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Journal articles on the topic 'Dopaminergic nigrostriatal pathway'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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1

Clark, Elisia, Laura Struzyna, Wisberty Gordián-Vélez, and Kacy Cullen. "3433 Tissue Engineered Nigrostriatal Pathway as a Test-Bed for Evaluating Axonal Pathophysiology in Parkinson’s disease." Journal of Clinical and Translational Science 3, s1 (2019): 25. http://dx.doi.org/10.1017/cts.2019.60.

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OBJECTIVES/SPECIFIC AIMS: Selective loss of long-projecting neural circuitry is a common feature of many neurodegenerative diseases, such as the vulnerable nigrostriatal pathway in Parkinson’s disease (PD). Current in vitro approaches for studying disease development generally do not mimic complex anatomical features of the afflicted substrates such as long axonal pathways between stereotypical neural populations. Such exquisite features are not only crucial for neural systems function but may also contribute to the preferential vulnerability and pathophysiological progression of these structu

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2

Pérez-Valenzuela, Enzo Javier, María Estela Andrés Coke, Anthony A. Grace, and José Antonio Fuentealba Evans. "Adolescent Exposure to WIN 55212-2 Render the Nigrostriatal Dopaminergic Pathway Activated During Adulthood." International Journal of Neuropsychopharmacology 23, no. 9 (2020): 626–37. http://dx.doi.org/10.1093/ijnp/pyaa053.

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Abstract Background During adolescence, neuronal circuits exhibit plasticity in response to physiological changes and to adapt to environmental events. Nigrostriatal dopaminergic pathways are in constant flux during development. Evidence suggests a relationship between early use of cannabinoids and psychiatric disorders characterized by altered dopaminergic systems, such as schizophrenia and addiction. However, the impact of adolescent exposure to cannabinoids on nigrostriatal dopaminergic pathways in adulthood remains unclear. The aim of this research was to determine the effects of repeated

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3

Vilela Filho, Osvaldo. "Thalamic ventrobasal stimulation for pain relief: probable mechanisms, pathways and neurotransmitters." Arquivos de Neuro-Psiquiatria 52, no. 4 (1994): 578–84. http://dx.doi.org/10.1590/s0004-282x1994000400022.

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Thalamic ventrobasal (VB) stimulation, first performed by Mazars, in 1961, is a valuable means for treating central and deafferentation pain. The way it acts to achieve pain relief, however, is still a matter of controversy. In this paper, the author examines previously proposed hypotheses and suggests that VB stimulation induces pain relief by activation of a multisynaptyic inhibitory pathway to the medial thalamus, in which the dopaminergic nigrostriatal system exerts an important role and by modulation of abnormal activity in VB itself. The multisynaptic pathway involved, as well as the neu

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4

Colzato, Lorenza S., Heleen A. Slagter, Mischa de Rover, and Bernhard Hommel. "Dopamine and the Management of Attentional Resources: Genetic Markers of Striatal D2 Dopamine Predict Individual Differences in the Attentional Blink." Journal of Cognitive Neuroscience 23, no. 11 (2011): 3576–85. http://dx.doi.org/10.1162/jocn_a_00049.

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The attentional blink (AB)—a deficit in reporting the second of two target stimuli presented in close succession in a rapid sequence of distracters—has been related to processing limitations in working memory. Given that dopamine (DA) plays a crucial role working memory, the present study tested whether individual differences in the size of the AB can be predicted by differences in genetic predisposition related to the efficiency of dopaminergic pathways. Polymorphisms related to mesocortical and nigrostriatal dopaminergic pathways were considered, as well as polymorphisms related to norepinep

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5

Tashiro, Yuzuru, and Takaaki Inomoto. "Functional Injury of Dopaminergic Nigrostriatal Pathway caused by Progressive Hydrocephalus." Japanese Journal of Neurosurgery 14, no. 7 (2005): 456–61. http://dx.doi.org/10.7887/jcns.14.456.

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6

Dodd, CA, and BG Klein. "Pyrethroid and organophosphate insecticide exposure in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson’s disease: an immunohistochemical analysis of tyrosine hydroxylase and glial fibrillary acidic protein in dorsolateral striatum." Toxicology and Industrial Health 25, no. 1 (2009): 25–39. http://dx.doi.org/10.1177/0748233709102752.

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The pyrethroid insecticide permethrin and the organophosphate insecticide chlorpyrifos can experimentally produce Parkinson’s disease (PD)-associated changes in the dopaminergic nigrostriatal pathway, short of frank degeneration, although at doses considerably higher than from a likely environmental exposure. The ability of permethrin (200 mg/kg), chlorpyrifos (50 mg/kg), or combined permethrin + chlorpyrifos to facilitate nigrostriatal damage in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (30 mg/kg) C57BL/6 mouse model of PD was investigated in three separate experiments. Tyrosine

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7

Jeon, Hyongjun, Sun Ryu, Dongsoo Kim, Sungtae Koo, Ki-Tae Ha, and Seungtae Kim. "Acupuncture Stimulation at GB34 Restores MPTP-Induced Neurogenesis Impairment in the Subventricular Zone of Mice." Evidence-Based Complementary and Alternative Medicine 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/3971675.

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Adult neurogenesis has recently been considered a new therapeutic paradigm of Parkinson’s disease. In this study, we investigated whether acupuncture restores 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine- (MPTP-) induced impaired neurogenesis in the subventricular zone (SVZ). Male C57BL/6 mice were given 30 mg/kg of MPTP intraperitoneally once a day for 5 days, after which they were intraperitoneally injected with 50 mg/kg of bromodeoxyuridine (BrdU) and given acupuncture stimulation at HT7 or GB34 for 12 consecutive days. Dopaminergic neuronal survival in the nigrostriatal pathway and cell pr

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8

Huang, Chin-Chang, Nai-Shin Chu, Tzu-Chen Yen, Yau-Yau Wai, and Chin-Song Lu. "Dopamine Transporter Binding in Wilson's Disease." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 30, no. 2 (2003): 163–67. http://dx.doi.org/10.1017/s0317167100053464.

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ABSTRACT:Introduction:In Wilson's disease (WD), brain magnetic resonance images (MRI) show increased signal intensity in T2 weighted images in the lenticular nuclei, thalamus and brainstem, including the substantia nigra. A poor therapeutic response to levodopa in WD suggests the mechanism of a postsynaptic abnormality. However positron emission tomography studies show an involvement of the nigrostriatal presynaptic dopaminergic pathway.Case report:We report the clinical manifestations in a case of WD with akinetic-rigid syndrome and initial hesitation. The brain MRI showed an increased signal

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9

Kuan, Wei-Li, Emma Poole, Michael Fletcher, et al. "A novel neuroprotective therapy for Parkinson’s disease using a viral noncoding RNA that protects mitochondrial Complex I activity." Journal of Experimental Medicine 209, no. 1 (2011): 1–10. http://dx.doi.org/10.1084/jem.20111126.

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Parkinson’s disease (PD) is a neurodegenerative disorder that results in the loss of nigrostriatal dopamine neurons. The etiology of this cell loss is unknown, but it involves abnormalities in mitochondrial function. In this study, we have demonstrated that the administration of a novel noncoding p137 RNA, derived from the human cytomegaloviral β2.7 transcript, can prevent and rescue dopaminergic cell death in vitro and in animal models of PD by protecting mitochondrial Complex I activity. Furthermore, as this p137 RNA is fused to a rabies virus glycoprotein peptide that facilitates delivery o

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10

Dieb, Wisam, Omar Ouachikh, Franck Durif, and Aziz Hafidi. "Lesion of the dopaminergic nigrostriatal pathway induces trigeminal dynamic mechanical allodynia." Brain and Behavior 4, no. 3 (2014): 368–80. http://dx.doi.org/10.1002/brb3.214.

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11

Sáez-Zea, Carmen, Francisco Escamilla-Sevilla, Josefina Martínez-Simón, Marisa Arnedo, and Adolfo Mínguez-Castellanos. "Neuropsychological Deficits Associated with Destruction of the Right Nigrostriatal Pathway." Journal of the International Neuropsychological Society 19, no. 6 (2013): 729–34. http://dx.doi.org/10.1017/s1355617713000416.

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AbstractHemiparkinsonism secondary to a vascular mesencephalic lesion is infrequent; these patients offer an exceptional opportunity to study neuropsychological alterations attributable to unilateral dopaminergic denervation, shedding light on the pathophysiology of cognitive disorders in early-stage idiopathic Parkinson's disease (PD). From the investigation of our case, we conclude that destruction of the right nigrostriatal pathway is accompanied by deficits in executive functioning and verbal/visual memory similar to those observed in many patients with early-stage idiopathic PD. The more

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12

Park, Hyunjun, and Keun-A. Chang. "Therapeutic Potential of Repeated Intravenous Transplantation of Human Adipose-Derived Stem Cells in Subchronic MPTP-Induced Parkinson’s Disease Mouse Model." International Journal of Molecular Sciences 21, no. 21 (2020): 8129. http://dx.doi.org/10.3390/ijms21218129.

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Parkinson’s disease (PD) is the second most common neurodegenerative disease, which is clinically and pathologically characterized by motor dysfunction and the loss of dopaminergic neurons in the substantia nigra, respectively. PD treatment with stem cells has long been studied by researchers; however, no adequate treatment strategy has been established. The results of studies so far have suggested that stem cell transplantation can be an effective treatment for PD. However, PD is a progressively deteriorating neurodegenerative disease that requires long-term treatment, and this has been insuf

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13

Mcgrath, John, Elishia Lintz, Barry J. Hoffer, Greg A. Gerhardt, E. Matthew Quintero, and Ann-Charlotte Granholm. "Adeno-Associated Viral Delivery of GDNF Promotes Recovery of Dopaminergic Phenotype following a Unilateral 6-Hydroxydopamine Lesion." Cell Transplantation 11, no. 3 (2002): 215–27. http://dx.doi.org/10.3727/096020198389988.

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Glial cell line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor for dopamine neurons that has been proposed for use in the treatment of Parkinson's disease (PD). Previous studies using viral vectors to deliver GDNF in rodent models of PD have entailed administering the virus either prior to or immediately after neurotoxin-induced lesions, when the nigrostriatal pathway is largely intact, a paradigm that does not accurately reflect the clinical situation encountered with Parkinson's patients. In this study, recombinant adeno-associated virus carrying the gene encoding GDNF (r

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14

Snow, B. J., M. Bhatt, W. R. Martin, D. Li, and D. B. Calne. "The nigrostriatal dopaminergic pathway in Wilson's disease studied with positron emission tomography." Journal of Neurology, Neurosurgery & Psychiatry 54, no. 1 (1991): 12–17. http://dx.doi.org/10.1136/jnnp.54.1.12.

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15

Mendez, Ivar, Damaso Sadi, and Murray Hong. "Reconstruction of the Nigrostriatal Pathway by Simultaneous Intrastriatal and Intranigral Dopaminergic Transplants." Journal of Neuroscience 16, no. 22 (1996): 7216–27. http://dx.doi.org/10.1523/jneurosci.16-22-07216.1996.

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16

Barata-Antunes, Sandra, Fábio G. Teixeira, Bárbara Mendes-Pinheiro, et al. "Impact of Aging on the 6-OHDA-Induced Rat Model of Parkinson’s Disease." International Journal of Molecular Sciences 21, no. 10 (2020): 3459. http://dx.doi.org/10.3390/ijms21103459.

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Parkinson’s disease (PD) is the second most common age-related neurodegenerative disorder. The neurodegeneration leading to incapacitating motor abnormalities mainly occurs in the nigrostriatal pathway due to the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Several animal models have been developed not only to better understand the mechanisms underlying neurodegeneration but also to test the potential of emerging disease-modifying therapies. However, despite aging being the main risk factor for developing idiopathic PD, most of the studies do not use aged animals.

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17

Chen, Shur Tzu, Jih Ing Chuang, Mei Huei Hong, and Eric I.-Chian Li. "Melatonin attenuates MPP+-induced neurodegeneration and glutathione impairment in the nigrostriatal dopaminergic pathway." Journal of Pineal Research 32, no. 4 (2002): 262–69. http://dx.doi.org/10.1034/j.1600-079x.2002.01871.x.

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18

Zuddas, Alessandro, Francesca Vaglini, Francesco Fornai, and Giovanni U. Corsini. "Selective lesion of the nigrostriatal dopaminergic pathway by MPTP and acetaldehydehyde or diethyldithiocarbamate." Neurochemistry International 20 (March 1992): 287–93. http://dx.doi.org/10.1016/0197-0186(92)90254-o.

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19

Granado, Noelia, Sara Ares-Santos, Esther O’Shea, Carlos Vicario-Abejón, M. Isabel Colado, and Rosario Moratalla. "Selective Vulnerability in Striosomes and in the Nigrostriatal Dopaminergic Pathway After Methamphetamine Administration." Neurotoxicity Research 18, no. 1 (2009): 48–58. http://dx.doi.org/10.1007/s12640-009-9106-1.

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20

Castel, M. N., C. Malgouris, J. C. Blanchard, and P. M. Laduron. "Retrograde axonal transport of neurotensin in the dopaminergic nigrostriatal pathway in the rat." Neuroscience 36, no. 2 (1990): 425–30. http://dx.doi.org/10.1016/0306-4522(90)90438-a.

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21

Yang, Yihang, Bo Pang, Zihao Liu, et al. "1-Trichloromethyl-1,2,3,4-tetrahydro-beta-carboline (TaClo) Induces the Apoptosis of Dopaminergic Neurons via Oxidative Stress and Neuroinflammation." Oxidative Medicine and Cellular Longevity 2019 (March 7, 2019): 1–12. http://dx.doi.org/10.1155/2019/1292891.

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Several in vitro studies have revealed the neurotoxicity of 1-trichloromethyl-1,2,3,4-tetrahydro-beta-carboline (TaClo). However, the underlying mechanism has not been completely elucidated, particularly in vivo. This study was designed to study the neurotoxicity of TaClo in vivo by stereotactically injecting TaClo into the striatum of Wistar rats. After the TaClo injections, rats were subjected to an open field test, and their distance travelled and tracks showed decreasing trends over time. The results of liquid chromatography-mass spectrometry analysis showed that the motor dysfunction of t

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22

Chung, Young Cheul, Yoon-Seong Kim, Eugene Bok, Tae Young Yune, Sungho Maeng, and Byung Kwan Jin. "MMP-3 Contributes to Nigrostriatal Dopaminergic Neuronal Loss, BBB Damage, and Neuroinflammation in an MPTP Mouse Model of Parkinson’s Disease." Mediators of Inflammation 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/370526.

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The present study examined whether matrix metalloproteinase-3 (MMP-3) participates in the loss of dopaminergic (DA) neurons in the nigrostriatal pathway in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease with blood brain barrier (BBB) damage and infiltration of peripheral immune cells. Tyrosine hydroxylase (TH) immunostaining of brain sections from MPTP-treated mice showed that MPTP induced significant degeneration of nigrostriatal DA neurons. Moreover, FITC-labeled albumin detection and immunostaining revealed that MPTP caused damage to the BBB and inc

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23

Hung, Hui-Chuan, and Eminy H. Y. Lee. "The mesolimbic dopaminergic pathway is more resistant than the nigrostriatal dopaminergic pathway to MPTP and MPP+ toxicity: role of BDNF gene expression." Molecular Brain Research 41, no. 1-2 (1996): 16–26. http://dx.doi.org/10.1016/0169-328x(96)00062-9.

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24

Bor-Seng-Shu, Edson, José Luiz Pedroso, Daniel Ciampi de Andrade, et al. "Transcranial sonography in Parkinson's disease." Einstein (São Paulo) 10, no. 2 (2012): 242–46. http://dx.doi.org/10.1590/s1679-45082012000200022.

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Transcranial sonography has become a useful tool in the differential diagnosis of parkinsonian syndromes. This is a non-invasive, low cost procedure. The main finding on transcranial sonography in patients with idiopathic Parkinson's disease is an increased echogenicity of the mesencephalic substantia nigra region. This hyperechogenicity is present in more than 90% of cases, and reflects a dysfunction in the dopaminergic nigrostriatal pathway. This study discussed how the hyperechogenicity of the substantia nigra may facilitate the differential diagnosis of parkinsonian syndromes.

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25

Kawahata, Ichiro, and Kohji Fukunaga. "Degradation of Tyrosine Hydroxylase by the Ubiquitin-Proteasome System in the Pathogenesis of Parkinson’s Disease and Dopa-Responsive Dystonia." International Journal of Molecular Sciences 21, no. 11 (2020): 3779. http://dx.doi.org/10.3390/ijms21113779.

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Nigrostriatal dopaminergic systems govern physiological functions related to locomotion, and their dysfunction leads to movement disorders, such as Parkinson’s disease and dopa-responsive dystonia (Segawa disease). Previous studies revealed that expression of the gene encoding nigrostriatal tyrosine hydroxylase (TH), a rate-limiting enzyme of dopamine biosynthesis, is reduced in Parkinson’s disease and dopa-responsive dystonia; however, the mechanism of TH depletion in these disorders remains unclear. In this article, we review the molecular mechanism underlying the neurodegeneration process i

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Liu, Zhaohui, and Hoi-Hung Cheung. "Stem Cell-Based Therapies for Parkinson Disease." International Journal of Molecular Sciences 21, no. 21 (2020): 8060. http://dx.doi.org/10.3390/ijms21218060.

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Parkinson disease (PD) is a neurological movement disorder resulting primarily from damage to and degeneration of the nigrostriatal dopaminergic pathway. The pathway consists of neural populations in the substantia nigra that project to the striatum of the brain where they release dopamine. Diagnosis of PD is based on the presence of impaired motor features such as asymmetric or unilateral resting tremor, bradykinesia, and rigidity. Nonmotor features including cognitive impairment, sleep disorders, and autonomic dysfunction are also present. No cure for PD has been discovered, and treatment st

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27

Booij, Jan, and Henk W. Berendse. "Monitoring therapeutic effects in Parkinson's disease by serial imaging of the nigrostriatal dopaminergic pathway." Journal of the Neurological Sciences 310, no. 1-2 (2011): 40–43. http://dx.doi.org/10.1016/j.jns.2011.07.029.

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28

Eberling, Jamie L., Adrian P. Kells, Philip Pivirotto, et al. "Functional Effects of AAV2-GDNF on the Dopaminergic Nigrostriatal Pathway in Parkinsonian Rhesus Monkeys." Human Gene Therapy 20, no. 5 (2009): 511–18. http://dx.doi.org/10.1089/hum.2008.201.

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29

Sasaki, Kazuo, Hiroshi Suda, and Hiroshi Watanabe. "An inhibitory entopedunculo-lateral habenular feedback pathway on the nigrostriatal dopaminergic system in rats." Neuroscience Research Supplements 15 (January 1990): S73. http://dx.doi.org/10.1016/0921-8696(90)90249-3.

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30

Sasaki, Kazuo, Hiroshi Suda, and Hiroshi Watanabe. "An inhibitory entopedunculo-lateral habenular feedback pathway on the nigrostriatal dopaminergic system in rats." Neuroscience Research Supplements 11 (January 1990): S73. http://dx.doi.org/10.1016/0921-8696(90)90672-p.

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31

Ciammola, A., J. Sassone, B. Poletti, N. Mencacci, R. Benti, and V. Silani. "Atypical Parkinsonism Revealing a Late Onset, Rigid and Akinetic Form of Huntington's Disease." Case Reports in Neurological Medicine 2011 (2011): 1–3. http://dx.doi.org/10.1155/2011/696953.

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Huntington's disease (HD) is a rare hereditary neurodegenerative disorder characterized in over 90 percent of cases by chorea as the presenting motor symptom. We report a 54-year-old male who presented with Parkinsonism as the initial symptom of the disease. Genetic analysis revealed expansion of 40 CAG repeats, and brain MRI showed both severe caudate nuclei and cortical atrophy. Single-photon emission computed tomography (SPECT) imaging of the dopamine transporter showed nigrostriatal pathway degeneration. Here, we also describe his 2 years of clinical followup after ensuing dopaminergic sti

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32

Fontoura, Jéssica Lopes, Camila Baptista, Flávia de Brito Pedroso, José Augusto Pochapski, Edmar Miyoshi, and Marcelo Machado Ferro. "Depression in Parkinson’s Disease: The Contribution from Animal Studies." Parkinson's Disease 2017 (2017): 1–8. http://dx.doi.org/10.1155/2017/9124160.

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Besides being better known for causing motor impairments, Parkinson’s disease (PD) can also cause many nonmotor symptoms, like depression and anxiety, which can cause significant loss of life quality and may not respond to regular drugs treatment. In this review, we discuss the depression in PD, based on data from studies in humans and rodents. Depression frequency seems higher in PD patients than in general population, despite high variation in data due to diagnosis disparities. Development of depression in PD seems more likely to be caused by the nigrostriatal pathway degeneration than as a

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33

Wang, Shuang, Yan Zhao, Jie Gao, et al. "In Vivo Effect of a 5-HT7 Receptor Agonist on 5-HT Neurons and GABA Interneurons in the Dorsal Raphe Nuclei of Sham and PD Rats." American Journal of Alzheimer's Disease & Other Dementiasr 32, no. 2 (2017): 73–81. http://dx.doi.org/10.1177/1533317516685425.

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The 5-hydroxytryptamine (5-HT; serotonin) neurotransmission is severely affected by the degeneration of nigrostriatal dopaminergic neurons. Here, we report the effects of the systemic administration of the 5-HT7 receptor agonist AS-19. In sham rats, the mean response of the 5-HT neurons in the dorsal raphe nucleus (DRN) to systemic AS-19 was excitatory and the mean response of the γ-aminobutyric acid (GABA) interneurons was inhibitory. In Parkinson disease (PD) rats, the same dose did not affect the 5-HT neurons and only high doses (640 μg/kg intravenous) were able to the increase GABA interne

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34

Lee, Tony Tung-Yin, Cheng-Fang Tsai, Tsung-Hsun Hsieh, et al. "Ectopic Pregnancy-Derived Human Trophoblastic Stem Cells Regenerate Dopaminergic Nigrostriatal Pathway to Treat Parkinsonian Rats." PLoS ONE 7, no. 12 (2012): e52491. http://dx.doi.org/10.1371/journal.pone.0052491.

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35

Johnston, Louisa C., Jamie Eberling, Philip Pivirotto, Piotr Hadaczek, Howard J. Federoff, and John Forsayeth. "Clinically relevant effects of AAV2-GDNF on the dopaminergic nigrostriatal pathway in aged Rhesus monkeys." Human Gene Therapy, ja (January 21, 2009): 090121133514017. http://dx.doi.org/10.1089/hgt.2008.137.

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36

Przedbroski, S., M. Leviver, H. Jiang, et al. "Dose-dependent lesions of the dopaminergic nigrostriatal pathway induced by instrastriatal injection of 6-hydroxydopamine." Neuroscience 67, no. 3 (1995): 631–47. http://dx.doi.org/10.1016/0306-4522(95)00066-r.

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37

Toledo-Aral, Juan J., Simón Méndez-Ferrer, Ricardo Pardal, Miriam Echevarrı́a, and José López-Barneo. "Trophic Restoration of the Nigrostriatal Dopaminergic Pathway in Long-Term Carotid Body-Grafted Parkinsonian Rats." Journal of Neuroscience 23, no. 1 (2003): 141–48. http://dx.doi.org/10.1523/jneurosci.23-01-00141.2003.

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Yu, Seong-Jin, Mikko Airavaara, Hui Shen, Jenny Chou, Brandon K. Harvey та Yun Wang. "Suppression of endogenous PPARγ increases vulnerability to methamphetamine-induced injury in mouse nigrostriatal dopaminergic pathway". Psychopharmacology 221, № 3 (2011): 479–92. http://dx.doi.org/10.1007/s00213-011-2595-7.

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39

Ingham, C. A., S. H. Hood, M. J. Mijnster, R. A. Baldock, and G. W. Arbuthnott. "Plasticity of striatopallidal terminals following unilateral lesion of the dopaminergic nigrostriatal pathway: a morphological study." Experimental Brain Research 116, no. 1 (1997): 39–49. http://dx.doi.org/10.1007/pl00005743.

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40

Kerkerian, Lydia, Olivier Bosler, Georges Pelletier, and André Nieoullon. "Striatal neuropeptide Y neurones are under the influence of the nigrostriatal dopaminergic pathway: Immunohistochemical evidence." Neuroscience Letters 66, no. 1 (1986): 106–12. http://dx.doi.org/10.1016/0304-3940(86)90174-6.

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41

Ünal, Bengi, Fulva Shah, Janish Kothari, and James M. Tepper. "Anatomical and electrophysiological changes in striatal TH interneurons after loss of the nigrostriatal dopaminergic pathway." Brain Structure and Function 220, no. 1 (2013): 331–49. http://dx.doi.org/10.1007/s00429-013-0658-8.

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42

Johnson, Michel, Donna M. Stone, Glen R. Hanson, and James W. Gibb. "Role of the dopaminergic nigrostriatal pathway in methamphetamine-induced depression of the neostriatal serotonergic system." European Journal of Pharmacology 135, no. 2 (1987): 231–34. http://dx.doi.org/10.1016/0014-2999(87)90616-9.

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43

Ingham, C. A., S. H. Hood, P. Taggart, and G. W. Arbuthnott. "Plasticity of Synapses in the Rat Neostriatum after Unilateral Lesion of the Nigrostriatal Dopaminergic Pathway." Journal of Neuroscience 18, no. 12 (1998): 4732–43. http://dx.doi.org/10.1523/jneurosci.18-12-04732.1998.

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44

Fujita, Kyota, Yusaku Nakabeppu, and Mami Noda. "Therapeutic Effects of Hydrogen in Animal Models of Parkinson's Disease." Parkinson's Disease 2011 (2011): 1–9. http://dx.doi.org/10.4061/2011/307875.

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Since the first description of Parkinson's disease (PD) nearly two centuries ago, a number of studies have revealed the clinical symptoms, pathology, and therapeutic approaches to overcome this intractable neurodegenerative disease. 1-methy-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 6-hydroxydopamine (6-OHDA) are neurotoxins which produce Parkinsonian pathology. From the animal studies using these neurotoxins, it has become well established that oxidative stress is a primary cause of, and essential for, cellular apoptosis in dopaminergic neurons. Here, we describe the mechanism whereby oxi

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45

Baldwin, Heather A., Pyry P. Koivula, Julie C. Necarsulmer, Keith W. Whitaker, and Brandon K. Harvey. "Step Sequence is a Critical Gait Parameter of Unilateral 6-OHDA Parkinson's Rat Models." Cell Transplantation 26, no. 4 (2017): 659–67. http://dx.doi.org/10.3727/096368916x693059.

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Parkinson's disease is a progressive neurological disorder, marked by the loss of dopaminergic neurons in the nigrostriatal pathway that leads to abnormal gait, rigidity, slowness of movement, and tremor. The ability to recapitulate and measure the neurological sequelae in rodent models of Parkinson's disease is important for studying and evaluating potential therapeutics. Individual variability in lesion severity and injury progression are key factors in the 6-hydroxydopamine model that require normalization when evaluating therapeutic effects. The gait parameters that were found to be affect

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Samiotaki, Gesthimani, Camilo Acosta, Shutao Wang, and Elisa E. Konofagou. "Enhanced Delivery and Bioactivity of the Neurturin Neurotrophic Factor through Focused Ultrasound—Mediated Blood—Brain Barrier Opening in vivo." Journal of Cerebral Blood Flow & Metabolism 35, no. 4 (2015): 611–22. http://dx.doi.org/10.1038/jcbfm.2014.236.

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The blood—brain barrier (BBB) constitutes a major obstacle in brain drug delivery. Focused ultrasound (FUS) in conjunction with microbubbles has been shown to open the BBB noninvasively, locally, and transiently to allow large molecules diffusion. Neurturin (NTN), a member of the glial-derived neurotrophic factor (GDNF) family, has been demonstrated to have neuroprotective and regenerative effects on dopaminergic neurons in vivo using invasive drug delivery methods. The brain's ascending nigrostriatal pathway is severely damaged in Parkinson's disease (PD), and therefore the substantia nigra (

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Mehta, Vivek, Murray Hong, Julian Spears, and Ivar Mendez. "Enhancement of graft survival and sensorimotor behavioral recovery in rats undergoing transplantation with dopaminergic cells exposed to glial cell line-derived neurotrophic factor." Neurosurgical Focus 7, no. 3 (1999): E6. http://dx.doi.org/10.3171/foc.1999.7.3.7.

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The goal of this study was to investigate the ability of fetal dopaminergic neurons to improve complex sensorimotor behavior. The authors obtained ventral mesencephalic tissue from 14-day-old rat fetuses. The cells were exposed to glial cell line-derived neurotrophic factor (GDNF) prior to transplantation into rats with unilateral 6-hydroxydopamine lesions of the dopaminergic nigrostriatal pathway. Animals that received 400,000 cells exposed to GDNF demonstrated significant improvement in contralateral forelimb function and showed improvement in rotational behavior faster than animals that rec

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Acton, Paul D., and P. David Mozley. "Single Photon Emission Tomography Imaging in Parkinsonian Disorders: A Review." Behavioural Neurology 12, no. 1-2 (2000): 11–27. http://dx.doi.org/10.1155/2000/914154.

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Parkinsonian symptoms are associated with a number of neurodegenerative disorders, such as Parkinson’s disease, multiple system atrophy and progressive supranuclear palsy. Pathological evidence has shown clearly that these disorders are associated with a loss of neurons, particularly in the nigrostriatal dopaminergic pathway. Positron emission tomography (PET) and single photon emission tomography (SPECT) now are able to visualise and quantify changes in cerebral blood flow, glucose metabolism, and dopaminergic function produced by parkinsonian disorders. Both PET and SPECT have become importa

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Sanjari Moghaddam, Hossein, Ameneh Zare-Shahabadi, Farzaneh Rahmani, and Nima Rezaei. "Neurotransmission systems in Parkinson’s disease." Reviews in the Neurosciences 28, no. 5 (2017): 509–36. http://dx.doi.org/10.1515/revneuro-2016-0068.

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AbstractParkinson’s disease (PD) is histologically characterized by the accumulation of α-synuclein particles, known as Lewy bodies. The second most common neurodegenerative disorder, PD is widely known because of the typical motor manifestations of active tremor, rigidity, and postural instability, while several prodromal non-motor symptoms including REM sleep behavior disorders, depression, autonomic disturbances, and cognitive decline are being more extensively recognized. Motor symptoms most commonly arise from synucleinopathy of nigrostriatal pathway. Glutamatergic, γ-aminobutyric acid (G

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Cui, M., R. Aras, W. V. Christian, et al. "The organic cation transporter-3 is a pivotal modulator of neurodegeneration in the nigrostriatal dopaminergic pathway." Proceedings of the National Academy of Sciences 106, no. 19 (2009): 8043–48. http://dx.doi.org/10.1073/pnas.0900358106.

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