-ice performance. These results indicate that HIIT can be used to improve athletes' capability to produce maximal and explosive forces, likely through enhanced voluntary activation of their muscles and reduced antagonist coactivation. Therefore, HIIT can be recommended in preseason training to improve neuromuscular performance. However, a longer than 2½-week HIIT period is needed to improve on-ice performance in female ice-hockey players.
Renal Safety of Intra-Arterial Treatment after Acute Ischemic Stroke with Multimodal CT Imaging selection.
Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association, 2019

Multimodal computed tomography imaging is used to identify eligible patients for intra-arterial treatment. A concern with this method is the multiple use of iodinated contrast material which presents a possible risk of renal toxicity. We compared the safety of intra-arterial treatment versus intravenous treatment during acute ischemic stroke treatment with a focus on renal safety.
A novel mutation of Twinkle in Perrault syndrome: A not rare diagnosis?
Annals of human genetics, 2020

Perrault syndrome is a rare disorder characterized by ovarian dysgenesis, bilateral sensorineural hearing loss and associated with mutations in six mitochondrial proteins. Additional neurological features were also described. Herein, we report on a 27-year-old woman with Perrault syndrome (PS), moderate ataxia and axonal sensory-motor peripheral neuropathy in whom we identified compound heterozygous mutations in the TWNK gene (p.Val507Ile and the novel p.Phe248Ser variant). Fewer than 30 patients with PS have been reported worldwide. Neurological involvement is more frequently associated with mutations in TWNK and indicates possible genotype-phenotype correlations. TWNK mutations should be searched in patients with sensory ataxia, early onset bilateral sensorineural hearing loss, and ovarian dysfunction in women.
Froggy mouth: a new myofunctional approach to atypical swallowing.
European journal of paediatric dentistry, 2019

Atypical swallowing has a high incidence in adult and child populations. The treatment of the latter is generally achieved by the adoption of orthodontic appliances in conjunction with speech therapy. The aim of this article is to describe the clinical protocol of Froggy Mouth, an innovative myofunctional appliance designed to correct the atypical swallowing.
Temporal changes of oxidative stress markers in Escherichia coli K1-induced experimental meningitis in a neonatal rat model.
Neuroscience letters, 2017

Despite advances in antimicrobial therapy and advanced critical care neonatal bacterial meningitis has a mortality rate of over 10% and induces neurological sequelae in 20-50% of cases. Escherichia coli K1 (E. coli K1) is the most common gram-negative organism causing neonatal meningitis and is the second most common cause behind group B streptococcus. We previously reported that an E. coli K1 experimental meningitis infection in neonatal rats resulted in habituation and aversive memory impairment and a significant increase in cytokine levels in adulthood. In this present study, we investigated the oxidative stress profile including malondialdehyde (MDA) levels, carbonyl protein formation, myeloperoxidase activity (MPO) activity, superoxide dismutase (SOD) activity and catalase (CAT) activity 6, 12, 24, 48, 72 and 96h after E. coli K1 experimental meningitis infection. In addition, sulfhydryl groups, nitrite and nitrate levels and activity of the mitochondrial respiratory chain enzymes were also measured in the frontal cortex and hippocampus of neonatal rats. The results from this study demonstrated a significant increase in MDA, protein carbonyls and MPO activity and a simultaneous decrease in SOD activity in the hippocampus of the neonatal meningitis survivors but the same was not observed in frontal cortex. In addition, we also observed a significant increase in complex IV activity in the hippocampus and frontal cortex of meningitis survivor rats. Thus, the results from this study reaffirmed the possible role of oxidative stress, nitric oxide and its related compounds in the complex pathophysiology of E. coli K1-induced bacterial meningitis.
Hyperexcitability of rat thalamocortical networks after exposure to general anesthesia during brain development.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015

Prevailing literature supports the idea that common general anesthetics (GAs) cause long-term cognitive changes and neurodegeneration in the developing mammalian brain, especially in the thalamus. However, the possible role of GAs in modifying ion channels that control neuronal excitability has not been taken into consideration. Here we show that rats exposed to GAs at postnatal day 7 display a lasting reduction in inhibitory synaptic transmission, an increase in excitatory synaptic transmission, and concomitant increase in the amplitude of T-type calcium currents (T-currents) in neurons of the nucleus reticularis thalami (nRT). Collectively, this plasticity of ionic currents leads to increased action potential firing in vitro and increased strength of pharmacologically induced spike and wave discharges in vivo. Selective blockade of T-currents reversed neuronal hyperexcitability in vitro and in vivo. We conclude that drugs that regulate thalamic excitability may improve the safety of GAs used during early brain development.
Two novel loci, COBL and SLC10A2, for Alzheimer's disease in African Americans.
Alzheimer's & dementia : the journal of the Alzheimer's Association, 2017

African Americans' (AAs) late-onset Alzheimer's disease (LOAD) genetic risk profile is incompletely understood. Including clinical covariates in genetic analyses using informed conditioning might improve study power.
Using our brains to develop better policy.
Risk analysis : an official publication of the Society for Risk Analysis, 2012

Current governmental practices often use a method called weight of evidence (WoE) to integrate and weigh different sources of information in the process of reaching a decision. Recent advances in cognitive neuroscience have identified WoE-like processes in the brain, and we believe that these advances have the potential to improve current decision-making practices. In this article, we describe five specific areas where knowledge emerging from cognitive neuroscience may be applied to the challenges confronting decisionmakers who manage risks: (1) quantifying evidence, (2) comparing the value of different sources of evidence, (3) reaching a decision, (4) illuminating the role of subjectivity, and (5) adapting to new information. We believe that the brain is an appropriate model for structuring decision-making processes because the brain's network is designed for complex, flexible decision making, and because policy decisions that must ultimately depend on human judgment will be best served by methods that complement human abilities. Future discoveries in cognitive neuroscience will likely bring further applications to decision practice.
NPTX2 is a key component in the regulation of anxiety.
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2018

Anxiety disorders significantly impair quality of life. However, limited knowledge of the underlying mechanisms impedes the development of effective therapeutics. Previous studies have suggested that the expression of the Nptx2 gene is associated with anxiety, but the neurobiological processes underlying this association remain unclear. We generated multiple mouse models with knockout or overexpression of Nptx2 in specific brain regions and during different developmental stages to assess anxiety, adult neurogenesis, and glucocorticoid-related gene expression. Our results provide evidence that Nptx2 expression in the adult hippocampus regulates anxiety in mice. Eliminating Nptx2 expression in either the developing mouse brain or in adulthood leads to increased anxiety levels. The increase in anxiety was evident in hippocampus-specific Nptx2 knockout mice, but not in an amygdala specific knockouts. Gene expression analysis revealed increased expression of glucocorticoid receptor target genes in Nptx2 knockout mice after acute stress. Overexpression of Nptx2 in the hippocampus alleviates stress-induced anxious behaviors and reverses the changes in expression of glucocorticoid receptor related genes. In conclusion, we demonstrate that Nptx2 in the hippocampus performs a critical role in modulating anxiety, hippocampal cell proliferation, and glucocorticoid receptor related gene expression. Our results suggest Nptx2 may be a potential target for anxiolytic therapeutics.
Synaptic Inputs to the Mouse Dorsal Vagal Complex and Its Resident Preproglucagon Neurons.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019

Stress responses are coordinated by widespread neural circuits. Homeostatic and psychogenic stressors activate preproglucagon (PPG) neurons in the caudal nucleus of the solitary tract (cNTS) that produce glucagon-like peptide-1; published work in rodents indicates that these neurons play a crucial role in stress responses. While the axonal targets of PPG neurons are well established, their afferent inputs are unknown. Here we use retrograde tracing with cholera toxin subunit b to show that the cNTS in male and female mice receives axonal inputs similar to those reported in rats. Monosynaptic and polysynaptic inputs specific to cNTS PPG neurons were revealed using Cre-conditional pseudorabies and rabies viruses. The most prominent sources of PPG monosynaptic input include the lateral (LH) and paraventricular (PVN) nuclei of the hypothalamus, parasubthalamic nucleus, lateral division of the central amygdala, and Barrington's nucleus (Bar). Additionally, PPG neurons receive monosynaptic vagal sensory input from the nodose ganglia and spinal sensory input from the dorsal horn. Sources of polysynaptic input to cNTS PPG neurons include the hippocampal formation, paraventricular thalamus, and prefrontal cortex. Finally, cNTS-projecting neurons within PVN, LH, and Bar express the activation marker cFOS in mice after restraint stress, identifying them as potential sources of neurogenic stress-induced recruitment of PPG neurons. In summary, cNTS PPG neurons in mice receive widespread monosynaptic and polysynaptic input from brain regions implicated in coordinating behavioral and physiological stress responses, as well as from vagal and spinal sensory neurons. Thus, PPG neurons are optimally positioned to integrate signals of homeostatic and psychogenic stress.
Reduced medial prefrontal-subcortical connectivity in dysphoria: Granger causality analyses of rapid functional magnetic resonance imaging.
Brain connectivity, 2015

A cortico-limbic network consisting of the amygdala, medial prefrontal cortex (mPFC), and ventral striatum (vSTR) has been associated with altered function in emotional disorders. Here we used rapidly sampled functional magnetic resonance imaging and Granger causality analyses to assess the directional connectivity between these brain structures in a sample of healthy and age-matched participants endorsing moderate to severe depressive symptomatology as they viewed a series of natural scene stimuli varying systematically in pleasantness and arousal. Specifically during pleasant scene perception, dysphoric participants showed reduced activity in mPFC and vSTR, relative to healthy participants. In contrast, amygdala activity was enhanced to pleasant as well as unpleasant arousing scenes in both participant groups. Granger causality estimates of influence between mPFC and vSTR were significantly reduced in dysphoric relative to control participants during all picture contents. These findings provide direct evidence that during visual perception of evocative emotional stimuli, reduced reward-related activity in dysphoria is associated with dysfunctional causal connectivity between mPFC, amygdala, and vSTR.
Comprehensive Estimates of Potential Synaptic Connections in Local Circuits of the Rodent Hippocampal Formation by Axonal-Dendritic Overlap.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2021

A quantitative description of the hippocampal formation synaptic architecture is essential for understanding the neural mechanisms of episodic memory. Yet the existing knowledge of connectivity statistics between different neuron types in the rodent hippocampus only captures a mere 5% of this circuitry. We present a systematic pipeline to produce first-approximation estimates for most of the missing information. Leveraging the www.Hippocampome.org knowledge base, we derive local connection parameters between distinct pairs of morphologically identified neuron types based on their axonal-dendritic overlap within every layer and subregion of the hippocampal formation. Specifically, we adapt modern image analysis technology to determine the parcel-specific neurite lengths of every neuron type from representative morphologic reconstructions obtained from either sex. We then compute the average number of synapses per neuron pair using relevant anatomic volumes from the mouse brain atlas and ultrastructurally established interaction distances. Hence, we estimate connection probabilities and number of contacts for >1900 neuron type pairs, increasing the available quantitative assessments more than 11-fold. Connectivity statistics thus remain unknown for only a minority of potential synapses in the hippocampal formation, including those involving long-range (23%) or perisomatic (6%) connections and neuron types without morphologic tracings (7%). The described approach also yields approximate measurements of synaptic distances from the soma along the dendritic and axonal paths, which may affect signal attenuation and delay. Overall, this dataset fills a substantial gap in quantitatively describing hippocampal circuits and provides useful model specifications for biologically realistic neural network simulations, until further direct experimental data become available.
Leptin's effect on taste bud calcium responses and transmitter secretion.
Chemical senses, 2015

Leptin, a peptide hormone released by adipose tissue, acts on the hypothalamus to control cravings and appetite. Leptin also acts to decrease taste responses to sweet substances, though there is little detailed information regarding where leptin acts in the taste transduction cascade. The present study examined the effects of leptin on sweet-evoked responses and neuro transmitter release from isolated taste buds. Our results indicate that leptin moderately decreased sweet-evoked calcium mobilization in isolated mouse taste buds. We also employed Chinese hamster ovary biosensor cells to examine taste transmitter release from isolated taste buds. Leptin reduced ATP and increased serotonin release in response to sweet stimulation. However, leptin has no effect on bitter-evoked transmitter release, further showing that the action of leptin is sweet specific. Our results support those of previous studies, which state that leptin acts on taste tissue via the leptin receptor, most likely on Type II (Receptor) cells, but also possibly on Type III (Presynaptic) cells.
Diabetic aggravation of stroke and animal models.
Experimental neurology, 2017

Cerebral ischemia in diabetics results in severe brain damage. Different animal models of cerebral ischemia have been used to study the aggravation of ischemic brain damage in the diabetic condition. Since different disease conditions such as diabetes differently affect outcome following cerebral ischemia, the Stroke Therapy Academic Industry Roundtable (STAIR) guidelines recommends use of diseased animals for evaluating neuroprotective therapies targeted to reduce cerebral ischemic damage. The goal of this review is to discuss the technicalities and pros/cons of various animal models of cerebral ischemia currently being employed to study diabetes-related ischemic brain damage. The rational use of such animal systems in studying the disease condition may better help evaluate novel therapeutic approaches for diabetes related exacerbation of ischemic brain damage.
Molecular specializations of deep cortical layer analogs in songbirds.
Scientific reports, 2020

How the evolution of complex behavioral traits is associated with the emergence of novel brain pathways is largely unknown. Songbirds, like humans, learn vocalizations via tutor imitation and possess a specialized brain circuitry to support this behavior. In a comprehensive in situ hybridization effort, we show that the zebra finch vocal robust nucleus of the arcopallium (RA) shares numerous markers (e.g. SNCA, PVALB) with the adjacent dorsal intermediate arcopallium (AId), an avian analog of mammalian deep cortical layers with involvement in motor function. We also identify markers truly unique to RA and thus likely linked to modulation of vocal motor function (e.g. KCNC1, GABRE), including a subset of the known shared markers between RA and human laryngeal motor cortex (e.g. SLIT1, RTN4R, LINGO1, PLXNC1). The data provide novel insights into molecular features unique to vocal learning circuits, and lend support for the motor theory for vocal learning origin.
Olig1 Acetylation and Nuclear Export Mediate Oligodendrocyte Development.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015

The oligodendrocyte transcription factor Olig1 is critical for both oligodendrocyte development and remyelination in mice. Nuclear to cytoplasmic translocation of Olig1 protein occurs during brain development and in multiple sclerosis, but the detailed molecular mechanism of this translocation remains elusive. Here, we report that Olig1 acetylation and deacetylation drive its active translocation between the nucleus and the cytoplasm in both mouse and rat oligodendrocytes. We identified three functional nuclear export sequences (NES) localized in the basic helix-loop-helix domain and one specific acetylation site at Lys 150 (human Olig1) in NES1. Olig1 acetylation and deacetylation are regulated by the acetyltransferase CREB-binding protein and the histone deacetylases HDAC1, HDAC3, and HDAC10. Acetylation of Olig1 decreased its chromatin association, increased its interaction with inhibitor of DNA binding 2 and facilitated its retention in the cytoplasm of mature oligodendrocytes. These studies establish that acetylation of Olig1 regulates its chromatin dissociation and subsequent translocation to the cytoplasm and is required for its function in oligodendrocyte maturation.
Attentive scanning behavior drives one-trial potentiation of hippocampal place fields.
Nature neuroscience, 2014

The hippocampus is thought to have a critical role in episodic memory by incorporating the sensory input of an experience onto a spatial framework embodied by place cells. Although the formation and stability of place fields requires exploration, the interaction between discrete exploratory behaviors and the specific, immediate and persistent modifications of neural representations required by episodic memory has not been established. We recorded place cells in rats and found that increased neural activity during exploratory head-scanning behaviors predicted the formation and potentiation of place fields on the next pass through that location, regardless of environmental familiarity and across multiple testing days. These results strongly suggest that, during the attentive behaviors that punctuate exploration, place cell activity mediates the one-trial encoding of ongoing experiences necessary for episodic memory.
Silent reading: does the brain 'hear' both speech and voices?
Current biology : CB, 2013

Silent reading is a private experience that plays out in our imagination. Although we might primarily read for content, recent human brain neuroimaging and neuronal recording work is revealing the inner processes at play. Some of these involve experiencing voices.