Mice lacking Faim2 show increased cell death in the MPTP mouse model of Parkinson disease

2016 ◽  
Vol 139 (5) ◽  
pp. 848-857 ◽  
Author(s):  
Daniel Komnig ◽  
Jörg B. Schulz ◽  
Arno Reich ◽  
Björn H. Falkenburger
Keyword(s):  
Cell Death ◽  
Mouse Model ◽  
Parkinson Disease

scholarly journals Transduced Tat-DJ-1 protein protects against oxidative stress-induced SH-SY5Y cell death and Parkinson disease in a mouse model

2012 ◽  
Vol 33 (5) ◽  
pp. 471-478 ◽  
Author(s):  
Hoon Jae Jeong ◽  
Dae Won Kim ◽  
Su Jung Woo ◽  
Hye Ri Kim ◽  
So Mi Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Mouse Model ◽  
Parkinson Disease

Altered DAT function in a mouse model of Parkinson disease

2011 ◽  
Author(s):  
D. Leo ◽  
M. J. Bourque ◽  
C. Kortleven ◽  
E. A. Fon ◽  
L. E. Trudeau
Keyword(s):  
Mouse Model ◽  
Parkinson Disease

Poly(ADP-ribose) polymerase-1 gene ablation protects mice from ischemic renal injury

2005 ◽  
Vol 288 (2) ◽  
pp. F387-F398 ◽  
Author(s):  
Jianfeng Zheng ◽  
Kishor Devalaraja-Narashimha ◽  
Kurinji Singaravelu ◽  
Babu J. Padanilam
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Mouse Model ◽  
Renal Injury ◽  
Atp Depletion ◽  
Inflammatory Cascade ◽  
Renal Functions ◽  
Atp Levels ◽  
Ischemic Renal Injury ◽  
Parp 1

Increased generation of reactive oxygen species (ROS) and the subsequent DNA damage and excessive activation of poly(ADP-ribose) polymerase-1 (PARP-1) have been implicated in the pathogenesis of ischemic injury. We previously demonstrated that pharmacological inhibition of PARP protects against ischemic renal injury (IRI) in rats (Martin DR, Lewington AJ, Hammerman MR, and Padanilam BJ. Am J Physiol Regul Integr Comp Physiol 279: R1834–R1840, 2000). To further define the role of PARP-1 in IRI, we tested whether genetic ablation of PARP-1 attenuates tissue injury after renal ischemia. Twenty-four hours after reperfusion following 37 min of bilateral renal pedicle occlusion, the effects of the injury on renal functions in PARP−/− and PARP+/+ mice were assessed by determining glomerular filtration rate (GFR) and the plasma levels of creatinine. The levels of plasma creatinine were decreased and GFR was augmented in PARP−/− mice. Morphological evaluation of the kidney tissues showed that the extent of damage due to the injury in PARP−/− mice was less compared with their wild-type counterparts. The levels of ROS and DNA damage were comparable in the injured kidneys of PARP+/+ and PARP−/− mice. PARP activity was induced in ischemic kidneys of PARP+/+ mice at 6–24 h postinjury. At 6, 12, and 24 h after injury, ATP levels in the PARP+/+ mice kidney declined to 28, 26, and 43%, respectively, whereas it was preserved close to normal levels in PARP−/− mice. The inflammatory cascade was attenuated in PARP−/− mice as evidenced by decreased neutrophil infiltration and attenuated expression of inflammatory molecules such as TNF-α, IL-1β, and intercellular adhesion molecule-1. At 12 h postinjury, no apoptotic cell death was observed in PARP−/− mice kidneys. However, by 24 h postinjury, a comparable number of cells underwent apoptosis in both PARP−/− and PARP+/+ mice kidneys. Thus activation of PARP post-IRI contributes to cell death most likely by ATP depletion and augmentation of the inflammatory cascade in the mouse model. PARP ablation preserved ATP levels, renal functions, and attenuated inflammatory response in the setting of IRI in the mouse model. PARP inhibition may have clinical efficacy in preventing the progression of acute renal failure complications.

scholarly journals Infiltration of CD4+ lymphocytes into the brain contributes to neurodegeneration in a mouse model of Parkinson disease

2008 ◽  
Author(s):  
Vanessa Brochard ◽  
Béhazine Combadière ◽  
Annick Prigent ◽  
Yasmina Laouar ◽  
Aline Perrin ◽  
...  
Keyword(s):  
Mouse Model ◽  
Parkinson Disease ◽  
The Brain ◽  
Cd4 Lymphocytes

scholarly journals Conditional Haploinsufficiency of β-Catenin Aggravates Neuronal Damage in a Paraquat-Based Mouse Model of Parkinson Disease

2018 ◽  
Vol 56 (7) ◽  
pp. 5157-5166 ◽  
Author(s):  
Fanpeng Zhao ◽  
Sandra L. Siedlak ◽  
Sandy L. Torres ◽  
Qian Xu ◽  
Beisha Tang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Parkinson Disease ◽  
Neuronal Damage

scholarly journals Effects of Pergolide Mesilate on Metallothionein mRNAs Expression in a Mouse Model for Parkinson Disease

2009 ◽  
Vol 32 (10) ◽  
pp. 1813-1817 ◽  
Author(s):  
Shin-ichi Ono ◽  
Kohji Hirai ◽  
Ei-ichi Tokuda
Keyword(s):  
Mouse Model ◽  
Parkinson Disease

Hypokinetic Movement Disorders: Parkinson Disease

2021 ◽  
pp. 576-582
Author(s):  
Sarah M. Tisel ◽  
Bryan T. Klassen
Keyword(s):  
Cell Death ◽  
Substantia Nigra ◽  
Parkinson Disease ◽  
Movement Disorder ◽  
Movement Disorders ◽  
Dopaminergic Neurons ◽  
Microscopic Level ◽  
Rest Tremor ◽  
Macroscopic Level ◽  
Progressive Degeneration

Parkinson disease (PD) is the classic hypokinetic movement disorder and one of the most common and widely recognized neurodegenerative conditions. PD is distinct from parkinsonism, a term that refers to a syndrome of rest tremor, bradykinesia, rigidity, and postural instability. The mechanism behind the progressive degeneration and cell death that result in PD is not precisely understood. Substantia nigra depigmentation occurs on a macroscopic level and loss of dopaminergic neurons and gliosis on a microscopic level.

scholarly journals Hyperexcitability precedes motoneuron loss in the Smn2B/− mouse model of spinal muscular atrophy

2019 ◽  
Vol 122 (4) ◽  
pp. 1297-1311 ◽  
Author(s):  
K. A. Quinlan ◽  
E. J. Reedich ◽  
W. D. Arnold ◽  
A. C. Puritz ◽  
C. F. Cavarsan ◽  
...  
Keyword(s):  
Cell Death ◽  
Mouse Model ◽  
Action Potential ◽  
Spinal Muscular Atrophy ◽  
Postnatal Development ◽  
Motor Unit ◽  
Muscular Atrophy ◽  
Action Potential Firing ◽  
Motor Unit Number Estimation ◽  
Potential Firing

Spinal motoneuron dysfunction and loss are pathological hallmarks of the neuromuscular disease spinal muscular atrophy (SMA). Changes in motoneuron physiological function precede cell death, but how these alterations vary with disease severity and motoneuron maturational state is unknown. To address this question, we assessed the electrophysiology and morphology of spinal motoneurons of presymptomatic Smn2B/− mice older than 1 wk of age and tracked the timing of motor unit loss in this model using motor unit number estimation (MUNE). In contrast to other commonly used SMA mouse models, Smn2B/− mice exhibit more typical postnatal development until postnatal day (P)11 or 12 and have longer survival (~3 wk of age). We demonstrate that Smn2B/− motoneuron hyperexcitability, marked by hyperpolarization of the threshold voltage for action potential firing, was present at P9–10 and preceded the loss of motor units. Using MUNE studies, we determined that motor unit loss in this mouse model occurred 2 wk after birth. Smn2B/− motoneurons were also larger in size, which may reflect compensatory changes taking place during postnatal development. This work suggests that motoneuron hyperexcitability, marked by a reduced threshold for action potential firing, is a pathological change preceding motoneuron loss that is common to multiple models of severe SMA with different motoneuron maturational states. Our results indicate voltage-gated sodium channel activity may be altered in the disease process. NEW & NOTEWORTHY Changes in spinal motoneuron physiologic function precede cell death in spinal muscular atrophy (SMA), but how they vary with maturational state and disease severity remains unknown. This study characterized motoneuron and neuromuscular electrophysiology from the Smn2B/− model of SMA. Motoneurons were hyperexcitable at postnatal day (P)9–10, and specific electrophysiological changes in Smn2B/− motoneurons preceded functional motor unit loss at P14, as determined by motor unit number estimation studies.

Sign in / Sign up

Export Citation Format

Share Document