scholarly journals Daily Subacute Paraquat Exposure Decreases Muscle Function and Substantia Nigra Dopamine Level

2013 ◽  
pp. 313-321 ◽  
Author(s):  
M. A. FAHIM ◽  
S. SHEHAB ◽  
A. NEMMAR ◽  
A. ADEM ◽  
S. DHANASEKARAN ◽  
...  

The use of the herbicide paraquat (1,1'-dimethyl-4,4'-bipyridylium dichloride; PQ) which is widely used in agriculture is known to cause dopaminergic neurotoxicity. However, the mechanisms underlying this effect are not fully understood. This present study investigated the behavioral manifestations, motor coordination, and dopaminergic neurodegeneration following exposure to PQ. Male rats were injected with PQ (10 mg/kg i.p.) daily for three weeks. Rotarod systems were used for measuring locomotor activity and motor coordination. The effects of PQ on dorsiflexor, electrophysiologically-induced muscle contraction were studied. Dopamine concentrations in the ventral mesencephalon were measured by high performance liquid chromatography and the number of dopaminergic neurons in substantia nigra pars compacta was estimated by tyrosine hydroxylase immunohistochemistry. PQ induced difficulty in movement and significant reduction in motor activity and twitch tension at the dorsiflexor skeletal muscle. The number of tyrosine hydroxylase positive neurons was significantly less in the substantia nigra pars compacta and nigral dopamine level was significantly reduced in PQ treated animals (20.4±3.4 pg/mg) when compared with control animals (55.0±2.4 pg/mg wet tissue). Daily treatment of PQ for three weeks induces selective dopaminergic neuronal loss in the substantia nigra and significant behavioral and peripheral motor deficit effects.

2014 ◽  
Vol 1592 ◽  
pp. 101-112 ◽  
Author(s):  
Pamela Brambilla Bagatini ◽  
Léder Leal Xavier ◽  
Laura Tartari Neves ◽  
Lisiani Saur ◽  
Sílvia Barbosa ◽  
...  

2021 ◽  
Author(s):  
Lilit Vahan Darbinyan ◽  
Lilia Eduard Hambardzumyan ◽  
Larisa Paylak Manukyan ◽  
Karen Vazgen Simonyan ◽  
Carlos Augusto Carvalho de Vasconcelos ◽  
...  

Abstract Rotenone is involved in the degeneration of dopaminergic neurons, and curcumin may prevent or effectively slow the progression of Parkinson disease (PD). Previous research has shown that the naturally occurring phenolic compound curcumin can reduce inflammation and oxidation, making it a potential therapeutic agent for neurodegenerative diseases. The present study involves investigation of rotenone induced histological changes in the brain areas, hippocampus using Nissl staining after 35 day of subcutaneous injection administration of rotenone in adult male rats. In this study, we investigated whether curcumin protects against rotenone-induced dopaminergic neurotoxicity in a rat model by in vivo electrical recording from Substantia nigra pars compacta (SNc). Curcumin treatment significantly improved electrical activity of neurons in the SNc of rotenone-induced PD model rats. The pattern of histological alterations corresponds with electrophysiological manifestations.


2011 ◽  
Vol 49 (2) ◽  
pp. 398-402 ◽  
Author(s):  
H. T. Chang ◽  
W. K. Rumbeiha ◽  
J. S. Patterson ◽  
B. Puschner ◽  
A. P. Knight

Chronic ingestion of yellow star thistle ( Centaurea solstitialis) or Russian knapweed ( Acroptilon repens) causes nigropallidal encephalomalacia (NPE) in horses with an abrupt onset of neurologic signs characterized by dystonia of lips and tongue, inability to prehend food, depression, and locomotor deficits. The objectives of this study were to reexamine the pathologic alterations of NPE and to conduct an immunohistochemistry study using antibodies to tyrosine hydroxylase and α-synuclein, to determine whether NPE brains show histopathologic features resembling those in human Parkinson disease. Results confirm that the NPE lesions are located within the substantia nigra pars reticulata, sparing the cell bodies of the dopaminergic neurons in the substantia nigra pars compacta, and in the rostral portion of the globus pallidus, with partial disruption of dopaminergic (tyrosine hydroxylase–positive) fibers passing through the globus pallidus. No abnormal cytoplasmic inclusions like the Lewy bodies of human Parkinson disease were seen in these NPE brains. These findings indicate that equine NPE may serve as a large animal model of environmentally acquired toxic parkinsonism, with clinical phenotype directly attributable to lesions in globus pallidus and substantia nigra pars reticulata rather than to the destruction of dopaminergic neurons.


2011 ◽  
Vol 116 (4) ◽  
pp. 646-658 ◽  
Author(s):  
Tim D. Aumann ◽  
Kate Egan ◽  
Jamie Lim ◽  
Wah C. Boon ◽  
Chris R. Bye ◽  
...  

Author(s):  
Md. Ezazul Haque ◽  
Shofiul Azam ◽  
Mahbuba Akther ◽  
Duk-Yeon Cho ◽  
Kim In Su ◽  
...  

GPR4, a member of proton activated GPCRs group. Previously we have reported that GPR4 is constitutively active at physiological pH and knockout of GPR4 has shown to protect dopaminergic neuronal cells from caspase-dependent mitochondrial apoptotic cell death. In this study we have investigated the role of GPR4 in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) treated mice model of Parkinson’s disease. Subchronic administration of MPTP in mice produces oxidative stress induced apoptotic cell death of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and motor deficits. Treatment with NE52-QQ57, a selective antagonist of GPR4 reduced dopaminergic neuronal loss MPTP-intoxicated C57BL6/J mice and improved motor deficit and memory impairment. Co-treatment with NE52-QQ57 significantly decreases the protein level of proapoptotic marker (Bax), and increases the antiapoptotic marker (Bcl-2) in the SNpc and striatum tissue collected from the brain of MPTP inflicted mice. Further, MPTP induced activation of caspase 3 and cleavage of poly (ADP-ribose) polymerase (PARP) was significantly decreased in the SNpc and striatum tissue of NE52-QQ57 cotreated mice. Further mice receiving both MPTP and NE52-QQ57 mice showed significantly higher TH positive cells in the SNpc and striatum than MPTP treated mice alone. Moreover, NE52-QQ57 cotreatment improved the motor activity in the rotarod test and pole test and also improved spatial memory in Y maze test. Our findings suggest GPR4 as a potential therapeutic target for PD whereas the activation GPR4 is involved in the caspase mediated apoptotic cell death in SNpc and striatum of MPTP-intoxicated mice.


2018 ◽  
Vol 26 (2) ◽  
pp. 175-183
Author(s):  
Dmitriy N. Voronkov ◽  
Vladimir N. Salkov ◽  
Rudolf M. Khudoerkov

Background. Up to the moment there is no universally accepted scheme of spatial organization of the groups of neurons of substantia nigra pars compacta of the human midbrain. A detailed study of the architectonics of this structure is necessary for pathomorphological analysis of agerelated changes in the nervous tissue and the associated neurodegenerative diseases with selective death of dopamine neurons. Aim. To clarify the peculiarities of the morphochemical organization of the substantia nigra (SN) of a human brain and to create a threedimensional model of pars compacta. Materials and Methods. Threedimensional reconstruction of substantia nigra pars compacta was performed on the brain autopsy material of individuals without neurological pathology (n=10, between 52 to 84 years of age) using a method of computed morphometry. Sections of the midbrain were stained by Nissl method and by an immunohistochemical method for localization of tyrosine hydroxylase – a marker of dopamine. Results. In the SN pars compacta accumulations of neurons were identified in the form of 9 bands oriented in the rostrocaudal direction and including four areas: medial, lateral, dorsal and ventral. Morphometric analysis detected significant differences in the density of neurons and in expression of tyrosine hydroxylase between the areas of SN. Conclusion. A model of cellular organization of SN pars compacta proposed by us on the basis of threedimensional reconstruction is characterized by a high degree of detalization as compared to similar works, and shows expressed spatial differentiation of the groups of neurons of SN which should be taken into consideration in pathomorphological examinations.


Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1671 ◽  
Author(s):  
Chi-Lin Li ◽  
Yang-Hwei Tsuang ◽  
Tung-Hu Tsai

Schisandra chinensis (Turcz.) Baill. (S. chinensis) is a well-known botanical medicine and nutritional supplement that has been shown to have potential effects on neurodegeneration. To investigate the potential neuroprotective effect of S. chinensis fruit extract, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was used to induce behavioral disorders and dopaminergic neuronal damage in mice, and biochemical indicators were examined. Male C57BL/6 mice were used to establish the MPTP-induced parkinsonian syndrome model. Open field and rotarod tests were performed to evaluate the overall manifestation of motor deficits and rodent motor coordination. The mice were divided into 8 groups as follows: normal control; MPTP alone (25 mg/kg, i.p.); S. chinensis extract pretreatment (0.5, 1.5, 5 g/kg, p.o.); and S. chinensis extract treatment (0.5, 1.5, 5 g/kg, p.o.). Liquid chromatography coupled to electrochemical detection was used to monitor neurochemicals in the striatum. Tyrosine hydroxylase content was measured by immunohistochemistry, and biochemical antioxidative indicators were used to evaluate the potential neuroprotective effects of S. chinensis fruit extract. The results demonstrated that treatment with S. chinensis fruit extract ameliorated MPTP-induced deficits in behavior, exercise balance, dopamine level, dopaminergic neurons, and tyrosine hydroxylase-positive cells in the striatum of mice. Among the pretreated and treatment groups, a high dose of S. chinensis fruit extract was the most effective treatment. In conclusion, S. chinensis fruit extract is a potential herbal drug candidate for the amelioration and prevention of Parkinson’s disease.


2011 ◽  
Vol 1382 ◽  
pp. 173-180 ◽  
Author(s):  
Patrícia S. do Nascimento ◽  
Gisele A. Lovatel ◽  
Sílvia Barbosa ◽  
Jocemar Ilha ◽  
Lígia A. Centenaro ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document