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Journal articles on the topic 'Nigro-striatal pathway'

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Published: 4 June 2021

Last updated: 1 February 2022

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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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11

Iannielli, Angelo, Giovanni Stefano Ugolini, Chiara Cordiglieri, Simone Bido, Alicia Rubio, Gaia Colasante, Marco Valtorta, Tommaso Cabassi, Marco Rasponi, and Vania Broccoli. "Reconstitution of the Human Nigro-striatal Pathway on-a-Chip Reveals OPA1-Dependent Mitochondrial Defects and Loss of Dopaminergic Synapses." Cell Reports 29, no. 13 (December 2019): 4646–56. http://dx.doi.org/10.1016/j.celrep.2019.11.111.

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12

Delli Pizzi, Stefano, Cosmo Rossi, Vincenzo Di Matteo, Ennio Esposito, Simone Guarnieri, Maria Addolorata Mariggiò, Raffaella Franciotti, et al. "Morphological and Metabolic Changes in the Nigro-Striatal Pathway of Synthetic Proteasome Inhibitor (PSI)-Treated Rats: A MRI and MRS Study." PLoS ONE 8, no. 2 (February 19, 2013): e56501. http://dx.doi.org/10.1371/journal.pone.0056501.

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13

Edwards III, Gamez, Armijo, Kramm, Morales, Taylor-Presse, Schulz, Soto, and Moreno-Gonzalez. "Peripheral Delivery of Neural Precursor Cells Ameliorates Parkinson’s Disease-Associated Pathology." Cells 8, no. 11 (October 30, 2019): 1359. http://dx.doi.org/10.3390/cells8111359.

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: Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by loss of motor control due to a wide loss of dopaminergic neurons along the nigro-striatal pathway. Some of the mechanisms that contribute to this cell death are inflammation, oxidative stress, and misfolded alpha-synuclein-induced toxicity. Current treatments are effective at managing the early motor symptoms of the disease, but they become ineffective over time and lead to adverse effects. Previous research using intracerebral stem cell therapy for treatment of PD has provided promising results; however, this method is very invasive and is often associated with unacceptable side effects. In this study, we used an MPTP-injected mouse model of PD and intravenously administered neural precursors (NPs) obtained from mouse embryonic and mesenchymal stem cells. Clinical signs and neuropathology were assessed. Female mice treated with NPs had improved motor function and reduction in the neuroinflammatory response. In terms of safety, there were no tumorigenic formations or any detectable adverse effect after treatment. Our results suggest that peripheral administration of stem cell-derived NPs may be a promising and safe therapy for the recovery of impaired motor function and amelioration of brain pathology in PD.

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14

Irvin, Dwain K., Deniz Kirik, Anders Björklund, and Lachlan H. Thompson. "In vivo gene delivery to proliferating cells in the striatum generated in response to a 6-hydroxydopamine lesion of the nigro-striatal dopamine pathway." Neurobiology of Disease 30, no. 3 (June 2008): 343–52. http://dx.doi.org/10.1016/j.nbd.2008.02.006.

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15

Andrés, Marı́a Estela, Katia Gysling, and Gonzalo Bustos. "Differential regulation of dopamine release by N-methyl-d-aspartate receptors in rat striatum after partial and extreme lesions of the nigro-striatal pathway." Brain Research 797, no. 2 (June 1998): 255–66. http://dx.doi.org/10.1016/s0006-8993(98)00381-3.

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16

Burbach, J. P. H., P. Cazorla, and M. P. Smidt. "Molecular players in the development and maintenance of mesencephalic dopamine systems." Acta Neuropsychiatrica 11, no. 2 (June 1999): 71–73. http://dx.doi.org/10.1017/s0924270800036206.

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Several psychiatric diseases are considered to be neuro-developmental disorders. Amongst these are schizophrenia and autism, in which genetic and environmental components have been indicated. In these disorders intrinsic molecular mechanisms of brain development may be deranged due to genetic predispositions, or modified by external influences. Brain development is a delicate process of well-tuned cellular proliferation and differentiation of multipotent neural progenitor cells driven by spatiotemporal cues. One of the fundamental mechanisms is the interaction between external signals, e.g. growth factors, and internal regulators, e.g. transcription factors. An important transmitter system involved in behavioural and affective functions relevant for psychiatric disorders is the mesencephalic dopamine (DA) system. The mesencephalic DA system is organized in two anatomically and functionally different systems. DA neurons in the ventral tegmental area project to the mesolimbic system and are mostly related to control of behaviour. It has been implicated in drug addiction and affective disorders like dipolar disorder and schizophrenia. The dopamine system of the substantia nigra (nigro-striatal pathway) is implicated in movement control. Degeneration of this system, as in Parkinson's disease, or altered function in tardive dyskinesia have highlighted its importance in human disease. Recent findings in molecular neurobiology have provided the first clues to molecular mechanisms involved in developing and mature DA neurons. These may have clinical implications in novel therapeutic strategies.

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17

Kuten, Jonathan, Adi Linevitz, Hedva Lerman, Nanette Freedman, Meir Kestenbaum, Tamara Shiner, Nir Giladi, and Einat Even-Sapir. "[18F] FDOPA PET may confirm the clinical diagnosis of Parkinson's disease by imaging the nigro-striatal pathway and the sympathetic cardiac innervation: Proof-of-concept study." Journal of Integrative Neuroscience 19, no. 3 (2020): 489. http://dx.doi.org/10.31083/j.jin.2020.03.196.

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18

Annese, V., María-Trinidad Herrero, M. Di Pentima, A. Gomez, L. Lombardi, C. M. Ros, V. De Pablos, E. Fernandez-Villalba, and Maria Egle De Stefano. "Metalloproteinase-9 contributes to inflammatory glia activation and nigro-striatal pathway degeneration in both mouse and monkey models of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinsonism." Brain Structure and Function 220, no. 2 (February 21, 2014): 703–27. http://dx.doi.org/10.1007/s00429-014-0718-8.

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19

Abarca, Jorge, and Gonzalo Bustos. "Differential regulation of glutamate, aspartate and γ-amino-butyrate release by N-methyl-d-aspartate receptors in rat striatum after partial and extensive lesions to the nigro-striatal dopamine pathway." Neurochemistry International 35, no. 1 (July 1999): 19–33. http://dx.doi.org/10.1016/s0197-0186(99)00029-7.

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20

Lyras, L., B. Y. Zeng, G. McKenzie, R. K. B. Pearce, B. Halliwell, and P. Jenner. "Chronic high dose L-DOPA alone or in combination with the COMT inhibitor entacapone does not increase oxidative damage or impair the function of the nigro-striatal pathway in normal cynomologus monkeys." Journal of Neural Transmission 109, no. 1 (January 1, 2002): 53–67. http://dx.doi.org/10.1007/s702-002-8236-2.

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21

Aebischer, P., S. R. Winn, P. A. Tresco, C. B. Jaeger, and L. A. Greene. "Transplantation of Polymer Encapsulated Neurotransmitter Secreting Cells: Effect of the Encapsulation Technique." Journal of Biomechanical Engineering 113, no. 2 (May 1, 1991): 178–83. http://dx.doi.org/10.1115/1.2891231.

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Deficits associated with neurological diseases may be improved by the transplantation within the brain lesioned target structure of polymer encapsulated cells releasing the missing neurotransmitter. Surrounding cells with a permselective membrane of appropriate molecular weight cut-off allows inward diffusion of nutrients and outward diffusion of neurotransmitters, but prevents immunoglobulins or immune cells from reaching the transplant. This technique therefore allows transplantation of postmitotic cells across species. It also permits neural grafting of transformed cell lines since the polymer capsule prevents the formation of tumors by physically sequestering the transplanted tissue. In the present study, we compared the ability of dopaminesecreting cells, encapsulated by 2 different methods, to reverse experimental Parkinson’s disease, a neurodegenerative disease characterized by motor disturbances due to a lack of dopamine within the striatum following degeneration of the dopaminergic nigro-striatal pathway. PC12 cells were loaded in polyelectrolyte-based microcapsules or thermoplastic-based macrocapsules and maintained in vitro or transplanted in a rat experimental Parkinson model for 4 weeks. Chemically-induced depolarization increased the in vitro release of dopamine from macrocapsules over time, while no increase in release was observed from microcapsules. Encapsulated PC12 cells were able to reduce lesion-induced rotational asymmetry in rats for at least 4 weeks, regardless of the encapsulation technique used. With both encapsulation methods, PC12 cell viability was greater in vivo than in vitro which suggests that the striatum releases trophic factors for PC12 cells. More brain tissue damage was observed with microcapsules than macrocapsules, possibly the result of the difficulty of manipulating the more fragile microcapsules. Material resembling alginate was observed in the brain parenchyma surrounding the microcapsules, whereas no structural changes were observed with poly (acrylonitrile vinyl chloride) based capsules 4 weeks post-implantation. This fact raises questions about the in vivo stability of polyelectrolyte-based capsules implanted in the nervous system. We conclude that the implantation of polymer-encapsulated cells may provide a means for long-term delivery of neurotransmitters providing adequate encapsulation technology.

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22

Iseki, Eizo, Wami Marui, Ryoko Yamamoto, Takashi Togo, Omi Katsuse, Masanori Kato, Takeshi Iwatsubo, Kenji Kosaka, and Heii Arai. "The nigro-striatal and nigro-amygdaloid pathways undergo different degeneration processes in brains of dementia with Lewy bodies." Neuroscience Letters 380, no. 1-2 (May 2005): 161–65. http://dx.doi.org/10.1016/j.neulet.2005.01.056.

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23

Paolini Paoletti, Federico, Lorenzo Gaetani, and Lucilla Parnetti. "The Challenge of Disease-Modifying Therapies in Parkinson’s Disease: Role of CSF Biomarkers." Biomolecules 10, no. 2 (February 19, 2020): 335. http://dx.doi.org/10.3390/biom10020335.

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The development of disease modifying strategies in Parkinson’s disease (PD) largely depends on the ability to identify suitable populations after accurate diagnostic work-up. Therefore, patient molecular profiling and disease subtyping are mandatory. Thus far, in clinical trials, PD has been considered to be a “single entity”. Conversely, in front of the common feature of nigro-striatal degeneration, PD is pathogenically heterogeneous with a series of several biological and molecular pathways that differently contribute to clinical development and progression. Currently available diagnostic criteria for PD mainly rely on clinical features and imaging biomarkers, thus missing to identify the contribution of pathophysiological pathways, also failing to catch abnormalities occurring in the early stages of disease. Cerebrospinal fluid (CSF) is a promising source of biomarkers, with the high potential for reflecting early changes occurring in PD brain. In this review, we provide an overview on CSF biomarkers in PD, discussing their association with different molecular pathways involved either in pathophysiology or progression in detail. Their potential application in the field of disease modifying treatments is also discussed.

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24

Cheng, Hsiao-Chun, and Robert E. Burke. "The WldSmutation delays anterograde, but not retrograde, axonal degeneration of the dopaminergic nigro-striatal pathwayin vivo." Journal of Neurochemistry 113, no. 3 (May 2010): 683–91. http://dx.doi.org/10.1111/j.1471-4159.2010.06632.x.

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25

Bastianetto, S., L. Rouquier, G. Perrault, and D. j. Sanger. "DTG-induced circling behaviour in rats may involve the interaction between σ sites and nigro-striatal dopaminergic pathways." Neuropharmacology 34, no. 3 (March 1995): 281–87. http://dx.doi.org/10.1016/0028-3908(94)00156-m.

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26

Duarte Azevedo, Marcelo, Sibilla Sander, and Liliane Tenenbaum. "GDNF, A Neuron-Derived Factor Upregulated in Glial Cells during Disease." Journal of Clinical Medicine 9, no. 2 (February 7, 2020): 456. http://dx.doi.org/10.3390/jcm9020456.

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In a healthy adult brain, glial cell line-derived neurotrophic factor (GDNF) is exclusively expressed by neurons, and, in some instances, it has also been shown to derive from a single neuronal subpopulation. Secreted GDNF acts in a paracrine fashion by forming a complex with the GDNF family receptor α1 (GFRα1), which is mainly expressed by neurons and can act in cis as a membrane-bound factor or in trans as a soluble factor. The GDNF/GFRα1 complex signals through interactions with the “rearranged during transfection” (RET) receptor or via the neural cell adhesion molecule (NCAM) with a lower affinity. GDNF can also signal independently from GFRα1 by interacting with syndecan-3. RET, which is expressed by neurons involved in several pathways (nigro–striatal dopaminergic neurons, motor neurons, enteric neurons, sensory neurons, etc.), could be the main determinant of the specificity of GDNF’s pro-survival effect. In an injured brain, de novo expression of GDNF occurs in glial cells. Neuroinflammation has been reported to induce GDNF expression in activated astrocytes and microglia, infiltrating macrophages, nestin-positive reactive astrocytes, and neuron/glia (NG2) positive microglia-like cells. This disease-related GDNF overexpression can be either beneficial or detrimental depending on the localization in the brain and the level and duration of glial cell activation. Some reports also describe the upregulation of RET and GFRα1 in glial cells, suggesting that GDNF could modulate neuroinflammation.

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27

Oakley, N. R., A. G. Hayes, and M. J. Sheehan. "Effect of typical and atypical neuroleptics on the behavioural consequences of activation by muscimol of mesolimbic and nigro-striatal dopaminergic pathways in the rat." Psychopharmacology 105, no. 2 (October 1991): 204–8. http://dx.doi.org/10.1007/bf02244310.

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28

"Study of the nigro-striatal dopaminergic pathway by microdialysis and HPLC with electrochemical detection." Journal of Neuroscience Methods 29, no. 3 (September 1989): 289. http://dx.doi.org/10.1016/0165-0270(89)90191-x.

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29

"Microdialysis studies of local apomorphine effects on dopamine release in the nigro-striatal pathway." Journal of Neuroscience Methods 29, no. 3 (September 1989): 290. http://dx.doi.org/10.1016/0165-0270(89)90193-3.

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30

Sabel, B. A., G. L. Dunbar, W. M. Butler, and D. G. Stein. "GM1 gangliosides stimulate neuronal reorganization and reduce rotational asymmetry after hemitransections of the nigro-striatal pathway." Experimental Brain Research 60, no. 1 (September 1985). http://dx.doi.org/10.1007/bf00237015.

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31

Escobar, Angélica P., Jonathan Martínez-Pinto, Francisco Silva-Olivares, Ramón Sotomayor-Zárate, and Pablo R. Moya. "Altered Grooming Syntax and Amphetamine-Induced Dopamine Release in EAAT3 Overexpressing Mice." Frontiers in Cellular Neuroscience 15 (June 21, 2021). http://dx.doi.org/10.3389/fncel.2021.661478.

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The excitatory amino acid transporter EAAT3 plays an important role in the neuronal uptake of glutamate regulating the activation of glutamate receptors. Polymorphisms in the gene-encoding EAAT3 have been associated with obsessive–compulsive disorder (OCD), although the mechanisms underlying this relationship are still unknown. We recently reported that mice with increased EAAT3 expression in forebrain neurons (EAAT3glo/CMKII) display behavioral and synaptic features relevant to OCD, including increased grooming, higher anxiety-like behavior and altered cortico-striatal synaptic function. The dopamine neurotransmitter system is implicated in ritualistic behaviors. Indeed, dopaminergic neurons express EAAT3, and mice lacking EAAT3 exhibit decreased dopamine release and decreased expression of the dopamine D1 receptor. Moreover, EAAT3 plays a role on the effect of the psychostimulant amphetamine. As such, we sought to determine if the OCD-like behavior in EAAT3glo/CMKII mice is accompanied by altered nigro-striatal dopaminergic transmission. The aim of this study was to analyze dopamine transmission both in basal conditions and after an acute challenge of amphetamine, using behavioral, neurochemical, molecular, and cellular approaches. We found that in basal conditions, EAAT3glo/CMKII mice performed more grooming events and that they remained in phase 1 of the grooming chain syntax compared with control littermates. Administration of amphetamine increased the number of grooming events in control mice, while EAAT3glo/CMKII mice remain unaffected. Interestingly, the grooming syntax of amphetamine-control mice resembled that of EAAT3glo/CMKII mice in basal conditions. Using in vivo microdialysis, we found decreased basal dopamine levels in EAAT3glo/CMKII compared with control mice. Unexpectedly, we found that after acute amphetamine, EAAT3glo/CMKII mice had a higher release of dopamine compared with that of control mice, suggesting that EAAT3 overexpression leads to increased dopamine releasability. To determine postsynaptic effect of EAAT3 overexpression over dopamine transmission, we performed Western blot analysis of dopaminergic proteins and found that EAAT3glo/CMKII mice have higher expression of D2 receptors, suggesting a higher inhibition of the indirect striatal pathway. Together, the data indicate that EAAT3 overexpression impacts on dopamine transmission, making dopamine neurons more sensitive to the effect of amphetamine and leading to a disbalance between the direct and indirect striatal pathways that favors the performance of repetitive behaviors.

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32

Patricio, Felipe, Alan Axel Morales-Andrade, Aleidy Patricio-Martínez, and Ilhuicamina Daniel Limón. "Cannabidiol as a Therapeutic Target: Evidence of its Neuroprotective and Neuromodulatory Function in Parkinson’s Disease." Frontiers in Pharmacology 11 (December 15, 2020). http://dx.doi.org/10.3389/fphar.2020.595635.

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The phytocannabinoids of Cannabis sativa L. have, since ancient times, been proposed as a pharmacological alternative for treating various central nervous system (CNS) disorders. Interestingly, cannabinoid receptors (CBRs) are highly expressed in the basal ganglia (BG) circuit of both animals and humans. The BG are subcortical structures that regulate the initiation, execution, and orientation of movement. CBRs regulate dopaminergic transmission in the nigro-striatal pathway and, thus, the BG circuit also. The functioning of the BG is affected in pathologies related to movement disorders, especially those occurring in Parkinson’s disease (PD), which produces motor and non-motor symptoms that involving GABAergic, glutamatergic, and dopaminergic neural networks. To date, the most effective medication for PD is levodopa (l-DOPA); however, long-term levodopa treatment causes a type of long-term dyskinesias, l-DOPA-induced dyskinesias (LIDs). With neuromodulation offering a novel treatment strategy for PD patients, research has focused on the endocannabinoid system (ECS), as it participates in the physiological neuromodulation of the BG in order to control movement. CBRs have been shown to inhibit neurotransmitter release, while endocannabinoids (eCBs) play a key role in the synaptic regulation of the BG. In the past decade, cannabidiol (CBD), a non-psychotropic phytocannabinoid, has been shown to have compensatory effects both on the ECS and as a neuromodulator and neuroprotector in models such as 6-hydroxydopamine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), and reserpine, as well as other PD models. Although the CBD-induced neuroprotection observed in animal models of PD has been attributed to the activation of the CB1 receptor, recent research conducted at a molecular level has proposed that CBD is capable of activating other receptors, such as CB2 and the TRPV-1 receptor, both of which are expressed in the dopaminergic neurons of the nigro-striatal pathway. These findings open new lines of scientific inquiry into the effects of CBD at the level of neural communication. Cannabidiol activates the PPARγ, GPR55, GPR3, GPR6, GPR12, and GPR18 receptors, causing a variety of biochemical, molecular, and behavioral effects due to the broad range of receptors it activates in the CNS. Given the low number of pharmacological treatment alternatives for PD currently available, the search for molecules with the therapeutic potential to improve neuronal communication is crucial. Therefore, the investigation of CBD and the mechanisms involved in its function is required in order to ascertain whether receptor activation could be a treatment alternative for both PD and LID.

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33

Patricio, Felipe, Alan Axel Morales-Andrade, Aleidy Patricio-Martínez, and Ilhuicamina Daniel Limón. "Cannabidiol as a Therapeutic Target: Evidence of its Neuroprotective and Neuromodulatory Function in Parkinson’s Disease." Frontiers in Pharmacology 11 (December 15, 2020). http://dx.doi.org/10.3389/fphar.2020.595635.

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Abstract:

The phytocannabinoids of Cannabis sativa L. have, since ancient times, been proposed as a pharmacological alternative for treating various central nervous system (CNS) disorders. Interestingly, cannabinoid receptors (CBRs) are highly expressed in the basal ganglia (BG) circuit of both animals and humans. The BG are subcortical structures that regulate the initiation, execution, and orientation of movement. CBRs regulate dopaminergic transmission in the nigro-striatal pathway and, thus, the BG circuit also. The functioning of the BG is affected in pathologies related to movement disorders, especially those occurring in Parkinson’s disease (PD), which produces motor and non-motor symptoms that involving GABAergic, glutamatergic, and dopaminergic neural networks. To date, the most effective medication for PD is levodopa (l-DOPA); however, long-term levodopa treatment causes a type of long-term dyskinesias, l-DOPA-induced dyskinesias (LIDs). With neuromodulation offering a novel treatment strategy for PD patients, research has focused on the endocannabinoid system (ECS), as it participates in the physiological neuromodulation of the BG in order to control movement. CBRs have been shown to inhibit neurotransmitter release, while endocannabinoids (eCBs) play a key role in the synaptic regulation of the BG. In the past decade, cannabidiol (CBD), a non-psychotropic phytocannabinoid, has been shown to have compensatory effects both on the ECS and as a neuromodulator and neuroprotector in models such as 6-hydroxydopamine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), and reserpine, as well as other PD models. Although the CBD-induced neuroprotection observed in animal models of PD has been attributed to the activation of the CB1 receptor, recent research conducted at a molecular level has proposed that CBD is capable of activating other receptors, such as CB2 and the TRPV-1 receptor, both of which are expressed in the dopaminergic neurons of the nigro-striatal pathway. These findings open new lines of scientific inquiry into the effects of CBD at the level of neural communication. Cannabidiol activates the PPARγ, GPR55, GPR3, GPR6, GPR12, and GPR18 receptors, causing a variety of biochemical, molecular, and behavioral effects due to the broad range of receptors it activates in the CNS. Given the low number of pharmacological treatment alternatives for PD currently available, the search for molecules with the therapeutic potential to improve neuronal communication is crucial. Therefore, the investigation of CBD and the mechanisms involved in its function is required in order to ascertain whether receptor activation could be a treatment alternative for both PD and LID.

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