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https://www.readbyqxmd.com/read/29051496/evidence-for-a-task-dependent-switch-in-subthalamo-nigral-basal-ganglia-signaling
#1
Jay J Jantz, Masayuki Watanabe, Ron Levy, Douglas P Munoz
Basal ganglia (BG) can either facilitate or inhibit movement through excitatory and inhibitory pathways; however whether these opposing signals are dynamically regulated during healthy behavior is not known. Here, we present compelling neurophysiological evidence from three complimentary experiments in non-human primates, indicating task-specific changes in tonic BG pathway weightings during saccade behavior with different cognitive demands. First, simultaneous local field potential recording in the subthalamic nucleus (STN; BG input) and substantia nigra pars reticulata (SNr; BG output) reveals task-dependent shifts in subthalamo-nigral signals...
October 19, 2017: Nature Communications
https://www.readbyqxmd.com/read/29050386/brain-monoamine-oxidase-b-and-a-in-human-parkinsonian-dopamine-deficiency-disorders
#2
Junchao Tong, Gausiha Rathitharan, Jeffrey H Meyer, Yoshiaki Furukawa, Lee-Cyn Ang, Isabelle Boileau, Mark Guttman, Oleh Hornykiewicz, Stephen J Kish
See Jellinger (doi:10.1093/awx190) for a scientific commentary on this article. The enzyme monoamine oxidases (B and A subtypes, encoded by MAOB and MAOA, respectively) are drug targets in the treatment of Parkinson's disease. Inhibitors of MAOB are used clinically in Parkinson's disease for symptomatic purposes whereas the potential disease-modifying effect of monoamine oxidase inhibitors is debated. As astroglial cells express high levels of MAOB, the enzyme has been proposed as a brain imaging marker of astrogliosis, a cellular process possibly involved in Parkinson's disease pathogenesis as elevation of MAOB in astrocytes might be harmful...
September 1, 2017: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/29037828/chemogenetic-modulation-of-cholinergic-interneurons-reveals-their-regulating-role-on-the-direct-and-indirect-output-pathways-from-the-striatum
#3
Patrick Aldrin-Kirk, Andreas Heuer, Daniella Rylander Ottosson, Marcus Davidsson, Bengt Mattsson, Tomas Björklund
The intricate balance between dopaminergic and cholinergic neurotransmission in the striatum has been thoroughly difficult to characterize. It was initially described as a seesaw with a competing function of dopamine versus acetylcholine. Recent technical advances however, have brought this view into question suggesting that the two systems work rather in concert with the cholinergic interneurons (ChIs) driving dopamine release. In this study, we have utilized two transgenic Cre-driver rat lines, a choline acetyl transferase ChAT-Cre transgenic rat and a novel double-transgenic tyrosine hydroxylase TH-Cre/ChAT-Cre rat to further elucidate the role of striatal ChIs in normal motor function and in Parkinson's disease...
October 13, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/29036383/nigral-stress-induced-dopamine-release-in-clinical-high-risk-and-antipsychotic-na%C3%A3-ve-schizophrenia
#4
Huai-Hsuan Tseng, Jeremy J Watts, Michael Kiang, Ivonne Suridjan, Alan A Wilson, Sylvain Houle, Pablo M Rusjan, Romina Mizrahi
Background: Striatal dopamine (DA) synthesis capacity and release are elevated in schizophrenia (SCZ) and its putative prodrome, the clinical high risk (CHR) state. Striatal DA function results from the activity of midbrain DA neurons projecting mainly from the substantia nigra (SN). Elevated stress-induced DA release in SCZ and CHR was observed in the striatum; however, whether it is also elevated in the SN is unclear. The current study aims to determine whether nigral DA release in response to a validated stress task is altered in CHR and in antipsychotic-naïve SCZ...
June 13, 2017: Schizophrenia Bulletin
https://www.readbyqxmd.com/read/29031913/chronic-pain-and-pain-processing-in-parkinson-s-disease
#5
REVIEW
Pierre J Blanchet, Christine Brefel-Courbon
Pain is experienced by the vast majority of patients living with Parkinson's disease. It is most often of nociceptive origin, but may also be ascribed to neuropathic (radicular or central) or miscellaneous sources. The recently validated King's Parkinson's Disease Pain Scale is based on 7 domains including musculoskeletal pain, chronic body pain (central or visceral), fluctuation-related pain, nocturnal pain, oro-facial pain, pain with discolouration/oedema/swelling, and radicular pain. The basal ganglia integrate incoming nociceptive information and contribute to coordinated motor responses in pain avoidance and nocifensive behaviors...
October 12, 2017: Progress in Neuro-psychopharmacology & Biological Psychiatry
https://www.readbyqxmd.com/read/29018335/a-connectomic-analysis-of-the-human-basal-ganglia-network
#6
Alberto Cacciola, Alessandro Calamuneri, Demetrio Milardi, Enricomaria Mormina, Gaetana Chillemi, Silvia Marino, Antonino Naro, Giuseppina Rizzo, Giuseppe Anastasi, Angelo Quartarone
The current model of basal ganglia circuits has been introduced almost two decades ago and has settled the basis for our understanding of basal ganglia physiology and movement disorders. Although many questions are yet to be answered, several efforts have been recently made to shed new light on basal ganglia function. The traditional concept of "direct" and "indirect" pathways, obtained from axonal tracing studies in non-human primates and post-mortem fiber dissection in the human brain, still retains a remarkable appeal but is somehow obsolete...
2017: Frontiers in Neuroanatomy
https://www.readbyqxmd.com/read/28978491/complement-receptor-3-mediates-nadph-oxidase-activation-and-dopaminergic-neurodegeneration-through-a-src-erk-dependent-pathway
#7
Liyan Hou, Ke Wang, Cong Zhang, Fuqiang Sun, Yuning Che, Xiulan Zhao, Dan Zhang, Huihua Li, Qingshan Wang
Microglial NADPH oxidase (Nox2) plays a key role in chronic neuroinflammation and related dopaminergic neurodegeneration in Parkinson's disease (PD). However, the mechanisms behind Nox2 activation remain unclear. Here, we revealed the critical role of complement receptor 3 (CR3), a microglia-specific pattern recognition receptor, in Nox2 activation and subsequent dopaminergic neurodegeneration by using paraquat and maneb-induced PD model. Suppression or genetic deletion of CR3 impeded paraquat and maneb-induced activation of microglial Nox2, which was associated with attenuation of dopaminergic neurodegeneration...
September 27, 2017: Redox Biology
https://www.readbyqxmd.com/read/28969384/the-l444p-gba1-mutation-enhances-alpha-synuclein-induced-loss-of-nigral-dopaminergic-neurons-in-mice
#8
Anna Migdalska-Richards, Michal Wegrzynowicz, Raffaella Rusconi, Giulio Deangeli, Donato A Di Monte, Maria G Spillantini, Anthony H V Schapira
Mutations in glucocerebrosidase 1 (GBA1) represent the most prevalent risk factor for Parkinson's disease. The molecular mechanisms underlying the link between GBA1 mutations and Parkinson's disease are incompletely understood. We analysed two aged (24-month-old) Gba1 mouse models, one carrying a knock-out mutation and the other a L444P knock-in mutation. A significant reduction of glucocerebrosidase activity was associated with increased total alpha-synuclein accumulation in both these models. Gba1 mutations alone did not alter the number of nigral dopaminergic neurons nor striatal dopamine levels...
October 1, 2017: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/28966738/olfactory-impairment-is-related-to-rem-sleep-deprivation-in-rotenone-model-of-parkinson-s-disease
#9
Mariana F Aurich, Lais S Rodrigues, Adriano D S Targa, Ana Carolina D Noseda, Flávia D W Cunha, Marcelo M S Lima
INTRODUCTION: Olfactory dysfunction affects about 85-90% of Parkinson's disease (PD) patients with severe deterioration in the ability of discriminate several types of odors. In addition, studies reported declines in olfactory performances during a short period of sleep deprivation. Besides, PD is also known to strongly affect the occurrence and maintenance of rapid eye movement (REM) sleep. METHODS: Therefore, we investigated the mechanisms involved on discrimination of a social odor (dependent on the vomeronasal system) and a non-social odor (related to the main olfactory pathway) in the rotenone model of PD...
January 2017: Sleep Science
https://www.readbyqxmd.com/read/28960595/spinal-lewy-body-pathology-in-older-adults-without-an-antemortem-diagnosis-of-parkinson-s-disease
#10
Aron S Buchman, Sukriti Nag, Sue E Leurgans, Jared Miller, Veronique G J M VanderHorst, David A Bennett, Julie A Schneider
OBJECTIVE: To test the hypothesis that Lewy body pathology (LBs) is present in the spinal cord of older community-dwelling adults without a clinical diagnosis of Parkinson's disease (PD). METHODS: We studied 162 prospective autopsies from older adults with PD (N=6) and without PD (N=156). We documented the presence of LBs in cerebrum and brainstem structures from each of the 6 regions used for Braak PD staging and 4 spinal cord levels (C5/6, T7, L4/5 and S4/5). Parkinsonism proximate to death was based on a previously validated measure present if 2 or more of the 4 signs of parkinsonism were present based on a modified version of the Unified Parkinson's Disease Rating Scale (UPDRS)...
September 28, 2017: Brain Pathology
https://www.readbyqxmd.com/read/28940353/repeated-dose-oral-n-acetylcysteine-in-parkinson-s-disease-pharmacokinetics-and-effect-on-brain-glutathione-and-oxidative-stress
#11
Lisa D Coles, Paul J Tuite, Gülin Öz, Usha R Mishra, Reena V Kartha, Kathleen M Sullivan, James C Cloyd, Melissa Terpstra
Parkinson's disease (PD) is associated with oxidative stress and decreased nigral glutathione (GSH), suggesting that therapies that boost GSH may have a disease-modifying effect. Intravenous administration of a high dose of N-acetylcysteine (NAC), a well-known antioxidant and GSH precursor, increases blood and brain GSH in individuals with PD and with Gaucher disease and in healthy controls. To characterize the pharmacokinetics of repeated high oral doses of NAC and their effect on brain and blood oxidative stress measures, we conducted a 4-week open-label prospective study of oral NAC in individuals with PD (n = 5) and in healthy controls (n = 3)...
September 22, 2017: Journal of Clinical Pharmacology
https://www.readbyqxmd.com/read/28927576/loss-of-microrna-7-regulation-leads-to-%C3%AE-synuclein-accumulation-and-dopaminergic-neuronal-loss-in%C3%A2-vivo
#12
Kirsty J McMillan, Tracey K Murray, Nora Bengoa-Vergniory, Oscar Cordero-Llana, Jane Cooper, Amy Buckley, Richard Wade-Martins, James B Uney, Michael J O'Neill, Liang F Wong, Maeve A Caldwell
Abnormal alpha-synuclein (α-synuclein) expression and aggregation is a key characteristic of Parkinson's disease (PD). However, the exact mechanism(s) linking α-synuclein to the other central feature of PD, dopaminergic neuron loss, remains unclear. Therefore, improved cell and in vivo models are needed to investigate the role of α-synuclein in dopaminergic neuron loss. MicroRNA-7 (miR-7) regulates α-synuclein expression by binding to the 3' UTR of the Synuclein Alpha Non A4 Component of Amyloid Precursor (SNCA) gene and inhibiting its translation...
October 4, 2017: Molecular Therapy: the Journal of the American Society of Gene Therapy
https://www.readbyqxmd.com/read/28924005/nigral-glutamatergic-neurons-control-the-speed-of-locomotion
#13
Dimitri Ryczko, Swantje Grätsch, Laura Schläger, Avo Keuyalian, Zakaria Boukhatem, Claudia Garcia, François Auclair, Ansgar Büschges, Réjean Dubuc
The mesencephalic locomotor region (MLR) plays a crucial role in locomotor control. In vertebrates, stimulation of the MLR at increasing intensities elicits locomotion of growing speed. This effect has been presumed to result from higher brain inputs activating the MLR like a dimmer switch. Here, we show in lampreys (Petromyzon marinus) of either sex that incremental stimulation of a region homologous to the mammalian substantia nigra pars compacta (SNc) evokes increasing activation of MLR cells with a graded increase in the frequency of locomotor movements...
October 4, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28920936/dopamine-induces-soluble-%C3%AE-synuclein-oligomers-and-nigrostriatal-degeneration
#14
Danielle E Mor, Elpida Tsika, Joseph R Mazzulli, Neal S Gould, Hanna Kim, Malcolm J Daniels, Shachee Doshi, Preetika Gupta, Jennifer L Grossman, Victor X Tan, Robert G Kalb, Kim A Caldwell, Guy A Caldwell, John H Wolfe, Harry Ischiropoulos
Parkinson's disease (PD) is defined by the loss of dopaminergic neurons in the substantia nigra and the formation of Lewy body inclusions containing aggregated α-synuclein. Efforts to explain dopamine neuron vulnerability are hindered by the lack of dopaminergic cell death in α-synuclein transgenic mice. To address this, we manipulated both dopamine levels and α-synuclein expression. Nigrally targeted expression of mutant tyrosine hydroxylase with enhanced catalytic activity increased dopamine levels without damaging neurons in non-transgenic mice...
September 18, 2017: Nature Neuroscience
https://www.readbyqxmd.com/read/28903492/editor-s-highlight-nlrp3-is-required-for-inflammatory-changes-and-nigral-cell-loss-resulting-from-chronic-intragastric-rotenone-exposure-in-mice
#15
Eileen M Martinez, Alison L Young, Yash R Patankar, Brent L Berwin, Li Wang, Katharine M von Herrmann, Jaclyn M Weier, Matthew C Havrda
Complex interactions between genetic and environmental factors are widely believed to underlie the incidence and progression of Parkinson's disease (PD). Rotenone is a naturally occurring metabolic toxin employed as an insecticide and piscicide identified as a risk factor for the development of PD in agricultural workers. The Nlrp3 inflammasome is an intracellular mediator that can initiate an inflammatory cascade in response to cellular stress. Reports by others indicating that NLRP3 expression was detectable in tissues obtained from Alzheimer's disease patients and that the PD-associated protein α-synuclein could activate inflammasomes in cultured glial cells, prompted us to test the prediction that Nlrp3 was required for the development of Parkinson's-like changes resulting from rotenone exposure in mice...
September 1, 2017: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/28900002/modeling-parkinson-s-disease-pathology-by-combination-of-fibril-seeds-and-%C3%AE-synuclein-overexpression-in-the-rat-brain
#16
Poonam Thakur, Ludivine S Breger, Martin Lundblad, Oi Wan Wan, Bengt Mattsson, Kelvin C Luk, Virginia M Y Lee, John Q Trojanowski, Anders Björklund
Although a causative role of α-synuclein (α-syn) is well established in Parkinson's disease pathogenesis, available animal models of synucleinopathy do not replicate the full range of cellular and behavioral changes characteristic of the human disease. This study was designed to generate a more faithful model of Parkinson's disease by injecting human α-syn fibril seeds into the rat substantia nigra (SN), in combination with adenoassociated virus (AAV)-mediated overexpression of human α-syn, at levels that, by themselves, are unable to induce acute dopamine (DA) neurodegeneration...
September 26, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28884460/potassium-channels-a-potential-therapeutic-target-for-parkinson-s-disease
#17
REVIEW
Xiaoyan Chen, Bao Xue, Jun Wang, Haixia Liu, Limin Shi, Junxia Xie
The pathogenesis of the second major neurodegenerative disorder, Parkinson's disease (PD), is closely associated with the dysfunction of potassium (K(+)) channels. Therefore, PD is also considered to be an ion channel disease or neuronal channelopathy. Mounting evidence has shown that K(+) channels play crucial roles in the regulations of neurotransmitter release, neuronal excitability, and cell volume. Inhibition of K(+) channels enhances the spontaneous firing frequency of nigral dopamine (DA) neurons, induces a transition from tonic firing to burst discharge, and promotes the release of DA in the striatum...
September 7, 2017: Neuroscience Bulletin
https://www.readbyqxmd.com/read/28881616/repetitive-transcranial-magnetic-stimulation-for-treatment-of-lactacystin-induced-parkinsonian-rat-model
#18
Maowen Ba, Guozhao Ma, Chao Ren, Xuwen Sun, Min Kong
The dysfunction of ubiquitin-proteasome system is an important pathogenesis in the neurodegenerative process of Parkinson's disease. Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive and potential method in treating Parkinson's disease. To investigate whether rTMS has neuroprotective effects in parkinsonian rat model induced by ubiquitin-proteasome system impairment, we gave rTMS daily for 4 weeks to proteasome inhibitor, lactacystin-induced parkinsonian rat model. Rotational behavior test demonstrated that rTMS obviously reduced apomorphine-induced turning number in parkinsonian rats...
August 1, 2017: Oncotarget
https://www.readbyqxmd.com/read/28822080/soluble-epoxide-hydrolase-inhibition-attenuates-mptp-induced-neurotoxicity-in-the-nigrostriatal-dopaminergic-system-involvement-of-%C3%AE-synuclein-aggregation-and-er-stress
#19
Hui-Ju Huang, Yi-Ting Wang, Hui-Ching Lin, Yi-Hsuan Lee, Anya Maan-Yuh Lin
Soluble epoxide hydrolase (sEH) is widely expressed in the mammalian brain and possesses dual enzymatic activities, including C-terminal epoxide hydrolase (C-EH) which degrades epoxyeicosatrienoic acid (EET), a beneficial arachidonic acid metabolite. In the present study, the neuroprotective effect of sEH inhibition on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurodegeneration of nigrostriatal dopaminergic system was investigated using genetic and pharmacological approaches. MPTP (15 mg/kg) was intraperitoneally injected in sEH knockout (KO) mice and C57BL/6J mice as wild-type (WT) mice...
August 18, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28811225/alpha-synuclein-ferrireductase-activity-is-detectible-in-vivo-is-altered-in-parkinson-s-disease-and-increases-the-neurotoxicity-of-dopal
#20
Jennifer S McDowall, Ioanna Ntai, Kevin C Honeychurch, John P Hart, Philippe Colin, Bernard L Schneider, David R Brown
The normal cellular role of α-synuclein is of potential importance in understanding diseases in which an aggregated form of the protein has been implicated. A potential loss or change in the normal function of α-synuclein could play a role in the aetiology of diseases such as Parkinson's disease. Recently, it has been suggested that α-synuclein could cause the enzymatic reduction of iron and a cellular increase in Fe(II) levels. Experiments were carried out to determine if such activity could be measured in vivo...
August 12, 2017: Molecular and Cellular Neurosciences
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