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Relevant bibliographies by topics / Nigro-striatal pathway

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Academic literature on the topic 'Nigro-striatal pathway'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Nigro-striatal pathway"

1

Darbin, Olivier, Xingxing Jin, Christof Von Wrangel, Kerstin Schwabe, Atsushi Nambu, Dean K. Naritoku, Joachim K. Krauss, and Mesbah Alam. "Neuronal Entropy-Rate Feature of Entopeduncular Nucleus in Rat Model of Parkinson’s Disease." International Journal of Neural Systems 26, no. 02 (February 21, 2016): 1550038. http://dx.doi.org/10.1142/s0129065715500380.

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The function of the nigro-striatal pathway on neuronal entropy in the basal ganglia (BG) output nucleus, i.e. the entopeduncular nucleus (EPN) was investigated in the unilaterally 6-hyroxydopamine (6-OHDA)-lesioned rat model of Parkinson’s disease (PD). In both control subjects and subjects with 6-OHDA lesion of dopamine (DA) the nigro-striatal pathway, a histological hallmark for parkinsonism, neuronal entropy in EPN was maximal in neurons with firing rates ranging between 15 and 25[Formula: see text]Hz. In 6-OHDA lesioned rats, neuronal entropy in the EPN was specifically higher in neurons with firing rates above 25[Formula: see text]Hz. Our data establishes that the nigro-striatal pathway controls neuronal entropy in motor circuitry and that the parkinsonian condition is associated with abnormal relationship between firing rate and neuronal entropy in BG output nuclei. The neuronal firing rates and entropy relationship provide putative relevant electrophysiological information to investigate the sensory-motor processing in normal condition and conditions such as movement disorders.

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2

Pangestiningsih, Tri Wahyu, Woro Danur Wendo, Yulfia Nelymalik Selan, Filphin Adolfin Amalo, Nemay Anggadewi Ndaong, and Victor Lenda. "Histological Features of Catecholaminergic Neuron in Substantia Nigra Induced by Paraquat Dichloride (1,1-dimethyl-4,4 bipyridinium) in Wistar Rat as A Model of Parkinson Disease." Indonesian Journal of Biotechnology 19, no. 1 (December 31, 2015): 91. http://dx.doi.org/10.22146/ijbiotech.8638.

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Paraquat dichloride has been used by farmers as a herbicide to kill the grass. On the other hand, paraquatdichloride is harmful if enters to the body, causing Parkinson’s disease, since it is disrupting dopamineproduction in the substantia nigra pars compacta or dopamine pathways Nigro striatal pathway. The studywas done to fi nd out the histological changes of catecholaminergic neurons and Nigro striatal pathway causedby paraquat dichloride treatment in Wistar rats as a model of Parkinson’s disease.Twenty-two Wistar rats 3,5 months old were divided into 4 groups, 5 rats each. Group I (control group)were injected with aquabidest, while groups II, III, and IV were injected intraperitoneally with paraquatdichloride in aquabidest, with the dosage 5 , 10 and 15 mg/kg bw respectively. The rats were injected onceper week for 6 weeks. Three days after the last injection, the rats were anesthetized using xylasin (2 mg/kg)and ketamine (20 mg/kg) intramuscularly, and then were intracardiac perfused using physiological saline asprerinse solution, followed by 10% buffered formalin solution as a fi xative. After animals were fi xed, the brainswere removed and embedded in paraffi n block and cut in 12 μm thickness for immunohistochemistry stainingusing tyrosine hydroxylase antibody. The results of staining then were observed under light microscope andanalyzed descriptively.The results showed that the catecholaminergic neurons were distributed in the substantia nigrapars compacta in all treatment groups, however, the cell density were found decreased only in group IV.Catecholaminergic neurons appear in the bipolar and multipolar form, while dopamine ‘Nigro striatal pathway’was found exist in all treatment groups. From our study, histologycally the decreased of catecholaminergicneurons is only found in rats that received paraquat dichloride in dose 15 mg/kg bw for 6 weeks.

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3

Barbagallo, Gaetano, Maria Sierra-Peña, Federico Nemmi, Anne Pavy-Le Traon, Wassilios G. Meissner, Olivier Rascol, and Patrice Péran. "Multimodal MRI assessment of nigro-striatal pathway in multiple system atrophy and Parkinson disease." Movement Disorders 31, no. 3 (December 17, 2015): 325–34. http://dx.doi.org/10.1002/mds.26471.

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4

PITTALUGA, A., P. VERSACE, M. MARCHI, and M. RAITERI. "[3]PIRENZEPINE BINDING IN RAT CORPUS STRIATUM DECREASES AFTER HEMITRANSECTION OF THE NIGRO-STRIATAL PATHWAY." Fundamental & Clinical Pharmacology 1, no. 5 (September 10, 1987): 317–25. http://dx.doi.org/10.1111/j.1472-8206.1987.tb00569.x.

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5

Kirshner, Michal, Ronit Galron, Dan Frenkel, Gil Mandelbaum, Yosef Shiloh, Zhao-Qi Wang, and Ari Barzilai. "Malfunctioning DNA Damage Response (DDR) Leads to the Degeneration of Nigro-Striatal Pathway in Mouse Brain." Journal of Molecular Neuroscience 46, no. 3 (September 16, 2011): 554–68. http://dx.doi.org/10.1007/s12031-011-9643-y.

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6

Monahan, J., Z. Ling, and P. M. Carvey. "Prenatal lipopolysaccharide (LPS) exposure alters the trophic environment of the developing nigro-striatal dopamine (DA) pathway." Brain, Behavior, and Immunity 24 (August 2010): S6—S7. http://dx.doi.org/10.1016/j.bbi.2010.07.020.

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7

SAVASTA, M., A. DUBOIS, and B. SCATTON. "LACK OF EVIDENCE FOR AXONAL TRANSPORT OF D1AND D2RECEPTORS IN THE NIGRO-STRIATAL PATHWAY OF THE RAT." Fundamental & Clinical Pharmacology 2, no. 6 (November 12, 1988): 499–507. http://dx.doi.org/10.1111/j.1472-8206.1988.tb00651.x.

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8

Galati, S., J. C. Moeller, and D. Ferrazzoli. "P3. Pathological synchronization of the rat basal ganglia following the functional blockade of the nigro-striatal pathway." Clinical Neurophysiology 123, no. 10 (October 2012): e102. http://dx.doi.org/10.1016/j.clinph.2012.03.053.

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9

Aluf, Yuval, Jacob Vaya, Soliman Khatib, Yelena Loboda, and John P. M. Finberg. "Selective inhibition of monoamine oxidase A or B reduces striatal oxidative stress in rats with partial depletion of the nigro-striatal dopaminergic pathway." Neuropharmacology 65 (February 2013): 48–57. http://dx.doi.org/10.1016/j.neuropharm.2012.08.023.

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10

Mizuta, Eiji, Hidehiko Nabatame, Akinori Akaike, Masashi Sasa, and Shuji Takaori. "Differential supersensitization of dopamine D1 and D2 receptors after unilateral lesioning of the nigro-striatal pathway: studies on rotational behavior." Japanese Journal of Pharmacology 46 (1988): 239. http://dx.doi.org/10.1016/s0021-5198(19)57558-8.

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Dissertations / Theses on the topic "Nigro-striatal pathway"

1

O'Callaghan, John Francis Xavier. "Mechanisms in neurochemical modulation in the substantia nigra : an electrophysiological study." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260149.

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2

Schurig, Katja. "Tissue engineering for reconstructing the central dopaminergic nigro-striatal pathway in Parkinson’s disease: Cutting edge cell culture studies." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2013. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-112900.

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Although neurotransplantation of primary fetal cells into the striatum of patients with Parkinson’s disease (PD) has been reported to be effective, poor clinical outcome and severe side effects lower clinical long-term results. A major drawback of cell replacement therapies in PD is the low cell survival and lacking regeneration of the neuronal circuitries due to the ectopic transplantation of cells into the host striatum. More anatomic and functional integration could potentially be reached by an orthotopic cell transplantation into their natural position within the rostral mesencephalon at the site of the Substantia nigra, where dopaminergic cells get lost in PD. The aim of the thesis was to provide the scientific basis for the use of injectable bioscaffols containing chemo-attractants promoting cell survival, differentiation and axo-dendritic outgrowth of dopaminergic cells. With the so called “bridging” transplantation technology an artificial axon pathway between the substantia nigra and the striatum with targeted nigro-striatal re-innervation should be generated. Thereby, the central dopaminergic nigro-striatal pathway would be reconstructed enabling a fully integration of grafted neurons into the basal ganglia circuitries. The main focus of the thesis was to explore the influence of bioscaffolds on cell survival and morphology of dopaminergic neurons in vitro. The investigations included isolation of primary fetal mesencephalic cells and fetal mesencephalic neural stem cells (NSCs) from embryonic (E14) mouse brain and their culture on ECM compounds and starPEG-heparin hydrogels. Initial characterizations of the gels showed separate as well as simultaneous immobilization and release of growth factors demonstrating that hydrogels could serve as an efficient storage and delivery system for growth factors. The axo-dendritic outgrowth of dopaminergic cells including primary branching, total branching and neurite elongation; cell survival studies; cell type analysis and cell migration were analyzed by immunostaining. Both cell sources showed distinct growth properties depending on the stiffness of the gel material and the presence of biomolecules with increased cell survival by the presence of RGD and FGF-2 in the hydrogel independent of network characteristic. Moreover, the presence of RGD on hydrogels was found to initiate differentiation of NSCs, whereas FGF-2 bound to hydrogels was shown to promote the viability of undifferentiated cells. Additionally, survival and axo-dendritic outgrowth of dopaminergic cells were observed to be affected by the gel properties: RGD or FGF-2 modification of hydrogels with intermediate network density showed the best results for dopaminergic growth. With the addition of GDNF to hydrogels the total amount of cells decreased strongly by an equal quantity of dead cells compared to FGF-2 bound hydrogels. Furthermore, differential effects were found for the survival of different brain cells depending on the growth factor which is loaded. GDNF was found to increase the survival of astrocytes, whereas FGF-2 bound to gels stimulated the viability of oligodendrocyte precursor cells. No differential effects were found for the survival of NSCs and mature neuronal cells on GDNF or FGF-2 bound gels. By showing the penetration of primary fetal mesencephalic cells expressing MMPs as endogenous endopeptidases into MMP-cleavable hydrogels, the potential biodegradability of the starPEG-heparin hydrogels was demonstrated. Together the findings provide the in vitro proof-of-principle data for combining dopaminergic neurons or predopaminergic NSCs with biomaterials for reconstructing the central dopaminergic nigro-striatal pathway by the “bridging” transplantation strategy as an alternative transplantation approach in PD. Further studies should focus on three-dimensional cell culture studies using starPEG-heparin hydrogels with cleavable peptide sequences and their functionalization with gradients of axon guidance molecules to selectively promote dopaminergic outgrowth.

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3

Schurig, Katja [Verfasser], Carsten [Akademischer Betreuer] Werner, and Alexander [Akademischer Betreuer] Storch. "Tissue engineering for reconstructing the central dopaminergic nigro-striatal pathway in Parkinson’s disease: Cutting edge cell culture studies / Katja Schurig. Gutachter: Carsten Werner ; Alexander Storch. Betreuer: Carsten Werner ; Alexander Storch." Dresden : Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2013. http://d-nb.info/1068152168/34.

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4

Schurig, Katja. "Tissue engineering for reconstructing the central dopaminergic nigro-striatal pathway in Parkinson’s disease: Cutting edge cell culture studies." Doctoral thesis, 2011. https://tud.qucosa.de/id/qucosa%3A26874.

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Abstract:

Although neurotransplantation of primary fetal cells into the striatum of patients with Parkinson’s disease (PD) has been reported to be effective, poor clinical outcome and severe side effects lower clinical long-term results. A major drawback of cell replacement therapies in PD is the low cell survival and lacking regeneration of the neuronal circuitries due to the ectopic transplantation of cells into the host striatum. More anatomic and functional integration could potentially be reached by an orthotopic cell transplantation into their natural position within the rostral mesencephalon at the site of the Substantia nigra, where dopaminergic cells get lost in PD. The aim of the thesis was to provide the scientific basis for the use of injectable bioscaffols containing chemo-attractants promoting cell survival, differentiation and axo-dendritic outgrowth of dopaminergic cells. With the so called “bridging” transplantation technology an artificial axon pathway between the substantia nigra and the striatum with targeted nigro-striatal re-innervation should be generated. Thereby, the central dopaminergic nigro-striatal pathway would be reconstructed enabling a fully integration of grafted neurons into the basal ganglia circuitries. The main focus of the thesis was to explore the influence of bioscaffolds on cell survival and morphology of dopaminergic neurons in vitro. The investigations included isolation of primary fetal mesencephalic cells and fetal mesencephalic neural stem cells (NSCs) from embryonic (E14) mouse brain and their culture on ECM compounds and starPEG-heparin hydrogels. Initial characterizations of the gels showed separate as well as simultaneous immobilization and release of growth factors demonstrating that hydrogels could serve as an efficient storage and delivery system for growth factors. The axo-dendritic outgrowth of dopaminergic cells including primary branching, total branching and neurite elongation; cell survival studies; cell type analysis and cell migration were analyzed by immunostaining. Both cell sources showed distinct growth properties depending on the stiffness of the gel material and the presence of biomolecules with increased cell survival by the presence of RGD and FGF-2 in the hydrogel independent of network characteristic. Moreover, the presence of RGD on hydrogels was found to initiate differentiation of NSCs, whereas FGF-2 bound to hydrogels was shown to promote the viability of undifferentiated cells. Additionally, survival and axo-dendritic outgrowth of dopaminergic cells were observed to be affected by the gel properties: RGD or FGF-2 modification of hydrogels with intermediate network density showed the best results for dopaminergic growth. With the addition of GDNF to hydrogels the total amount of cells decreased strongly by an equal quantity of dead cells compared to FGF-2 bound hydrogels. Furthermore, differential effects were found for the survival of different brain cells depending on the growth factor which is loaded. GDNF was found to increase the survival of astrocytes, whereas FGF-2 bound to gels stimulated the viability of oligodendrocyte precursor cells. No differential effects were found for the survival of NSCs and mature neuronal cells on GDNF or FGF-2 bound gels. By showing the penetration of primary fetal mesencephalic cells expressing MMPs as endogenous endopeptidases into MMP-cleavable hydrogels, the potential biodegradability of the starPEG-heparin hydrogels was demonstrated. Together the findings provide the in vitro proof-of-principle data for combining dopaminergic neurons or predopaminergic NSCs with biomaterials for reconstructing the central dopaminergic nigro-striatal pathway by the “bridging” transplantation strategy as an alternative transplantation approach in PD. Further studies should focus on three-dimensional cell culture studies using starPEG-heparin hydrogels with cleavable peptide sequences and their functionalization with gradients of axon guidance molecules to selectively promote dopaminergic outgrowth.

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Book chapters on the topic "Nigro-striatal pathway"

1

Cruz-Sánchez, F. F., A. Cardozo, C. Castejón, E. Tolosa, and M. L. Rossi. "Aging and the nigro-striatal pathway." In Dementia in Parkinsonism, 9–25. Vienna: Springer Vienna, 1997. http://dx.doi.org/10.1007/978-3-7091-6846-2_2.

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2

Oakley, N. R., and M. J. Sheehan. "The Effect of Haloperidol and Clozapine on the Behavioural Consequences of Stimulating Mesolimbic and Nigro-Striatal Dopaminergic Pathways in the Rat." In Animal Models in Psychopharmacology, 285–88. Basel: Birkhäuser Basel, 1991. http://dx.doi.org/10.1007/978-3-0348-6419-0_27.

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