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Similar Time Course (similar + time_course)
Selected AbstractsCortical and subcortical correlates of functional electrical stimulation of wrist extensor and flexor muscles revealed by fMRIHUMAN BRAIN MAPPING, Issue 3 2009Armin Blickenstorfer Abstract The main scope of this study was to test the feasibility and reliability of FES in a MR-environment. Functional Electrical Stimulation (FES) is used in the rehabilitation therapy of patients after stroke or spinal cord injury to improve their motor abilities. Its principle lies in applying repeated electrical stimulation to the relevant nerves or muscles for eliciting either isometric or concentric contractions of the treated muscles. In this study we report cerebral activation patterns in healthy subjects undergoing fMRI during FES stimulation. We stimulated the wrist extensor and flexor muscles in an alternating pattern while BOLD-fMRI was recorded. We used both block and event-related designs to demonstrate their feasibility for recording FES activation in the same cortical and subcortical areas. Six out of fifteen subjects repeated the experiment three times within the same session to control intraindividual variance. In both block and event-related design, the analysis revealed an activation pattern comprising the contralateral primary motor cortex, primary somatosensory cortex and premotor cortex; the ipsilateral cerebellum; bilateral secondary somatosensory cortex, the supplementary motor area and anterior cingulate cortex. Within the same subjects we observed a consistent replication of the activation pattern shown in overlapping regions centered on the peak of activation. Similar time course within these regions were demonstrated in the event-related design. Thus, both techniques demonstrate reliable activation of the sensorimotor network and eventually can be used for assessing plastic changes associated with FES rehabilitation treatment. Hum Brain Mapp, 2009. © 2008 Wiley-Liss, Inc. [source] The chondroitin sulphate proteoglycan brevican is upregulated by astrocytes after entorhinal cortex lesions in adult ratsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 7 2000Niklas Thon Abstract The chondroitin sulphate proteoglycan brevican is one of the most abundant extracellular matrix molecules in the adult rat brain. It is primarily synthesized by astrocytes and is believed to influence astroglial motility during development and under certain pathological conditions. In order to study a potential role of brevican in the glial reaction after brain injury, its expression was analysed following entorhinal cortex lesion in rats (12 h, 1, 2, 4, 10, 14 and 28 days and 6 months post lesion). In situ hybridization and immunohistochemistry were employed to study brevican mRNA and protein, respectively, in the denervated outer molecular layer of the fascia dentata and at the lesion site. In both regions brevican mRNA was upregulated between 1 and 4 days post lesion. The combination of in situ hybridization with immunohistochemistry for glial fibrillary acidic protein demonstrated that many brevican mRNA-expressing cells are astrocytes. In the denervated zone of the fascia dentata, immunostaining for brevican was increased by 4 days, reached a maximum by 4 weeks and remained detectable up to 6 months post lesion. Electron microscopic immunocytochemistry showed that brevican is a component of the extracellular matrix compartment. At the lesion site a similar time course of brevican upregulation was observed. These data demonstrate that brevican is upregulated in areas of brain damage as well as in areas denervated by a lesion. They suggest a role of brevican in reactive gliosis and are compatible with the hypothesis that brevican is involved in the synaptic reorganization of denervated brain areas. [source] Electrical Remodeling and Atrial Dilation During Atrial Tachycardia are Influenced by Ventricular Rate: Role of Developing TachycardiomyopathyJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2001BAS A. SCHOONDERWOERD M.D. Atrial Remodeling in Tachycardiomyopathy. Introduction: Atrial fibrillation (AF) and congestive heart failure (CHF) are two clinical entities that often coincide. Our aim was to establish the influence of concomitant high ventricular rate and consequent development of CHF on electrical remodeling and dilation during atrial tachycardia. Methods and Results: A total of 14 goats was studied. Five goats were subjected to 3:1 AV pacing (A-paced group, atrial rate 240 beats/min, ventricular rate 80 beats/min). Nine goats were subjected to rapid 1:1 AV pacing (AV-paced group, atrial and ventricular rates 240 beats/min). During 4 weeks, right atrial (RA) and left ventricular (LV) diameters were measured during sinus rhythm. Atrial effective refractory periods (AERP) and inducibility of AF were assessed at three basic cycle lengths (BCL). After 4 weeks of rapid AV pacing, RA and LV diameters had increased to 151% and 113% of baseline, whereas after rapid atrial pacing alone, these parameters were unchanged. Right AERP (157 ± 10 msec vs 144 ± 16 msec at baseline with BCL of 400 msec in the A-paced and AV-paced group, respectively) initially decreased in both groups, reaching minimum values within 1 week. Subsequently, AERP partially recovered in AV-paced goats, whereas AERP remained short in A-paced goats (79 ± 7 msec vs 102 ± 12 msec after 4 weeks; P < 0.05). Left AERP demonstrated a similar time course. Inducibility of AF increased in both groups and reached a maximum during the first week in both groups, being 20% and 48% in the A-paced and AV-paced group, respectively. Conclusion: Nature and time course of atrial electrical remodeling and dilation during atrial tachycardia are influenced by concurrent high ventricular rate and consequent development of CHF. [source] Water diffusion in a rat glioma during ganciclovir-thymidine kinase gene therapy-induced programmed cell death in vivo: Correlation with cell densityJOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 4 2004Piia K. Valonen MSc Abstract Purpose To study the characteristics of diffusion magnetic resonance imaging (MRI) contrast in a rat brain BT4C glioma during progression of ganciclovir (GCV)-thymidine kinase gene therapy-induced programmed cell death (PCD) in vivo. Materials and Methods The trace of the diffusion tensor (Dav = 1/3Trace ), T2, and spin density were determined by MRI and the apparent diffusion coefficient (ADC) of water by diffusion nuclear MR (NMR) spectroscopy using largely varying b values and diffusion times (tD) at 4.7 T. Cell count and apoptotic cells were quantified by histological means. Results Decline in cell count was strongly associated with increase in both Dav and T2. Spin density ratio between tumor and contralateral parietal cortex increased with a very similar time course as Dav and T2, indicating net water gain into the eradicating tumor. Diffusion spectroscopy showed a nonmonoexponential signal decay at all tD values ranging from 14,192 msec. During PCD, the ADC of the component yielding fast diffusion coefficient (D1), as acquired with tD , 47 msec, increased with kinetics similar to those of Dav (tD = 4.8 msec). The fractional size of D1 increased by 10% to 15% throughout the entire tD range. Apparent water residence time of the slow diffusion component, D2, shortened from a value of 38.3 ± 1.7 msec on day 0 to 33.4 ± 0.5 msec by day 8. Conclusion The present results show that reduced cell density and increased water content, leading to altered water microenvironment, are associated with increased water diffusion coefficient in eradicating gliomas as a result of PCD. J. Magn. Reson. Imaging 2004;19:389,396. © 2004 Wiley-Liss, Inc. [source] In Vivo Time-Course Changes in Ethanol Levels Sampled With Subcutaneous MicrodialysisALCOHOLISM, Issue 3 2008Eric A. Engleman Background:, The objective of this study was to determine time-course changes in in vivo ethanol (EtOH) concentrations using a novel subcutaneous (s.c.) microdialysis sampling technique. The hypothesis to be tested was that EtOH concentrations in the s.c. fluid would reflect blood EtOH concentrations. If this is the case, then s.c. microdialysis could allow a more detailed analysis of changes in in vivo levels of EtOH under different drinking paradigms. Methods:, Adult male and female Wistar rats and male alcohol-preferring (P) rats were used in this study. A loop-style microdialysis probe was designed for s.c. applications. After initial in vitro characterization, probes were implanted under the skin between the shoulder blades. Animals were allowed to recover 4 to 24 hours prior to microdialysis collection (2.0 ,l/min flow rate with isotonic saline). In vivo microdialysis experiments were then conducted to determine (i) the extraction fraction (or clearance) using EtOH no-net-flux (NNF) coupled with the alcohol clamp method, (ii) the dose,response and time-course effects after systemic EtOH administration and to compare with blood EtOH levels, and (iii) the time-course changes in EtOH levels during and after an EtOH drinking episode. Results:, In vivo probe recovery (extraction fraction) obtained using the alcohol clamp method was 69 ± 3%, and was comparable to the in vitro recovery of 73 ± 2%. For the EtOH dose,response experiment, rats injected i.p. with 0.5, 1.0, or 2.0 g/kg EtOH showed a clear dose,response effect in the s.c. dialysate samples. Peak concentrations (70, 123, and 203 mg%, respectively) were reached by 15 minutes after injection. In an experiment comparing levels of EtOH in s.c. dialysis and arterial blood samples in rats administered 1.0 g/kg EtOH, similar time-course changes in in vivo EtOH concentrations were observed with both i.g. and i.p. EtOH administration. In P rats drinking 15% EtOH during a 1-hour scheduled access period, EtOH levels in s.c. microdialysates rose rapidly over the session and peaked at approximately 50 mg% at 60 to 80 minutes. Conclusions:, Overall, these experiments indicate that s.c. EtOH and blood EtOH concentrations follow a similar time course. Moreover, s.c. microdialysis can be useful as an experimental approach for determining detailed time-course changes in in vivo EtOH concentrations associated with alcohol drinking episodes. [source] Platelet Recruitment in the Murine Hepatic Microvasculature During Experimental Sepsis: Role of NeutrophilsMICROCIRCULATION, Issue 2 2006GEORG SINGER ABSTRACT Objectives: Sepsis is a major clinical problem that often results in the dysfunction or failure of multiple organs, including the liver. While inflammatory cell activation has been implicated as an early critical event in sepsis-induced liver dysfunction, there is growing evidence for the involvement of activated platelets in this pathologic process. Methods: Intravital microscopy was used in this study to assess the magnitude and time course of platelet adhesion in the liver microcirculation during experimental sepsis and to determine whether the platelet accumulation is linked to leukocyte infiltration. The adhesion of platelets and leukocytes in terminal hepatic venules (THV) and sinusoids was quantified at 2, 4, and 6 h after abdominal sepsis induced by cecal ligation and puncture (CLP). Results: While the rolling and firm adhesion of platelets and leukocytes in THV were not altered in the first 2 h after CLP, platelet recruitment was observed at 4 h and further elevated at 6 h after CLP. Leukocyte adhesion in THV exhibited a similar time course. A similar accumulation of blood cells in sinusoids was noted after CLP. This was accompanied by an increased number of nonperfused sinusoids. CLP-induced leukocyte and platelet recruitment in THV and sinusoids was attenuated in mice rendered neutropenic with anti-neutrophil serum. Conclusion: These findings indicate that sepsis is associated with a neutrophil-dependent recruitment of platelets in the liver microcirculation that impairs sinusoidal perfusion and may contribute to the liver dysfunction associated with sepsis. [source] Flufenamic acid blocks depolarizing afterpotentials and phasic firing in rat supraoptic neuronesTHE JOURNAL OF PHYSIOLOGY, Issue 2 2002Masoud Ghamari-Langroudi Depolarizing afterpotentials (DAPs) that follow action potentials in magnocellular neurosecretory cells (MNCs) are thought to underlie the generation of phasic firing, a pattern that optimizes vasopressin release from the neurohypophysis. Previous work has suggested that the DAP may result from the Ca2+ -dependent reduction of a resting K+ conductance. Here we examined the effects of flufenamic acid (FFA), a blocker of Ca2+ -dependent non-selective cation (CAN) channels, on DAPs and phasic firing using intracellular recordings from supraoptic MNCs in superfused explants of rat hypothalamus. Application of FFA, but not solvent (0.1 % DMSO), reversibly inhibited (IC50+ 13.8 ,m; R+ 0.97) DAPs and phasic firing with a similar time course, but had no significant effects (P > 0.05) on membrane potential, spike threshold and input resistance, nor on the frequency and amplitude of spontaneous synaptic potentials. Moreover, FFA did not affect (P > 0.05) the amplitude, duration, undershoot, or frequency-dependent broadening of action potentials elicited during the spike trains used to evoke DAPs. These findings suggest that FFA inhibits the DAP by directly blocking the channels responsible for its production, rather than by interfering with Ca2+ influx. They also support a role for DAPs in the generation of phasic firing in MNCs. Finally, the absence of a depolarization and increased membrane resistance upon application of FFA suggests that the DAP in MNCs may not be due to the inhibition of resting K+ current, but to the activation of CAN channels. [source] Relationship of Static and Dynamic Mechanisms in Vestibuloocular Reflex Compensation,THE LARYNGOSCOPE, Issue 2 2005FACS, Shawn D. Newlands MD Abstract Objectives/Hypothesis: We tested the hypothesis that recovery of dynamic oculomotor behavior (specifically the vestibuloocular reflex [VOR]) after a unilateral labyrinthectomy (UL) is independent from static deficit recovery (e.g., spontaneous nystagmus). This hypothesis predicts that VOR recovery from peripheral vestibular lesions that do not cause static symptoms, such as unilateral semicircular canal plugging (UCP), would have a similar time course and magnitude as recovery from a lesion that creates both a static and dynamic imbalance, such as UL. Furthermore, animals compensated after UCP would be expected to retain their compensated VOR response after the additional insult of ipsilateral labyrinthectomy. Study Design: An experimental study in the Mongolian gerbil animal model. Methods: The horizontal VOR was measured from both eyes using infrared video-oculography on gerbils before and after UCP, UL, or ipsilateral labyrinthectomy after a previous UCP. Eye movements were recorded during yaw rotation in the dark. Results: UL resulted in a more severe acute deficit than the UCP. Over several weeks, the UCP animals compensated their horizontal VOR, particularly on rotation toward the intact side, quicker and more completely than the UL animals. Animals that underwent ipsilateral labyrinthectomy 8 to 11 weeks after UCP demonstrated preservation of the improved gain, particularly on rotation toward the intact labyrinth. However, the difference between the UL groups with or without precedent UCP was not retained after 72 hours, and long-term compensation was poorest in the UL after UCP group. Conclusions: Plasticity in dynamic vestibular reflexes induced by UCP is preserved after a subsequent UL. However, neurologic events during the first and second day after UL appear to limit, change, or suppress the long-term dynamic compensation of the VOR, regardless of whether the animal had a previous UCP. [source] Astrocytes are More Resistant to Focal Cerebral Ischemia Than Neurons and Die by a Delayed NecrosisBRAIN PATHOLOGY, Issue 4 2009Günfer Gürer Abstract Several recent reports proposed that astrocyte death might precede neuronal demise after focal ischemia, contrary to the conventional view that astrocytes are more resistant to injury than neurons. Interestingly, there are findings supporting each of these opposing views. To clarify these controversies, we assessed astrocyte viability after 2-h middle cerebral artery occlusion in mice. In contrast to neighboring neurons, astrocytes were alive and contained glycogen across the ischemic area 6 h after reperfusion, and at the expanding outer border of the infarct at later time points. These glycogen-positive astrocytes had intact plasma membranes. Astrocytes lost plasmalemma integrity much later than neurons: 19 ± 22 (mean ± standard deviation), 58 ± 14 and 69 ± 3% of astrocytes in the perifocal region became permeable to propidium iodide (PI) at 6, 24, 72 h after ischemia, respectively, in contrast to 81 ± 2, 96 ± 3, 97 ± 2% of neurons. Although more astrocytes in the cortical and subcortical core regions were PI-positive, their numbers were considerably less than those of neurons. Lysosomal rupture (monitored by deoxyribonuclease II immunoreactivity) followed a similar time course. Cytochrome-c immunohistochemistry showed that astrocytes maintained mitochondrial integrity longer than neurons. EM confirmed that astrocyte ultrastructure including mitochondria and lysosomes disintegrated much later than that of neurons. We also found that astrocytes died by a delayed necrosis without significantly activating apoptotic mechanisms although they rapidly swelled at the onset of ischemia. [source] Migraine: a review and future directions for treatmentACTA NEUROLOGICA SCANDINAVICA, Issue 2 2006M. Linde Migraine is a chronic, neurological disorder generally manifesting itself in attacks with severe headache, nausea and an increased reactivity to sensory stimuli. A low migraine threshold is set by genetic factors, although the phenotype also modulates the manifestations. The 1-year prevalence is approximately 13% and is higher among women. Patients usually experience neuropsychological dysfunction, and sometimes also reversible focal neurological symptoms. The trajectories of the characteristic symptoms of acute migraine usually follow a similar time course, indicating a reciprocal underlying mechanism. A central nervous system hyperexcitability has been demonstrated in neurophysiological studies. The dibilitating effects of migraine are not confined to the attacks per se. Many individuals do not recover completely between the attacks and most report a negative impact on the most important life domains, and an interest in testing other treatments. Young persons have a higher frequency of attacks. Acute treatment should routinely be initiated with an analgesic plus a prokinetic anti-emetic. Triptans must not be provided early during the attack to ensure their efficacy. The natural course of attacks is commonly only temporarily altered by acute treatment. Non-pharmacological treatment and drugs may be equally viable in prophylaxis for migraine. In more complicated cases, conjoint therapy should be considered. New strategies to improve adherence with existing therapeutic regimens might yield greater benefits than will new pharmacological agents. [source] Tests for presynaptic modulation of corticospinal terminals from peripheral afferents and pyramidal tract in the macaqueTHE JOURNAL OF PHYSIOLOGY, Issue 1 2006A. Jackson The efficacy of sensory input to the spinal cord can be modulated presynaptically during voluntary movement by mechanisms that depolarize afferent terminals and reduce transmitter release. It remains unclear whether similar influences are exerted on the terminals of descending fibres in the corticospinal pathway of Old World primates and man. We investigated two signatures of presynaptic inhibition of the macaque corticospinal pathway following stimulation of the peripheral nerves of the arm (median, radial and ulnar) and the pyramidal tract: (1) increased excitability of corticospinal axon terminals as revealed by changes in antidromically evoked cortical potentials, and (2) changes in the size of the corticospinal monosynaptic field potential in the spinal cord. Conditioning stimulation of the pyramidal tract increased both the terminal excitability and monosynaptic fields with similar time courses. Excitability was maximal between 7.5 and 10 ms following stimulation and returned to baseline within 40 ms. Conditioning stimulation of peripheral nerves produced no statistically significant effect in either measure. We conclude that peripheral afferents do not exert a presynaptic influence on the corticospinal pathway, and that descending volleys may produce autogenic terminal depolarization that is correlated with enhanced transmitter release. Presynaptic inhibition of afferent terminals by descending pathways and the absence of a reciprocal influence of peripheral input on corticospinal efficacy would help to preserve the fidelity of motor commands during centrally initiated movement. [source] | |||||||||||||