scholarly journals Effect of Photobiomodulation in Rescuing Lipopolysaccharide-Induced Dopaminergic Cell Loss in the Male Sprague–Dawley Rat

Biomolecules ◽  
2019 ◽  
Vol 9 (8) ◽  
pp. 381 ◽  
Author(s):  
O’Brien ◽  
Austin
Keyword(s):  
Cell Death ◽  
Cell Loss ◽  
Lesion Size ◽  
Motor Deficits ◽  
Sprague Dawley ◽  
Dopaminergic Cell ◽  
Sprague Dawley Rats ◽  
Neuroprotective Therapy ◽  
Potential Benefits ◽  
Inflammatory Component

Photobiomodulation (PBM) provides neuroprotection against dopaminergic cell death and associated motor deficits in rodent and primate models of Parkinson’s disease (PD). However, it has not yet been tested in the lipopolysaccharide (LPS) model of PD, which leads to dopaminergic cell death through microglia-evoked neuroinflammation. We investigated whether transcranial PBM could protect against dopaminergic cell death within the substantia nigra in male Sprague–Dawley rats following supranigral LPS injection. PBM fully protected rats from 10 µg LPS which would have otherwise caused 15% cell loss, but there was no significant neuroprotection at a 20 µg dose that led to a 50% lesion. Cell loss at this dose varied according to the precise site of injection and correlated with increased local numbers of highly inflammatory amoeboid microglia. Twenty microgram LPS caused motor deficits in the cylinder, adjusted stepping and rotarod tests that correlated with dopaminergic cell loss. While PBM caused no significant improvement at the group level, motor performance on all three tests no longer correlated with the lesion size caused by 20 µg LPS in PBM-treated rats, suggesting extranigral motor improvements in some animals. These results provide support for PBM as a successful neuroprotective therapy against the inflammatory component of early PD, provided inflammation has not reached a devastating level, as well as potential benefits in other motor circuitries.

Intralesional Patterns of MRI ADC Maps Predict Outcome in Experimental Stroke

2015 ◽  
Vol 39 (5-6) ◽  
pp. 293-301 ◽  
Author(s):  
Isabel Lestro Henriques ◽  
María Gutiérrez-Fernández ◽  
Berta Rodríguez-Frutos ◽  
Jaime Ramos-Cejudo ◽  
Laura Otero-Ortega ◽  
...  
Keyword(s):  
Cell Death ◽  
Functional Outcome ◽  
Lesion Size ◽  
Artery Occlusion ◽  
Experimental Stroke ◽  
Acute Ischemia ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Ischemic Tissue ◽  
Cerebral Artery Occlusion

Background: After acute ischemia, the tissue that is at risk of infarction can be detected by perfusion-weighted imaging/diffusion-weighted imaging (PWI/DWI) mismatch but the time that is needed to process PWI limits its use. As DWI is highly sensitive to acute ischemic tissue damage, we hypothesized that different ADC patterns represent areas with a different potential for recovery. Methods: In a model of permanent middle cerebral artery occlusion (pMCAO), Sprague-Dawley rats were randomly distributed to sham surgery and pMCAO. We further separated the pMCAO group according to intralesional ADC pattern (homogeneous or heterogeneous). At 24 h after ischemia induction, we analyzed lesion size, functional outcome, cell death expression, and brain protection markers including ROS enzyme NOX-4. MRI included DWI (ADC maps), DTI (tractography), and PWI (CBF, CBV and MTT). Results: The lesion size was similar in pMCAO rats. Animals with a heterogeneous pattern in ADC maps showed better functional outcome in Rotarod test (p = 0.032), less expression of cell death (p = 0.014) and NOX-4 (p = 0.0063), higher intralesional CBF (p = 0.0026) and larger PWI/DWI mismatch (p = 0.007). Conclusions: In a rodent model for ischemic stroke, intralesional heterogeneity in ADC maps was related to better functional outcome in lesions of similar size and interval after pMCAO. DWI ADC maps may assist in the early identification of ischemic tissue with an increased potential for recovery as higher expression of acute protection markers, lower expression of cell death, increased PWI/DWI mismatch, and higher intralesional CBF were present in animals with a heterogeneous ADC pattern.

scholarly journals High-Fat-High-Fructose Diet Decreases Hippocampal Neuron Number in Male Rats

2020 ◽  
Vol 12 (1) ◽  
pp. 1-7
Author(s):  
Inggita Kusumastuty ◽  
Frinny Sembiring ◽  
Sri Andarini ◽  
Dian Handayani
Keyword(s):  
Cell Death ◽  
Nerve Cell ◽  
Hippocampal Neurons ◽  
Sprague Dawley ◽  
High Fat ◽  
Group I ◽  
Sprague Dawley Rats ◽  
High Fructose ◽  
Group Ii ◽  
Nerve Cell Death

BACKGROUND: Consumption of foods and drinks high in energy, fat, and/or sugar beyond the recommended quantities can cause obesity, which triggers the incidence of brain nerve cell death related to oxidative stress, high levels of tumor necrosis factor (TNF)-α and triglycerides, and low high-density lipoprotein (HDL) levels. Progressive nerve cell death causes decreasing cognitive performance. This study aims to prove that an American Institute of Nutrition committee in 1993 (AIN-93M) diet modified with high-fat-high-fructose (HFHF) can decrease the number of hippocampal neurons. A decrease in the number of hippocampal neurons indicates progressive nerve cell death.METHODS: An experimental study using a post-test control group design was carried out using male Sprague Dawley rats. Samples were selected using simple random sampling to divide them into two groups, Group I was AIN-93M-modified HFHF diet (n=14) and Group II was AIN-93M standard (n=16). The number of visible neurons was measured in the hippocampus area of Sprague Dawley rats’ brains, stained with haemotoxylin and eosin (H&E) and scanned under 400x magnification. Neurons were counted in 10 visual fields using the "Cell_Count" application.RESULTS: The data were analysed by Pearson’s correlation test using SPSS. The results show that rats in Group I had a greater weight gain and fewer neurons than those in the Group II (p=0.023, r=-0.413).CONCLUSION: The consumption of foods high in fat and fructose can cause an increase in nerve cell death, as shown by the decrease in the number of hippocampal neurons.KEYWORDS: brain nerve cells, high fat, high fructose, increased body weight

Disrupted basal ganglia output during movement preparation in hemi-parkinsonian mice is consistent with behavioral deficits

2021 ◽  
Author(s):  
Anand Tekriwal ◽  
Mario J. Lintz ◽  
John A Thompson ◽  
Gidon Felsen
Keyword(s):  
Basal Ganglia ◽  
Cell Loss ◽  
Motor Deficits ◽  
Movement Preparation ◽  
Rate Model ◽  
Model Framework ◽  
Behavioral Deficits ◽  
Dopaminergic Cell ◽  
Clinical Observations ◽  
External Stimuli

Parkinsonian motor deficits are associated with elevated inhibitory output from the basal ganglia (BG). However, several features of Parkinson's disease (PD) have not been accounted for by this simple "classical rate model" framework, including the observation in PD patients that movements guided by external stimuli are less impaired than otherwise-identical movements generated based on internal goals. Is this difference due to divergent processing within the BG itself, or to the recruitment of extra-BG pathways by sensory processing? In addition, surprisingly little is known about precisely when, in the sequence from selecting to executing movements, BG output is altered by PD. Here, we address these questions by recording activity in the SNr, a key BG output nucleus, in hemiparkinsonian mice performing a well-controlled behavioral task requiring stimulus-guided and internally-specified directional movements. We found that hemiparkinsonian mice exhibited a bias ipsilateral to the side of dopaminergic cell loss that was stronger when movements were internally specified rather than stimulus guided, consistent with clinical observations in parkinsonian patients. We further found that changes in parkinsonian SNr activity during movement preparation were consistent with the ipsilateral behavioral bias, as well as its greater magnitude for internally-specified movements. While these findings are inconsistent with some aspects of the classical rate model, they are accounted for by a related "directional rate model" positing that SNr output phasically over-inhibits motor output in a direction-specific manner. These results suggest that parkinsonian changes in BG output underlying movement preparation contribute to the greater deficit in internally-specified than stimulus-guided movements.

scholarly journals Synergistic toxicity in an in vivo model of neurodegeneration through the co-expression of human TDP-43M337V and tauT175D protein

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Alexander J. Moszczynski ◽  
Madeline Harvey ◽  
Niveen Fulcher ◽  
Cleusa de Oliveira ◽  
Patrick McCunn ◽  
...  
Keyword(s):  
Tau Protein ◽  
Sensorimotor Gating ◽  
In Vivo Model ◽  
Motor Deficits ◽  
Sprague Dawley ◽  
Tau Pathology ◽  
Adult Rats ◽  
Sprague Dawley Rats ◽  
Somatic Gene Transfer

Abstract Although it has been suggested that the co-expression of multiple pathological proteins associated with neurodegeneration may act synergistically to induce more widespread neuropathology, experimental evidence of this is sparse. We have previously shown that the expression of Thr175Asp-tau (tauT175D) using somatic gene transfer with a stereotaxically-injected recombinant adeno-associated virus (rAAV9) vector induces tau pathology in rat hippocampus. In this study, we have examined whether the co-expression of human tauT175D with mutant human TDP-43 (TDP-43M337V) will act synergistically. Transgenic female Sprague-Dawley rats that inducibly express mutant human TDP-43M337V using the choline acetyltransferase (ChAT) tetracycline response element (TRE) driver with activity modulating tetracycline-controlled transactivator (tTA) were utilized in these studies. Adult rats were injected with GFP-tagged tau protein constructs in a rAAV9 vector through bilateral stereotaxic injection into the hippocampus. Injected tau constructs were: wild-type GFP-tagged 2N4R human tau (tauWT; n = 8), GFP-tagged tauT175D 2N4R human tau (tauT175D, pseudophosphorylated, toxic variant, n = 8), and GFP (control, n = 8). Six months post-injection, mutant TDP-43M337V expression was induced for 30 days. Behaviour testing identified motor deficits within 3 weeks after TDP-43 expression irrespective of tau expression, though social behaviour and sensorimotor gating remained unchanged. Increased tau pathology was observed in the hippocampus of both tauWT and tauT175D expressing rats and tauT175D pathology was increased in the presence of cholinergic neuronal expression of human TDP-43M337V. These data indicate that co-expression of pathological TDP-43 and tau protein exacerbate the pathology associated with either individual protein.

Apoptotic Mode of Cell Death in Substantia Nigra Following Intranigral Infusion of the Parkinsonian Neurotoxin, MPP+ in Sprague-Dawley Rats: Cellular, Molecular and Ultrastructural Evidences

2007 ◽  
Vol 32 (7) ◽  
pp. 1238-1247 ◽  
Author(s):  
Rebecca Banerjee ◽  
Sen Sreetama ◽  
Karuppagounder S. Saravanan ◽  
Sailendra Nath Dey ◽  
Kochupurackal P. Mohanakumar
Keyword(s):  
Cell Death ◽  
Substantia Nigra ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

Age-dependent nerve cell loss in the brain of Sprague-Dawley rats: effect of long term acetyl-L-carnitine treatment

1990 ◽  
Vol 10 (2) ◽  
pp. 173-185 ◽  
Author(s):  
P. Napoleone ◽  
F. Ferrante ◽  
O. Ghirardi ◽  
M.T. Ramacci ◽  
F. Amenta
Keyword(s):  
Nerve Cell ◽  
Cell Loss ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Age Dependent ◽  
The Brain

scholarly journals α-Synuclein binds and sequesters PIKE-L into Lewy bodies, triggering dopaminergic cell death via AMPK hyperactivation

2017 ◽  
Vol 114 (5) ◽  
pp. 1183-1188 ◽  
Author(s):  
Seong Su Kang ◽  
Zhentao Zhang ◽  
Xia Liu ◽  
Fredric P. Manfredsson ◽  
Li He ◽  
...  
Keyword(s):  
Cell Death ◽  
Molecular Mechanisms ◽  
Critical Role ◽  
Lewy Bodies ◽  
Cell Loss ◽  
Dominant Negative ◽  
Dependent Manner ◽  
Ph Domain ◽  
Dopaminergic Cell ◽  
Neuroprotective Actions

The abnormal aggregation of fibrillar α-synuclein in Lewy bodies plays a critical role in the pathogenesis of Parkinson’s disease. However, the molecular mechanisms regulating α-synuclein pathological effects are incompletely understood. Here we show that α-synuclein binds phosphoinositide-3 kinase enhancer L (PIKE-L) in a phosphorylation-dependent manner and sequesters it in Lewy bodies, leading to dopaminergic cell death via AMP-activated protein kinase (AMPK) hyperactivation. α-Synuclein interacts with PIKE-L, an AMPK inhibitory binding partner, and this action is increased by S129 phosphorylation through AMPK and is decreased by Y125 phosphorylation via Src family kinase Fyn. A pleckstrin homology (PH) domain in PIKE-L directly binds α-synuclein and antagonizes its aggregation. Accordingly, PIKE-L overexpression decreases dopaminergic cell death elicited by 1-methyl-4-phenylpyridinium (MPP+), whereas PIKE-L knockdown elevates α-synuclein oligomerization and cell death. The overexpression of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or α-synuclein induces greater dopaminergic cell loss and more severe motor defects in PIKE-KO and Fyn-KO mice than in wild-type mice, and these effects are attenuated by the expression of dominant-negative AMPK. Hence, our findings demonstrate that α-synuclein neutralizes PIKE-L’s neuroprotective actions in synucleinopathies, triggering dopaminergic neuronal death by hyperactivating AMPK.

Inhalation of formaldehyde and xylene induces apoptotic cell death in the lung tissue

2009 ◽  
Vol 25 (7) ◽  
pp. 455-461 ◽  
Author(s):  
M. Sandikci ◽  
K. Seyrek ◽  
H. Aksit ◽  
H. Kose
Keyword(s):  
Cell Death ◽  
Lung Tissue ◽  
Lymphoid Tissue ◽  
Apoptotic Cell ◽  
Apoptotic Cells ◽  
Sprague Dawley ◽  
Control Groups ◽  
Adult Rats ◽  
Lymphoid Follicles ◽  
Sprague Dawley Rats

The aim of this study was to determine the localization and number of apoptotic cells in lung tissue and bronchus-associated lymphoid tissue (BALT) of newborns, young, and adult rats exposed to formaldehyde (6 ppm) or technical xylene (300 ppm) for 6 weeks (8 h/day). A total of 27 female Sprague-Dawley rats were used. Apoptotic cells were mainly localized around the bronchus and bronchioles and relatively less frequently on the walls of alveoli and interalveolar septa both in control and experimental groups. In the BALT, reactive cells were localized in the area under the epithelium and distributed homogenously within the lymphoid follicles. The numbers of apoptotic cells in the lung tissue including the BALT were significantly higher in young and adult rats exposed to formaldehyde and xylene than those detected in control groups.

scholarly journals Disrupted basal ganglia output during movement preparation in hemi-parkinsonian mice accounts for behavioral deficits

2020 ◽  
Author(s):  
Anand Tekriwal ◽  
Mario J. Lintz ◽  
John A. Thompson ◽  
Gidon Felsen
Keyword(s):  
Basal Ganglia ◽  
Cell Loss ◽  
Motor Deficits ◽  
Movement Preparation ◽  
Rate Model ◽  
Model Framework ◽  
Behavioral Deficits ◽  
Dopaminergic Cell ◽  
Clinical Observations ◽  
External Stimuli

AbstractParkinsonian motor deficits are associated with elevated inhibitory output from the basal ganglia (BG). However, several features of Parkinson’s disease (PD) have not been accounted for by this simple “rate model” framework, including the observation in PD patients that movements guided by external stimuli are less impaired than otherwise-identical movements generated based on internal goals. Is this difference in impairment due to divergent processing within the BG itself, or to the recruitment of extra-BG pathways by sensory processing? In addition, surprisingly little is known about precisely when, in the sequence from selecting to executing movements, BG output is altered by PD. Here, we address these questions by recording activity in the SNr, a key BG output nucleus, in hemiparkinsonian (hemi-PD) mice performing a well-controlled behavioral task requiring stimulus-guided and internally-specified directional movements. We found that hemi-PD mice exhibited a bias ipsilateral to the side of dopaminergic cell loss that was stronger when movements were internally specified rather than stimulus guided, consistent with clinical observations in parkinsonian patients. We further found that changes in parkinsonian SNr activity during movement preparation could account for the ipsilateral behavioral bias, as well as its greater magnitude for internally-specified movements, consistent with some aspects of the rate model. These results suggest that parkinsonian changes in BG output underlying movement preparation contribute to the greater deficit in internally-specified than stimulus-guided movements.

scholarly journals Thymoquinone enhances sperm DNA integrity in nicotineinduced infertile male rats

2021 ◽  
Vol 18 (6) ◽  
pp. 1219-1225
Author(s):  
Farah Dayana Rosli ◽  
Noor Hashida Hashim ◽  
Yusmin Mohd Yusuf ◽  
Khairul Osman ◽  
Siti Fatimah Ibrahim ◽  
...  
Keyword(s):  
Normal Saline ◽  
Quantitative Polymerase Chain Reaction ◽  
Male Rats ◽  
Control Group ◽  
Dna Integrity ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Sperm Dna ◽  
Potential Benefits

Purpose: To assess the effects of thymoquinone (TQ) on the integrity of sperm DNA in nicotineinduced sperm impairment in rats. Methods: Adult male Sprague Dawley rats were randomized into four equal groups: control group received normal saline orally for 60 days; nicotine group was subcutaneously injected with 5 mg/kg/day nicotine for 30 days and then given normal saline for the next 30 days; TQ group was given normal saline for 30 days followed by TQ at 5 mg/kg/day for 30 days; and nicotine-TQ group received 5 mg/kg of nicotine for 30 days and 5mg/kg of TQ for another 30 days. Sperm DNA breakages were evaluated using Comet assay. The expression levels of protamine 1 (PT1) and transition nuclear protein 2 (Tnp2) genes which are essential for the proper compaction of the sperm DNA were analyzed by quantitative polymerase chain reaction (qPCR). Results: Thymoquinone significantly decreased DNA fragmentation in the sperm of nicotine-treated rats. However, there was no change in PT1 gene expression. Tnp2 was downregulated in the nicotine group and slightly upregulated in nicotine-TQ group (p < 0.05). Conclusion: The results demonstrate the potential benefits of TQ in improving sperm DNA quality of nicotine-induced male infertility.

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