rudyvdbrink/CitationDatabase huggingface dataset:
Transglutaminase inhibition protects against oxidative stress-induced neuronal death downstream of pathological ERK activation.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012

Molecular deletion of transglutaminase 2 (TG2) has been shown to improve function and survival in a host of neurological conditions including stroke, Huntington's disease, and Parkinson's disease. However, unifying schemes by which these cross-linking or polyaminating enzymes participate broadly in neuronal death have yet to be presented. Unexpectedly, we found that in addition to TG2, TG1 gene expression level is significantly induced following stroke in vivo or due to oxidative stress in vitro. Forced expression of TG1 or TG2 proteins is sufficient to induce neuronal death in Rattus norvegicus cortical neurons in vitro. Accordingly, molecular deletion of TG2 alone is insufficient to protect Mus musculus neurons from oxidative death. By contrast, structurally diverse inhibitors used at concentrations that inhibit TG1 and TG2 simultaneously are neuroprotective. These small molecules inhibit increases in neuronal transamidating activity induced by oxidative stress; they also protect neurons downstream of pathological ERK activation when added well after the onset of the death stimulus. Together, these studies suggest that multiple TG isoforms, not only TG2, participate in oxidative stress-induced cell death signaling; and that isoform nonselective inhibitors of TG will be most efficacious in combating oxidative death in neurological disorders.
Rectus Pulley Displacements without Abnormal Oblique Contractility Explain Strabismus in Superior Oblique Palsy.
Ophthalmology, 2016

Using high-resolution magnetic resonance imaging (MRI), we investigated whether rectus pulleys are significantly displaced in superior oblique (SO) palsy and whether displacements account for strabismus patterns.
Maternal care differentially affects neuronal excitability and synaptic plasticity in the dorsal and ventral hippocampus.
Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2015

Variations in early life maternal care modulate hippocampal development to program distinct emotional-cognitive phenotypes that persist into adulthood. Adult rat offspring that received low compared with high levels of maternal licking and grooming (low LG offspring) in early postnatal life show reduced long term potentiation (LTP) and impaired hippocampal-dependent memory, suggesting a 'detrimental' maternal effect on neural development. However, these studies focused uniquely on the dorsal hippocampus. Emerging evidence suggests a distinct role of the ventral hippocampus in mediating aggression, anxiety, and fear-memory formation, which are enhanced in low LG offspring. We report that variations in maternal care in the rat associate with opposing effects on hippocampal function in the dorsal and ventral hippocampus. Reduced pup licking associated with suppressed LTP formation in the dorsal hippocampus, but enhanced ventral hippocampal LTP. Ventral hippocampal neurons in low LG offspring fired action potentials at lower threshold voltages that were of larger amplitude and faster rise rate in comparison with those in high LG offspring. Furthermore, recordings of excitatory postsynaptic potential-to-spike coupling (E-S coupling) revealed an increase in excitability of ventral hippocampal CA1 neurons in low LG offspring. These effects do not associate with changes in miniature excitatory postsynaptic currents or paired-pulse facilitation, suggesting a specific effect of maternal care on intrinsic excitability. These findings suggest region-specific influences of maternal care in shaping neural development and synaptic plasticity.
A novel language-neutral Visual Cognitive Assessment Test (VCAT): validation in four Southeast Asian countries.
Alzheimer's research & therapy, 2018

Cognitive screeners are imperative for early diagnosis of dementia. The Visual Cognitive Assessment Test (VCAT) is a language-neutral, visual-based test which has proven useful for a multilingual population in a single-center study. However, its performance utility is unknown in a wider and more diverse Southeast Asian cohort.
Compact and Low-Power Neural Spike Compression Using Undercomplete Autoencoders.
IEEE transactions on neural systems and rehabilitation engineering : a publication of the IEEE Engineering in Medicine and Biology Society, 2019

Implantable microsystems that collect and transmit neural data are becoming very useful entities in the field of neuroscience. Limited by high data rates, on-chip compression is often required to transmit the recorded data without causing power dissipation at levels that would damage sensitive brain tissue. This paper presents a data compression system designed for brain-computer interfaces (BCIs) based on undercomplete autoencoders. To the best of our knowledge, the proposed system is the first to achieve an average spike reconstruction quality of 14-dB signal-to-noise-and-distortion ratio (SNDR) at a 32× compression ratio (CR), 18-dB SNDR at a 16× CR, 22-dB SNDR at an 8× CR, and 35-dB SNDR at a 4× CR of neural spikes. The spike detection and autoencoder-based compression modules are designed and implemented in a standard 45-nm CMOS process. The post-synthesis simulation results report that the compression module consumes between 1.4 and 222.5 [Formula: see text] of power per channel and takes between 0.018 and 0.082mm
Stereovision and augmented reality for closed-loop control of grasping in hand prostheses.
Journal of neural engineering, 2014

Technologically advanced assistive devices are nowadays available to restore grasping, but effective and effortless control integrating both feed-forward (commands) and feedback (sensory information) is still missing. The goal of this work was to develop a user friendly interface for the semi-automatic and closed-loop control of grasping and to test its feasibility.
Impact of acute bisphenol-A exposure upon intrauterine implantation of fertilized ova and urinary levels of progesterone and 17beta-estradiol.
Reproductive toxicology (Elmsford, N.Y.), 2008

Bisphenol-A (BPA), a monomer used in production of polycarbonate plastics and epoxy resins, has established estrogenic properties. We assessed the impact of acute and repeated subcutaneous BPA administration upon intrauterine implantation of fertilized ova and urinary levels of 17beta-estradiol and progesterone in inseminated female mice. In Experiment 1, females received varied doses of BPA on days 1-4 of gestation. Daily doses of 6.75 and 10.125mg/animal significantly reduced the number of implantation sites. Urinary progesterone was significantly reduced by the higher dose, but no other dose had an effect on progesterone levels and no dose altered estradiol levels. In Experiment 2, inseminated females received a single dose of BPA on days 0, 1, or 2 of gestation. A single dose of 10.125mg reduced the number of implantation sites when given on day 0 or day 1, and 6.75mg on day 1 also produced fewer implantation sites, but there was no such effect of any dose when administered on day 2. These data show a lower threshold for BPA-induced pregnancy disruption than previously reported, also indicating effects of just one exposure. They confirm that this disruption is due to the actions of BPA upon implantation sites, and show that higher doses can influence systemic progesterone levels.
Assessing the relationship between near-infrared spectroscopy-derived regional cerebral oxygenation and neurological dysfunction in critically ill adults: a prospective observational multicentre protocol, on behalf of the Canadian Critical Care Trials Group.
BMJ open, 2019

Survivors of critical illness frequently exhibit acute and chronic neurological complications. The underlying aetiology of this dysfunction remains unknown but may be associated with cerebral ischaemia. This study will use near-infrared spectroscopy to non-invasively quantify regional cerebral oxygenation (rSO
DeltaFosB is increased in the nucleus accumbens by amphetamine but not social housing or isolation in the prairie vole.
Neuroscience, 2012

The nucleus accumbens is a key region that mediates aspects of immediate and long-term adaptations to various stimuli. For example, both repeated amphetamine and pair-bonding increase dopamine D1 receptor binding in the nucleus accumbens of the monogamous prairie vole (Microtus ochrogaster). This upregulation has significant and stimulus-dependent behavioral consequences. A promising candidate for these and other adaptations is the transcription factor ΔfosB. ΔfosB is a highly stable protein that persists in the brain over long periods of time, leading to increasing and accumulating levels with repeated or continuous exposure to specific stimuli. Within the nucleus accumbens, ΔfosB is specifically increased in medium spiny neurons containing D1 receptors. To explore whether ΔfosB is altered by drug and social experience in prairie voles, we performed three separate experiments. In the first experiment, animals were treated with repeated injections of amphetamine and then brain tissue was analyzed for ΔfosB expression. As expected, 4 days of amphetamine treatment increased ΔfosB in the nucleus accumbens, consistent with previous findings in other laboratory species. In the second experiment, animals were housed for 10 days with one of three social partners: a familiar same-sex sibling, an unfamiliar same-sex partner, or an unfamiliar opposite-sex partner. Here, we predicted that 10 days of housing with an opposite-sex partner would act as a "social reward," leading to upregulation of ΔfosB expression in the nucleus accumbens. In a third experiment, we also investigated whether 10 days of social isolation would result in altered ΔfosB activity. We hypothesized that isolation would lead to decreased levels of nucleus accumbens ΔfosB, as seen in other studies. However, neither opposite-sex cohabitation nor social isolation affected ΔfosB expression in the nucleus accumbens. These findings suggest that social stimuli, in contrast to drugs of abuse, are not mediators of ΔfosB in this region in prairie voles.
Testosterone reduces functional connectivity during the 'Reading the Mind in the Eyes' Test.
Psychoneuroendocrinology, 2016

Women on average outperform men in cognitive-empathic abilities, such as the capacity to infer motives from the bodily cues of others, which is vital for effective social interaction. The steroid hormone testosterone is thought to play a role in this sexual dimorphism. Strikingly, a previous study shows that a single administration of testosterone in women impairs performance on the 'Reading the Mind in Eyes' Test (RMET), a task in which emotions have to be inferred from the eye-region of a face. This effect was mediated by the 2D:4D ratio, the ratio between the length of the index and ring finger, a proxy for fetal testosterone. Research in typical individuals, in individuals with autism spectrum conditions (ASC), and in individuals with brain lesions has established that performance on the RMET depends on the left inferior frontal gyrus (IFG). Using functional magnetic resonance imaging (fMRI), we found that a single administration of testosterone in 16 young women significantly altered connectivity of the left IFG with the anterior cingulate cortex (ACC) and the supplementary motor area (SMA) during RMET performance, independent of 2D:4D ratio. This IFG-ACC-SMA network underlies the integration and selection of sensory information, and for action preparation during cognitive empathic behavior. Our findings thus reveal a neural mechanism by which testosterone can impair emotion-recognition ability, and may link to the symptomatology of ASC, in which the same neural network is implicated.
Early spatial attentional modulation of inputs to the fovea.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010

Attending to a specific spatial location modulates responsivity of neurons with receptive fields processing that part of the environment. A major outstanding question is whether attentional modulation operates differently for the foveal (central) representation of the visual field than it does for the periphery. Indeed, recent animal electrophysiological recordings suggest that attention differentially affects spatial integration for central and peripheral receptive fields in primary visual cortex. In human electroencephalographic recordings, spatial attention to peripheral locations robustly modulates activity in early visual regions, but it has been claimed that this mechanism does not operate in foveal vision. Here, however, we show clear early attentional modulation of foveal stimulation with the same timing and cortical sources as seen for peripheral stimuli, demonstrating that attentional gain control operates similarly across the entire field of view. These results imply that covertly attending away from the center of gaze, which is a common paradigm in behavioral and electrophysiological studies of attention, results in a precisely timed push-pull mechanism. While the amplitude of the initial response to stimulation at attended peripheral locations is significantly increased beginning at 80 ms, the amplitude of the response to foveal stimulation begins to be attenuated.
Glutamate-based depression GBD.
Medical hypotheses, 2012

We describe a new term: glutamate-based depression (GBD). GBD is defined as a chronic depressive illness associated with environmental stress and diseases associated with altered glutamate neurotransmission. We hypothesize that glutamate-induced over-activation of extrasynaptic NMDA receptors in the subgenual cingulate area called Brodmann's 25 plays an important role in the etiology of depression and may be responsible for the high incidence of co-morbid depression associated in diseases with glutamate etiology. While depression is a syndrome with multiple possible etiologies, we propose that a disruption in glutamatergic neurotransmission may underline a substantial proportion of clinically observed depression. The high rates of depressive symptoms associated with various disorders in which altered glutamatergic functions have been identified, may suggest a common pathophysiological mechanism is underlying the diverse clinical presentations.
Hyperacute unilateral contrast-induced parotiditis during cerebral angiography.
Radiology case reports, 2018

An uncommon complication of iodinated contrast administration is the development of bilateral sialadenitis. We report a unique case of hyperacute unilateral parotiditis during diagnostic cerebral angiography of the external carotid artery, which mimicked possible iatrogenic vascular event associated with cerebral endovascular procedures. Discussion includes the differential diagnosis, diagnostic studies, and treatments for this unusual condition.
State-Dependent Cortical Unit Activity Reflects Dynamic Brain State Transitions in Anesthesia.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2020

Understanding the effects of anesthesia on cortical neuronal spiking and information transfer could help illuminate the neuronal basis of the conscious state. Recent investigations suggest that the brain state identified by local field potential spectrum is not stationary but changes spontaneously at a fixed level of anesthetic concentration. How cortical unit activity changes with dynamically transitioning brain states under anesthesia is unclear. Extracellular unit activity was measured with 64-channel silicon microelectrode arrays in cortical layers 5/6 of the primary visual cortex of chronically instrumented, freely moving male rats (
Statin Use and Risk of Cognitive Decline in the ADNI Cohort.
The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry, 2020

To investigate associations between statin use and cognitive change, as well as diagnostic conversion, in individuals with cognitively normal (CN) status, mild cognitive impairment (MCI), and dementia due to Alzheimer disease (AD-dementia).
Neuroanatomy and physiology of colorectal function and defaecation: from basic science to human clinical studies.
Neurogastroenterology and motility, 2009

Colorectal physiology is complex and involves programmed, coordinated interaction between muscular and neuronal elements. Whilst a detailed understanding remains elusive, novel information has emerged from recent basic science and human clinical studies concerning normal sensorimotor mechanisms and the organization and function of the key elements involved in the control of motility. This chapter summarizes these observations to provide a contemporary review of the neuroanatomy and physiology of colorectal function and defaecation.
Do astrocytes really exocytose neurotransmitters?
Nature reviews. Neuroscience, 2010

In the past 20 years, an extra layer of information processing, in addition to that provided by neurons, has been proposed for the CNS. Neuronally evoked increases of the intracellular calcium concentration in astrocytes have been suggested to trigger exocytotic release of the 'gliotransmitters' glutamate, ATP and D-serine. These are proposed to modulate neuronal excitability and transmitter release, and to have a role in diseases as diverse as stroke, epilepsy, schizophrenia, Alzheimer's disease and HIV infection. However, there is intense controversy about whether astrocytes can exocytose transmitters in vivo. Resolving this issue would considerably advance our understanding of brain function.
A new central post-stroke pain rat model: autologous blood injected thalamic hemorrhage involved increased expression of P2X4 receptor.
Neuroscience letters, 2018

Stroke is the leading cause of disability and death in the world. Central post-stroke pain (CPSP), a central neuropathic pain syndrome occurring after cerebral stroke, is a serious problem. But on account of the lack of reliable animal models, the mechanisms underlying CPSP remains poorly understood. To better understand of the pathophysiological basis of CPSP, we developed and characterized a new rat model of CPSP. This model is based on a hemorrhagic stroke lesion with intra-thalamic autologous blood (ITAB) injection in the ventral posterolateral nucleus of the thalamus. Behavioral analysis demonstrated that the animals displayed a significant decrease in mechanical allodynia threshold. We found a signiﬁcant increase in P2 × 4 receptor expression in microglia in thalamic peri-lesion tissues post-hemorrhage. The mechanical allodynia in rats with CPSP were reversed by blocking P2 × 4 receptors. A significant alleviation of mechanical allodynia was achieved following the administration of adrenergic antidepressants and antiepileptics. Meanwhile, we found a signiﬁcant decrease in P2 × 4 receptor expression after treatment with these drugs. Taken together, our results suggest that targeting P2 × 4 receptor may be effective in the treatment of CPSP.
Aspiration of parafalcine empyemas with flexible scope.
Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery, 2016

Subdural empyemas are considered neurosurgical emergencies, and the parafalcine location is particularly insidious. We revised the experience of general surgeons who are used to manage chronic pleural purulent collections with video-assisted thoracoscopy.
Projections from the rat pedunculopontine and laterodorsal tegmental nuclei to the anterior thalamus and ventral tegmental area arise from largely separate populations of neurons.
Brain structure & function, 2011

Cholinergic and non-cholinergic neurons in the brainstem pedunculopontine (PPT) and laterodorsal tegmental (LDT) nuclei innervate diverse forebrain structures. The cholinergic neurons within these regions send heavy projections to thalamic nuclei and provide modulatory input as well to midbrain dopamine cells in the ventral tegmental area (VTA). Cholinergic PPT/LDT neurons are known to send collateralized projections to thalamic and non-thalamic targets, and previous studies have shown that many of the afferents to the VTA arise from neurons that also project to midline and intralaminar thalamic nuclei. However, whether cholinergic projections to the VTA and anterior thalamus (AT) are similarly collateralized is unknown. Ultrastructural work from our laboratory has demonstrated that cholinergic axon varicosities in these regions differ both morphologically and with respect to the expression and localization of the high-affinity choline transporter. We therefore hypothesized that the cholinergic innervation to these regions is provided by separate sets of PPT/LDT neurons. Dual retrograde tract-tracing from the AT and VTA indicated that only a small percentage of the total afferent population to either region showed evidence of providing collateralized input to the other target. Cholinergic and non-cholinergic cells displayed a similarly low percentage of collateralization. These results are contrasted to a control case in which retrograde labeling from the midline paratenial thalamic nucleus and the VTA resulted in higher percentages of cholinergic and non-cholinergic dual-tracer labeled cells. Our results indicate that functionally distinct limbic target regions receive primarily segregated signaling from PPT/LDT neurons.
Nicotine potentiation of excitatory inputs to ventral tegmental area dopamine neurons.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011

Drug-induced changes in synaptic strength are hypothesized to contribute to appetitive behavior and addiction. Nicotine, the major addictive substance in tobacco, activates nicotinic receptors (nAChRs) to initiate a series of adaptive changes at the cellular and circuit levels in brain, particularly the ventral tegmental area (VTA). Our laboratory previously reported that nicotine facilitates induction of long-term potentiation (LTP) in VTA dopamine (DA) neurons by increasing glutamate release via activation of α7 nAChRs on the glutamate terminals, suggesting a critical presynaptic contribution of nicotine in LTP induction. In the present study, we used an in vitro exposure paradigm to study the effect of nicotine on excitatory synaptic strength. Brief exposure of nicotine to brain slices from drug-naive adult rats followed by a period of recovery resulted in an NMDA receptor (NMDAR)-dependent increase of AMPA receptor/NMDAR ratio in VTA DA neurons, which is consistent with the induction of LTP. These effects are similar to that induced by a single in vivo nicotine injection intraperitoneally. The induction of synaptic potentiation required excitation of DA neurons mediated by somatodendritic α4β2 nAChRs, as well as enhancement of NMDAR function via D(5) dopamine receptors, also on DA neurons. Nicotine-induced increase of presynaptic glutamate release also contributed to the induction of synaptic plasticity, likely through increased activation of NMDAR. These results identified important receptor systems involved in nicotine-induced long-term changes in excitatory synaptic input to VTA DA neurons. The data also revealed remarkable similarity in the mechanisms underlying synaptic plasticity induced by nicotine and cocaine in the VTA.