Neuronal correlates of impaired habituation in response to repeated trigemino-nociceptive but not to olfactory input in migraineurs: An fMRI study

Cephalalgia ◽  
2012 ◽  
Vol 33 (4) ◽  
pp. 256-265 ◽  
Author(s):  
A Stankewitz ◽  
E Schulz ◽  
A May
Keyword(s):  
Olfactory System ◽  
Time Course ◽  
Brain Activity ◽  
Sensory System ◽  
Blood Oxygen Level Dependent ◽  
Control Group ◽  
Specific Response ◽  
Similar Time ◽  
Pain Ratings ◽  
Olfactory Stimuli

Introduction: Using functional magnetic resonance imaging (fMRI), we aimed to explore the habituation behaviour to trigemino-nociceptive as well as olfactory stimuli in migraine patients. We exclusively focussed on intrasessional behavioural rating patterns and the related blood oxygen level dependent (BOLD) signal changes. Findings: We observed that groups significantly differ in the time course of pain intensity ratings during the stimulation session: whereas interictal migraineurs sensitized (increasing pain ratings), control subjects habituated (decreasing pain ratings). Pain ratings of ictal patients remained unchanged. This behaviour is accompanied by a similar time course of neuronal activity in the bilateral anterior insula, in the middle cingulate cortex and in the thalamus. In these areas, the brain activity increased in migraineurs but decreased in the control group during the session. In contrast to these findings, the rating patterns for the olfactory stimuli (rose odour) did not differ between patients and controls and a gradual decrease of perceived stimulus intensity was found in all three groups. This stimulus specific response may occur because the olfactory system is the only sensory system not passing the thalamus. Conclusion: Our data suggest that impaired habituation in functional brain systems in migraine is fundamental only to specific modalities including the trigemino-nociceptive, but, at least, excluding the olfactory system. Our findings further suggest that there is no single neuronal modulator responsible for the altered rating pattern in migraineurs.

Postnatal growth rate and gonadal development in circadian tau mutant hamsters reared in constant dim red light

Reproduction ◽  
2000 ◽  
pp. 327-330 ◽  
Author(s):  
RJ Lucas ◽  
JA Stirland ◽  
YN Mohammad ◽  
AS Loudon
Keyword(s):  
Time Course ◽  
Red Light ◽  
Somatic Growth ◽  
Postnatal Growth ◽  
Gonadal Development ◽  
Testicular Development ◽  
Wild Type ◽  
Similar Time ◽  
Syrian Hamsters ◽  
Body Weights

The role of the circadian clock in the reproductive development of Syrian hamsters (Mesocricetus auratus was examined in wild type and circadian tau mutant hamsters reared from birth to 26 weeks of age under constant dim red light. Testis diameter and body weights were determined at weekly intervals in male hamsters from 4 weeks of age. In both genotypes, testicular development, subsequent regression and recrudescence exhibited a similar time course. The age at which animals displayed reproductive photosensitivity, as exhibited by testicular regression, was unrelated to circadian genotype (mean +/- SEM: 54 +/- 3 days for wild type and 59 +/- 5 days for tau mutants). In contrast, our studies revealed a significant impact of the mutation on somatic growth, such that tau mutants weighed 18% less than wild types at the end of the experiment. Our study reveals that the juvenile onset of reproductive photoperiodism in Syrian hamsters is not timed by the circadian system.

scholarly journals Neurofilament Proteolysis after Focal Ischemia; When Do Cells Die after Experimental Stroke?

1999 ◽  
Vol 19 (6) ◽  
pp. 652-660 ◽  
Author(s):  
Jaroslaw Aronowski ◽  
Ki-Hyun Cho ◽  
Roger Strong ◽  
James C. Grotta
Keyword(s):  
Time Course ◽  
Infarct Volume ◽  
Focal Ischemia ◽  
Cellular Damage ◽  
Experimental Stroke ◽  
Infarct Core ◽  
Similar Time ◽  
The Core ◽  
Tetrazolium Staining ◽  
Previous Demonstration

To determine the occurrence and time-course of presumably irreversible subcellular damage after moderate focal ischemia, rats were subjected to 1, 3, 6, 9, or 24 hours of permanent unilateral middle cerebral and common carotid occlusion or 3 hours of reversible occlusion followed by 3, 6, or 21 hours of reperfusion. The topography and the extent of damage were analyzed with tetrazolium staining and immunoblot using an antibody capable of detecting breakdown of neurofilament. Neurofilament proteolysis began after 3 hours in the infarct core but was still incomplete in penumbral regions up to 9 hours. Similarly, tetrazolium-staining abnormalities were observed in the core of 50% of animals after 3 hours of ischemia. At 6 hours of permanent ischemia, infarct volume was maximal, and further prolongation of occlusion to 9 or 24 hours did not increase abnormal tetrazolium staining. In contrast to permanent ischemia and in agreement with the authors' previous demonstration of “reperfusion injury” in this model, prolongation of reperfusion from 3 hours to 6 and 21 hours after 3 hours of reversible occlusion gradually augmented infarct volume by 203% and 324%, respectively. Neurofilament proteolysis initiated approximately 3 hours after ischemia was quantitatively greatest in the core and extended during reperfusion to incorporate penumbra with a similar time course to that of tetrazolium abnormalities. These data demonstrate that, at least as measured by neurofilament breakdown and mitochondrial failure, extensive cellular damage is not present in penumbral regions for up to 9 hours, suggesting the potential for rescuing these regions by appropriate and timely neuroprotective strategies.

scholarly journals On the Role of Bilateral Brain Hypofunction and Abnormal Lateralization of Cortical Information Flow as Neural Underpinnings of Conventional Metaphor Processing Impairment in Schizophrenia: An fMRI and EEG Study

2021 ◽  
Author(s):  
Przemysław Adamczyk ◽  
Martin Jáni ◽  
Tomasz S. Ligeza ◽  
Olga Płonka ◽  
Piotr Błądziński ◽  
...  
Keyword(s):  
Information Flow ◽  
Language Processing ◽  
Time Course ◽  
Figurative Language ◽  
Neural Circuits ◽  
Effective Connectivity ◽  
Brain Regions ◽  
Blood Oxygenation ◽  
Control Group ◽  
Metaphor Processing

AbstractFigurative language processing (e.g. metaphors) is commonly impaired in schizophrenia. In the present study, we investigated the neural activity and propagation of information within neural circuits related to the figurative speech, as a neural substrate of impaired conventional metaphor processing in schizophrenia. The study included 30 schizophrenia outpatients and 30 healthy controls, all of whom were assessed with a functional Magnetic Resonance Imaging (fMRI) and electroencephalography (EEG) punchline-based metaphor comprehension task including literal (neutral), figurative (metaphorical) and nonsense (absurd) endings. The blood oxygenation level-dependent signal was recorded with 3T MRI scanner and direction and strength of cortical information flow in the time course of task processing was estimated with a 64-channel EEG input for directed transfer function. The presented results revealed that the behavioral manifestation of impaired figurative language in schizophrenia is related to the hypofunction in the bilateral fronto-temporo-parietal brain regions (fMRI) and various differences in effective connectivity in the fronto-temporo-parietal circuit (EEG). Schizophrenia outpatients showed an abnormal pattern of connectivity during metaphor processing which was related to bilateral (but more pronounced at the left hemisphere) hypoactivation of the brain. Moreover, we found reversed lateralization patterns, i.e. a rightward-shifted pattern during metaphor processing in schizophrenia compared to the control group. In conclusion, the presented findings revealed that the impairment of the conventional metaphor processing in schizophrenia is related to the bilateral brain hypofunction, which supports the evidence on reversed lateralization of the language neural network and the existence of compensatory recruitment of alternative neural circuits in schizophrenia.

scholarly journals TGF-β1 increases permeability of ciliated airway epithelia via redistribution of claudin 3 from tight junction into cell nuclei

2021 ◽  
Author(s):  
Carolin Schilpp ◽  
Robin Lochbaum ◽  
Peter Braubach ◽  
Danny Jonigk ◽  
Manfred Frick ◽  
...  
Keyword(s):  
Time Course ◽  
Atopic Asthma ◽  
Ciliated Cells ◽  
Cell Nuclei ◽  
Tissue Remodelling ◽  
Similar Time ◽  
Airway Epithelia ◽  
Epithelial Integrity ◽  
Motile Cilia ◽  
Tgf Β1

AbstractTGF-β1 is a major mediator of airway tissue remodelling during atopic asthma and affects tight junctions (TJs) of airway epithelia. However, its impact on TJs of ciliated epithelia is sparsely investigated. Herein we elaborated effects of TGF-β1 on TJs of primary human bronchial epithelial cells. We demonstrate that TGF-β1 activates TGF-β1 receptors TGFBR1 and TGFBR2 resulting in ALK5-mediated phosphorylation of SMAD2. We observed that TGFBR1 and -R2 localize specifically on motile cilia. TGF-β1 activated accumulation of phosphorylated SMAD2 (pSMAD2-C) at centrioles of motile cilia and at cell nuclei. This triggered an increase in paracellular permeability via cellular redistribution of claudin 3 (CLDN3) from TJs into cell nuclei followed by disruption of epithelial integrity and formation of epithelial lesions. Only ciliated cells express TGF-β1 receptors; however, nuclear accumulations of pSMAD2-C and CLDN3 redistribution were observed with similar time course in ciliated and non-ciliated cells. In summary, we demonstrate a role of motile cilia in TGF-β1 sensing and showed that TGF-β1 disturbs TJ permeability of conductive airway epithelia by redistributing CLDN3 from TJs into cell nuclei. We conclude that the observed effects contribute to loss of epithelial integrity during atopic asthma.

scholarly journals Effect of Resonant Frequency Vibration on Delayed Onset Muscle Soreness and Resulting Stiffness as Measured by Shear-Wave Elastography

2021 ◽  
Vol 18 (15) ◽  
pp. 7853
Author(s):  
Garrett C. Jones ◽  
Jonathan D. Blotter ◽  
Cameron D. Smallwood ◽  
Dennis L. Eggett ◽  
Darryl J. Cochrane ◽  
...  
Keyword(s):  
Resonant Frequency ◽  
Shear Wave ◽  
Time Course ◽  
Biceps Brachii ◽  
Shear Wave Elastography ◽  
Upper Body ◽  
Maximum Voluntary Isometric Contraction ◽  
Post Exercise ◽  
Significant Difference ◽  
Pain Ratings

This study utilized resonant frequency vibration to the upper body to determine changes in pain, stiffness and isometric strength of the biceps brachii after eccentric damage. Thirty-one participants without recent resistance training were randomized into three groups: a Control (C) group and two eccentric exercise groups (No vibration (NV) and Vibration (V)). After muscle damage, participants in the V group received upper body vibration (UBV) therapy for 5 min on days 1–4. All participants completed a visual analog scale (VAS), maximum voluntary isometric contraction (MVIC), and shear wave elastography (SWE) of the bicep at baseline (pre-exercise), 24 h, 48 h, and 1-week post exercise. There was a significant difference between V and NV at 24 h for VAS (p = 0.0051), at 24 h and 1-week for MVIC (p = 0.0017 and p = 0.0016, respectively). There was a significant decrease in SWE for the V group from 24–48 h (p = 0.0003), while there was no significant change in the NV group (p = 0.9341). The use of UBV resonant vibration decreased MVIC decrement and reduced VAS pain ratings at 24 h post eccentric damage. SWE was strongly negatively correlated with MVIC and may function as a predictor of intrinsic muscle state in the time course of recovery of the biceps brachii.

scholarly journals Clinical Value and Time Course of Pericoronary Fat Inflammation in Patients with Angiographically Nonobstructive Coronaries: A Preliminary Report

2021 ◽  
Vol 10 (8) ◽  
pp. 1786
Author(s):  
Valeria Pergola ◽  
Marco Previtero ◽  
Annagrazia Cecere ◽  
Vittorio Storer ◽  
Teresa Castiello ◽  
...  
Keyword(s):  
Cardiac Troponin ◽  
Preliminary Report ◽  
Time Course ◽  
Coronary Artery Stenosis ◽  
High Sensitivity ◽  
Control Group ◽  
Clinical Value ◽  
Coronary Ct ◽  
Electrocardiographic Changes ◽  
Acute Event

The introduction of high-sensitivity cardiac troponin allowed identifying a proportion of subjects with chest pain and electrocardiographic changes suggestive of myocardial infarction showing <50% coronary artery stenosis. PFAI is a coronary CT marker proved to predict outcome in ischemic heart disease. Based on CMR findings, patients were divided into myocarditis (n = 15), MINOCA (n = 14) and TTS (n = 9) groups. The aim was to estimate the value of pFAI in these groups compared to 12 controls. To evaluate the coronary inflammation “time course,” 20 patients underwent CMR and coronary CT scan within 8 days from the onset, the others within 60 days. There were higher values of pFAI in myocarditis (−86.45 HU), MINOCA (−84.63 HU) and TTS (−84.79 HU) compared to controls (−96.02 HU; p = 0.0077). Among patients who underwent CT within 8 days from onset, the MINOCA had a significantly higher pFAI value (−76.91 HU) compared to the control group (−96.02 HU; p = 0.0001). In the group that underwent CT later than 8 days, elevated pFAI values persisted only in the myocarditis and TTS groups, and there was no difference between MINOCA and controls. Our study shows that in patients with a diagnosis of MINOCA, there is acute coronary inflammation, which is more evident within one week from the acute event but tends to disappear with time.

scholarly journals Brain reactivity using fMRI to insomnia stimuli in insomnia patients with discrepancy between subjective and objective sleep

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Young-Bo Kim ◽  
Nambeom Kim ◽  
Jae Jun Lee ◽  
Seo-Eun Cho ◽  
Kyoung-Sae Na ◽  
...  
Keyword(s):  
Brain Activity ◽  
Blood Oxygen Level Dependent ◽  
Brain Regions ◽  
Cognitive Distortion ◽  
Sleep Diary ◽  
Bold Signal ◽  
Blood Oxygen Level ◽  
General Anxiety ◽  
Sleep Deficit ◽  
Perception Of Sleep

AbstractSubjective–objective discrepancy of sleep (SODS) might be related to the distorted perception of sleep deficit and hypersensitivity to insomnia-related stimuli. We investigated differences in brain activation to insomnia-related stimuli among insomnia patients with SODS (SODS group), insomnia patients without SODS (NOSODS group), and healthy controls (HC). Participants were evaluated for subjective and objective sleep using sleep diary and polysomnography. Functional magnetic resonance imaging was conducted during the presentation of insomnia-related (Ins), general anxiety-inducing (Gen), and neutral (Neu) stimuli. Brain reactivity to the contrast of Ins vs. Neu and Gen vs. Neu was compared among the SODS (n = 13), NOSODS (n = 15), and HC (n = 16) groups. In the SODS group compared to other groups, brain areas including the left fusiform, bilateral precuneus, right superior frontal gyrus, genu of corpus callosum, and bilateral anterior corona radiata showed significantly increased blood oxygen level dependent (BOLD) signal in the contrast of Ins vs. Neu. There was no brain region with significantly increased BOLD signal in the Gen vs. Neu contrast in the group comparisons. Increased brain activity to insomnia-related stimuli in several brain regions of the SODS group is likely due to these individuals being more sensitive to sleep-related threat and negative cognitive distortion toward insomnia.

scholarly journals Pseudo-streaming potentials in Necturus gallbladder epithelium. II. The mechanism is a junctional diffusion potential.

1992 ◽  
Vol 99 (3) ◽  
pp. 317-338 ◽  
Author(s):  
L Reuss ◽  
B Simon ◽  
C U Cotton
Keyword(s):  
Time Course ◽  
Bathing Solution ◽  
Intercellular Spaces ◽  
Similar Time ◽  
Streaming Potentials ◽  
Osmotic Water ◽  
Lateral Intercellular Spaces ◽  
Transepithelial Voltage ◽  
Time Courses ◽  
Good Agreement

The mechanisms of apparent streaming potentials elicited across Necturus gallbladder epithelium by addition or removal of sucrose from the apical bathing solution were studied by assessing the time courses of: (a) the change in transepithelial voltage (Vms). (b) the change in osmolality at the cell surface (estimated with a tetrabutylammonium [TBA+]-selective microelectrode, using TBA+ as a tracer for sucrose), and (c) the change in cell impermeant solute concentration ([TMA+]i, measured with an intracellular double-barrel TMA(+)-selective microelectrode after loading the cells with TMA+ by transient permeabilization with nystatin). For both sucrose addition and removal, the time courses of Vms were the same as the time courses of the voltage signals produced by [TMA+]i, while the time courses of the voltage signals produced by [TBA+]o were much faster. These results suggest that the apparent streaming potentials are caused by changes of [NaCl] in the lateral intercellular spaces, whose time course reflects the changes in cell water volume (and osmolality) elicited by the alterations in apical solution osmolality. Changes in cell osmolality are slow relative to those of the apical solution osmolality, whereas lateral space osmolality follows cell osmolality rapidly, due to the large surface area of lateral membranes and the small volume of the spaces. Analysis of a simple mathematical model of the epithelium yields an apical membrane Lp in good agreement with previous measurements and suggests that elevations of the apical solution osmolality elicit rapid reductions in junctional ionic selectivity, also in good agreement with experimental determinations. Elevations in apical solution [NaCl] cause biphasic transepithelial voltage changes: a rapid negative Vms change of similar time course to that of a Na+/TBA+ bi-ionic potential and a slow positive Vms change of similar time course to that of the sucrose-induced apparent streaming potential. We conclude that the Vms changes elicited by addition of impermeant solute to the apical bathing solution are pseudo-streaming potentials, i.e., junctional diffusion potentials caused by salt concentration changes in the lateral intercellular spaces secondary to osmotic water flow from the cells to the apical bathing solution and from the lateral intercellular spaces to the cells. Our results do not support the notion of junctional solute-solvent coupling during transepithelial osmotic water flow.

scholarly journals Association Between Brain Activation and Functional Connectivity

2018 ◽  
Vol 29 (5) ◽  
pp. 1984-1996 ◽  
Author(s):  
Dardo Tomasi ◽  
Nora D Volkow
Keyword(s):  
Functional Connectivity ◽  
Brain Activity ◽  
Low Frequency ◽  
Brain Activation ◽  
Blood Oxygen Level Dependent ◽  
Common Source ◽  
Functional Connectivity Density ◽  
Density Mapping ◽  
Human Connectome Project ◽  
Bold Responses

Abstract The origin of the “resting-state” brain activity recorded with functional magnetic resonance imaging (fMRI) is still uncertain. Here we provide evidence for the neurovascular origins of the amplitude of the low-frequency fluctuations (ALFF) and the local functional connectivity density (lFCD) by comparing them with task-induced blood-oxygen level dependent (BOLD) responses, which are considered a proxy for neuronal activation. Using fMRI data for 2 different tasks (Relational and Social) collected by the Human Connectome Project in 426 healthy adults, we show that ALFF and lFCD have linear associations with the BOLD response. This association was significantly attenuated by a novel task signal regression (TSR) procedure, indicating that task performance enhances lFCD and ALFF in activated regions. We also show that lFCD predicts BOLD activation patterns, as was recently shown for other functional connectivity metrics, which corroborates that resting functional connectivity architecture impacts brain activation responses. Thus, our findings indicate a common source for BOLD responses, ALFF and lFCD, which is consistent with the neurovascular origin of local hemodynamic synchrony presumably reflecting coordinated fluctuations in neuronal activity. This study also supports the development of task-evoked functional connectivity density mapping.

scholarly journals Correlation between Charge Movement and Ionic Current during Slow Inactivation in Shaker K+ Channels

1997 ◽  
Vol 110 (5) ◽  
pp. 579-589 ◽  
Author(s):  
Riccardo Olcese ◽  
Ramón Latorre ◽  
Ligia Toro ◽  
Francisco Bezanilla ◽  
Enrico Stefani
Keyword(s):  
Time Course ◽  
Voltage Dependence ◽  
Ionic Current ◽  
K Channel ◽  
Charge Movement ◽  
Slow Inactivation ◽  
Gating Currents ◽  
Similar Time ◽  
K Channels ◽  
Recovery From Inactivation

Prolonged depolarization induces a slow inactivation process in some K+ channels. We have studied ionic and gating currents during long depolarizations in the mutant Shaker H4-Δ(6–46) K+ channel and in the nonconducting mutant (Shaker H4-Δ(6–46)-W434F). These channels lack the amino terminus that confers the fast (N-type) inactivation (Hoshi, T., W.N. Zagotta, and R.W. Aldrich. 1991. Neuron. 7:547–556). Channels were expressed in oocytes and currents were measured with the cut-open-oocyte and patch-clamp techniques. In both clones, the curves describing the voltage dependence of the charge movement were shifted toward more negative potentials when the holding potential was maintained at depolarized potentials. The evidences that this new voltage dependence of the charge movement in the depolarized condition is associated with the process of slow inactivation are the following: (a) the installation of both the slow inactivation of the ionic current and the inactivation of the charge in response to a sustained 1-min depolarization to 0 mV followed the same time course; and (b) the recovery from inactivation of both ionic and gating currents (induced by repolarizations to −90 mV after a 1-min inactivating pulse at 0 mV) also followed a similar time course. Although prolonged depolarizations induce inactivation of the majority of the channels, a small fraction remains non–slow inactivated. The voltage dependence of this fraction of channels remained unaltered, suggesting that their activation pathway was unmodified by prolonged depolarization. The data could be fitted to a sequential model for Shaker K+ channels (Bezanilla, F., E. Perozo, and E. Stefani. 1994. Biophys. J. 66:1011–1021), with the addition of a series of parallel nonconducting (inactivated) states that become populated during prolonged depolarization. The data suggest that prolonged depolarization modifies the conformation of the voltage sensor and that this change can be associated with the process of slow inactivation.

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