scholarly journals Taurine Increases Zinc Preconditioning-Induced Prevention of Nitrosative Stress, Metabolic Alterations, and Motor Deficits in Young Rats following Intrauterine Ischemia

2021 ◽  
Vol 2021 ◽  
pp. 1-20
Author(s):  
Alejandro Gonzalez-Vazquez ◽  
Ana-Karina Aguilar-Peralta ◽  
Constantino Tomas-Sanchez ◽  
Victor-Manuel Blanco-Alvarez ◽  
Daniel Martinez-Fong ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Nitrosative Stress ◽  
Motor Behavior ◽  
Nutrient Deficiency ◽  
Motor Deficits ◽  
Cerebral Damage ◽  
Ischemic Brain ◽  
Taurine Treatment ◽  
Behavior Impairment ◽  
Ischemic Encephalopathy

Oxygen deprivation in newborns leads to hypoxic-ischemic encephalopathy, whose hallmarks are oxidative/nitrosative stress, energetic metabolism alterations, nutrient deficiency, and motor behavior disability. Zinc and taurine are known to protect against hypoxic-ischemic brain damage in adults and neonates. However, the combined effect of prophylactic zinc administration and therapeutic taurine treatment on intrauterine ischemia- (IUI-) induced cerebral damage remains unknown. The present work evaluated this issue in male pups subjected to transient IUI (10 min) at E17 and whose mothers received zinc from E1 to E16 and taurine from E17 to postnatal day 15 (PND15) via drinking water. We assessed motor alterations, nitrosative stress, lipid peroxidation, and the antioxidant system comprised of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). Enzymes of neuronal energetic pathways, such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH), were also evaluated. The hierarchization score of the protective effect of pharmacological strategies (HSPEPS) was used to select the most effective treatment. Compared with the IUI group, zinc, alone or combined with taurine, improved motor behavior and reduced nitrosative stress by increasing SOD, CAT, and GPx activities and decreasing the GSSG/GSH ratio in the cerebral cortex and hippocampus. Taurine alone increased the AST/ALT, LDH/ALT, and AST/LDH ratios in the cerebral cortex, showing improvement of the neural bioenergetics system. This result suggests that taurine improves pyruvate, lactate, and glutamate metabolism, thus decreasing IUI-caused cerebral damage and relieving motor behavior impairment. Our results showed that taurine alone or in combination with zinc provides neuroprotection in the IUI rat model.

scholarly journals Time-Interval Estimation Training Modulate Motor Behavior and Cerebral Cortex Activity in Parkinson Disease Patients: Preliminary Study

2019 ◽  
Vol 09 (01) ◽  
Author(s):  
Francisco Magalhaes ◽  
Victor Marinho ◽  
Carla Ayre ◽  
Kaline Rocha ◽  
Silmar Teixeira ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Parkinson Disease ◽  
Motor Behavior ◽  
Interval Estimation ◽  
Time Interval ◽  
Preliminary Study

scholarly journals Impact of Age and Sex on α-Syn (α-Synuclein) Knockdown-Mediated Poststroke Recovery

Stroke ◽  
2020 ◽  
Vol 51 (10) ◽  
pp. 3138-3141
Author(s):  
Bharath Chelluboina ◽  
Taehee Kim ◽  
Suresh L. Mehta ◽  
Joo-Yong Kim ◽  
Saivenkateshkomal Bathula ◽  
...  
Keyword(s):  
Brain Damage ◽  
Infarct Volume ◽  
Critical Role ◽  
Artery Occlusion ◽  
Motor Deficits ◽  
Ischemic Brain ◽  
Therapeutic Opportunity ◽  
Interfering Rna ◽  
Cerebral Artery Occlusion ◽  
Age And Sex

Background and Purpose: Increased expression of α-Syn (α-Synuclein) is known to mediate secondary brain damage after stroke. We presently studied if α-Syn knockdown can protect ischemic brain irrespective of sex and age. Methods: Adult and aged male and female mice were subjected to transient middle cerebral artery occlusion. α-Syn small interfering RNA (siRNA) was administered intravenous at 30 minutes or 3 hour reperfusion. Poststroke motor deficits were evaluated between day 1 and 7 and infarct volume was measured at day 7 of reperfusion. Results: α-Syn knockdown significantly decreased poststroke brain damage and improved poststroke motor function recovery in adult and aged mice of both sexes. However, the window of therapeutic opportunity for α-Syn siRNA is very limited. Conclusions: α-Syn plays a critical role in ischemic brain damage and preventing α-Syn protein expression early after stroke minimizes poststroke brain damage leading to better functional outcomes irrespective of age and sex.

scholarly journals Glycine Protects against Hypoxic-Ischemic Brain Injury by Regulating Mitochondria-Mediated Autophagy via the AMPK Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-29 ◽  
Author(s):  
Chen-chen Cai ◽  
Jiang-hu Zhu ◽  
Li-xia Ye ◽  
Yuan-yuan Dai ◽  
Ming-chu Fang ◽  
...  
Keyword(s):  
Pc12 Cells ◽  
Adenosine Monophosphate ◽  
Ischemic Brain Injury ◽  
Hypoxic Stress ◽  
Ischemic Brain ◽  
Ampk Pathway ◽  
Amp Activated Protein Kinase ◽  
Ischemic Encephalopathy

Hypoxic-ischemic encephalopathy (HIE) is detrimental to newborns and is associated with high mortality and poor prognosis. Thus, the primary aim of the present study was to determine whether glycine could (1) attenuate HIE injury in rats and hypoxic stress in PC12 cells and (2) downregulate mitochondria-mediated autophagy dependent on the adenosine monophosphate- (AMP-) activated protein kinase (AMPK) pathway. Experiments conducted using an in vivo HIE animal model and in vitro hypoxic stress to PC12 cells revealed that intense autophagy associated with mitochondrial function occurred during in vivo HIE injury and in vitro hypoxic stress. However, glycine treatment effectively attenuated mitochondria-mediated autophagy. Additionally, after identifying alterations in proteins within the AMPK pathway in rats and PC12 cells following glycine treatment, cyclosporin A (CsA) and 5-aminoimidazole-4-carboxamide-1-b-4-ribofuranoside (AICAR) were administered in these models and indicated that glycine protected against HIE and CoCl2 injury by downregulating mitochondria-mediated autophagy that was dependent on the AMPK pathway. Overall, glycine attenuated hypoxic-ischemic injury in neurons via reductions in mitochondria-mediated autophagy through the AMPK pathway both in vitro and in vivo.

Eye Movements of the Murine P/Q Calcium Channel Mutant Tottering, and the Impact of Aging

2006 ◽  
Vol 95 (3) ◽  
pp. 1588-1607 ◽  
Author(s):  
John S. Stahl ◽  
Robert A. James ◽  
Brian S. Oommen ◽  
Freek E. Hoebeek ◽  
Chris I. De Zeeuw
Keyword(s):  
Eye Movements ◽  
Calcium Channel ◽  
Motor Behavior ◽  
Motor Deficits ◽  
Ocular Motor ◽  
Gene Encoding ◽  
Optokinetic Reflex ◽  
Behavioral Abnormalities ◽  
Cross Axis ◽  
The Impact

Mice carrying mutations of the gene encoding the ion pore of the P/Q calcium channel (Cacna1a) are an instance in which cerebellar dysfunction may be attributable to altered electrophysiology and thus provide an opportunity to study how neuronal intrinsic properties dictate signal processing in the ocular motor system. P/Q channel mutations can engender multiple effects at the single neuron, circuit, and behavioral levels; correlating physiological and behavioral abnormalities in multiple allelic strains will ultimately facilitate determining which alterations of physiology are responsible for specific behavioral aberrations. We used videooculography to quantify ocular motor behavior in tottering mutants aged 3 mo to 2 yr and compared their performance to data previously obtained in the allelic mutant rocker and C57BL/6 controls. Tottering mutants shared numerous abnormalities with rocker, including upward deviation of the eyes at rest, increased vestibuloocular reflex (VOR) phase lead at low stimulus frequencies, reduced VOR gain at high stimulus frequencies, reduced gain of the horizontal and vertical optokinetic reflex, reduced time constants of the neural integrator, and reduced plasticity of the VOR as assessed in a cross-axis training paradigm. Unlike rocker, young tottering mutants exhibited normal peak velocities of nystagmus fast phases, arguing against a role for neuromuscular transmission defects in the attenuation of compensatory eye movements. Tottering also differed by exhibiting directional asymmetries of the gains of optokinetic reflexes. The data suggest at least four pathophysiological mechanisms (two congenital and two acquired) are required to explain the ocular motor deficits in the two Cacna1a mutant strains.

scholarly journals Adenovirus-Mediated Gene Transfer of Glial Cell Line-Derived Neurotrophic Factor Prevents Ischemic Brain Injury after Transient Middle Cerebral Artery Occlusion in Rats

1999 ◽  
Vol 19 (12) ◽  
pp. 1336-1344 ◽  
Author(s):  
Hisashi Kitagawa ◽  
Chihoko Sasaki ◽  
Kenichi Sakai ◽  
Atsushi Mori ◽  
Yasuhide Mitsumoto ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Brain Injury ◽  
Gene Transfer ◽  
Neurotrophic Factor ◽  
Treated Group ◽  
Artery Occlusion ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Gdnf Gene ◽  
Cerebral Artery Occlusion

To examine a possible protective effect of exogenous glial cell line-derived neurotrophic factor (GDNF) gene expression against ischemic brain injury, a replication-defective adenoviral vector containing GDNF gene (Ad-GDNF) was directly injected into the cerebral cortex at 1 day before 90 minutes of transient middle cerebral artery occlusion (MCAO) in rats. 2,3,5-Triphenyltetrazolium chloride staining showed that infarct volume of the Ad-GDNF-injected group at 24 hours after the transient MCAO was significantly smaller than that of vehicle- or Ad-LacZ-treated group. Enzyme-linked immunosorbent assay (ELISA) for immunoreactive GDNF demonstrated that GDNF gene products in the Ad-GDNF-injected group were higher than those of vehicle-treated group at 24 hours after transient MCAO. Immunoreactive GDNF staining was obviously detected in the cortex around the needle track just before or 24 hours after MCAO in the Ad-GDNF group, whereas no or slight GDNF staining was detected in the vehicle group. The numbers of TUNEL, immunoreactive caspase-3, and cytochrome c-positive neurons induced in the ipsilateral cerebral cortex at 24 hours after transient MCAO were markedly reduced by the Ad-GDNF group. These results suggest that the successful exogenous GDNF gene transfer ameliorates ischemic brain injury after transient MCAO in association with the reduction of apoptotic signals.

Sensory and non-sensory visual disorders in man and monkey

1982 ◽  
Vol 298 (1089) ◽  
pp. 3-13 ◽  
Keyword(s):  
Cerebral Cortex ◽  
Sensory Analysis ◽  
Receptive Fields ◽  
Visual Feature ◽  
Cerebral Damage ◽  
Visual Agnosia ◽  
Sensory Impairments ◽  
Visual Areas ◽  
Visual Disorders ◽  
Orientation Disparity

The posterior third of the cerebral cortex in monkeys consists of a patchwork of visual areas in each of which there is a ‘map’ of the retina. The details of the ‘map’ vary considerably from one area to another and one notable variation concerns the optimal visual feature to which the cells respond. Orientation, disparity, colour and movement are emphasized in separate areas that appear to be concerned with sensory analysis. Their existence and the possibility that brain damage is occasionally restricted chiefly to one such area may explain the rare highly selective visual sensory impairments that can follow posterior cerebral damage in man. Other areas are notable for having little or no retinotopic representation. Here the cells may have huge receptive fields and complex trigger features. When such regions are removed, the animal’s visual sensory abilities are intact but its recognition of patterns and objects is not. This condition resembles human visual agnosia.

scholarly journals Does Diffusion Tensor Imaging-Based Tractography at 3 Months of Age Contribute to the Prediction of Motor Outcome After Perinatal Arterial Ischemic Stroke?

Stroke ◽  
2011 ◽  
Vol 42 (12) ◽  
pp. 3410-3414 ◽  
Author(s):  
Niek E. van der Aa ◽  
Alexander Leemans ◽  
Frances J. Northington ◽  
Henrica L. van Straaten ◽  
Ingrid C. van Haastert ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Diffusion Tensor Imaging ◽  
Positive Predictive Value ◽  
Predictive Value ◽  
Neonatal Period ◽  
Motor Behavior ◽  
Diffusion Tensor ◽  
Motor Deficits ◽  
Arterial Ischemic Stroke ◽  
Perinatal Arterial Ischemic Stroke

Background and Purpose— After perinatal arterial ischemic stroke, diffusion-weighted imaging (DWI) and early evaluation of spontaneous motor behavior can be used to predict the development of unilateral motor deficits. The aim of this study was to investigate whether diffusion tensor imaging-based tractography at 3 months of age contributes to this prediction. Methods— Twenty-two infants with unilateral perinatal arterial ischemic stroke were included and scanned during the neonatal period. DWI was used to assess restricted diffusion in the cerebral peduncle. At the age of 3 months, diffusion tensor imaging-based tractography of the corticospinal tracts was performed along with assessment of the movement repertoire. The role of DWI, diffusion tensor imaging, and motor assessment in predicting unilateral motor deficits were compared by calculating the positive and negative predictive values for each assessment. Results— Eleven infants (50%) showed abnormal motor behavior at 3 months with subsequent development of unilateral motor deficits in 8 as determined at follow-up (9–48 months, positive predictive value 73%). Diffusion tensor imaging-based tractography correctly predicted the development of unilateral motor deficits in all 8 infants (positive predictive value 100%). A diagnostic neonatal DWI was available in 20 of 22 (91%) infants. Seven infants showed an abnormal DWI, resulting in unilateral motor deficits in 6 infants (positive predictive value 86%). All assessments had a negative predictive value of 100%. Conclusions— Diffusion tensor imaging-based tractography at 3 months can be used to predict neurodevelopmental outcome after perinatal arterial ischemic stroke. It has a similar predictive value as DWI in the neonatal period and can especially be of additional value in case of an indecisive neonatal DWI or unexpected abnormal early motor development.

scholarly journals Corticospinal vs Rubrospinal Revisited: An Evolutionary Perspective for Sensorimotor Integration

2021 ◽  
Vol 15 ◽  
Author(s):  
Rafael Olivares-Moreno ◽  
Paola Rodriguez-Moreno ◽  
Veronica Lopez-Virgen ◽  
Martín Macías ◽  
Moisés Altamira-Camacho ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cerebral Cortex ◽  
Sensorimotor Integration ◽  
Motor Deficits ◽  
Cns Injury ◽  
Evolutionary Perspective ◽  
Skilled Movement ◽  
Spinal Cord Level ◽  
Behavioral Evidence

The knowledge about how different subsystems participate and interplay in sensorimotor control is fundamental to understand motor deficits associated with CNS injury and movement recovery. The role of corticospinal (CS) and rubrospinal (RS) projections in motor control has been extensively studied and compared, and it is clear that both systems are important for skilled movement. However, during phylogeny, the emerging cerebral cortex took a higher hierarchical role controlling rubro-cerebellar circuits. Here, we present anatomical, neurophysiological, and behavioral evidence suggesting that both systems modulate complex segmental neuronal networks in a parallel way, which is important for sensorimotor integration at spinal cord level. We also highlight that, although specializations exist, both systems could be complementary and potentially subserve motor recovery associated with CNS damage.

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