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[PMID]: 29427284
[Au] Autor:Gutierrez A; Williams MT; Vorhees CV
[Ad] Address:Division of Neurology, Deptarment of Pediatrics, University of Cincinnati College of Medicine and Cincinnati Children's Research Foundation, Cincinnati, OH, 45229, USA.
[Ti] Title:A Single High Dose of Methamphetamine Reduces Monoamines and Impairs Egocentric and Allocentric Learning and Memory in Adult Male Rats.
[So] Source:Neurotox Res;, 2018 Feb 09.
[Is] ISSN:1476-3524
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Methamphetamine (MA) alters dopamine markers and cognitive function in heavy users. In rodents, there are MA dosing regimens that induce concordant effects using repeated administration at spaced intervals. These regimens are effective but complicate experiments designed to disentangle the effects of the drug on different brain regions in relation to their cognitive effects because of treatment spacing. In an effort to simplify the model, we tested whether a single dose of MA could induce the same monoamine and cognitive effects as multiple, spaced dosing without affecting survival. Adult male Sprague-Dawley rats were treated with 40 mg/kg MA subcutaneously once and tested starting 2 weeks later. MA-treated rats showed deficits in egocentric navigation in Cincinnati water maze, in spatial navigation in the Morris water maze, and in choosing a consistent problem-solving strategy in the Star water maze when given the option to show a preference. MA-treated rats had persistent dopamine and serotonin reductions in the neostriatum and nucleus accumbens, and serotonin reductions in the hippocampus of the same magnitude as in repetitive treatment models. The data demonstrate that a single dose recapitulates the neurocognitive and monoamine effects of multiple-dose regimens, thereby simplifying the model of MA-induced neurotoxicity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180222
[Lr] Last revision date:180222
[St] Status:Publisher
[do] DOI:10.1007/s12640-018-9871-9

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[PMID]: 28462585
[Au] Autor:Ye Z; Hammer A; Münte TF
[Ad] Address:1 Department of Neurology, University of Lübeck , Lübeck, Germany .
[Ti] Title:Pramipexole Modulates Interregional Connectivity Within the Sensorimotor Network.
[So] Source:Brain Connect;7(4):258-263, 2017 May.
[Is] ISSN:2158-0022
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Pramipexole is widely prescribed to treat Parkinson's disease but has been reported to cause impulse control disorders such as pathological gambling. Recent neurocomputational models suggested that D2 agonists may distort functional connections between the striatum and the motor cortex, resulting in impaired reinforcement learning and pathological gambling. To examine how D2 agonists modulate the striatal-motor connectivity, we carried out a pharmacological resting-state functional magnetic resonance imaging study with a double-blind randomized within-subject crossover design. We analyzed the medication-induced changes of network connectivity and topology with two approaches, an independent component analysis (ICA) and a graph theoretical analysis (GTA). The ICA identified the sensorimotor network (SMN) as well as other classical resting-state networks. Within the SMN, the connectivity between the right caudate nucleus and other cortical regions was weaker under pramipexole than under placebo. The GTA measured the topological properties of the whole-brain network at global and regional levels. Both the whole-brain network under placebo and that under pramipexole were identified as small-world networks. The two whole-brain networks were similar in global efficiency, clustering coefficient, small-world index, and modularity. However, the degree of the right caudate nucleus decreased under pramipexole mainly due to the loss of the connectivity with the supplementary motor area, paracentral lobule, and precentral and postcentral gyrus of the SMN. The two network analyses consistently revealed that pramipexole weakened the functional connectivity between the caudate nucleus and the SMN regions.
[Mh] MeSH terms primary: Benzothiazoles/pharmacology
Dopamine Agonists/pharmacology
Neostriatum/drug effects
Sensorimotor Cortex/drug effects
[Mh] MeSH terms secundary: Adult
Brain/diagnostic imaging
Brain/drug effects
Brain/physiology
Cross-Over Studies
Double-Blind Method
Functional Neuroimaging
Healthy Volunteers
Humans
Male
Motor Cortex/diagnostic imaging
Motor Cortex/drug effects
Motor Cortex/physiology
Neostriatum/diagnostic imaging
Neostriatum/physiology
Neural Pathways/diagnostic imaging
Neural Pathways/drug effects
Neural Pathways/physiology
Sensorimotor Cortex/diagnostic imaging
Sensorimotor Cortex/physiology
Young Adult
[Pt] Publication type:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Name of substance:0 (Benzothiazoles); 0 (Dopamine Agonists); 83619PEU5T (pramipexole)
[Em] Entry month:1801
[Cu] Class update date: 180130
[Lr] Last revision date:180130
[Js] Journal subset:IM
[Da] Date of entry for processing:170503
[St] Status:MEDLINE
[do] DOI:10.1089/brain.2017.0484

  3 / 7259 MEDLINE  
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[PMID]: 27773571
[Au] Autor:Xie K; Colgan LA; Dao MT; Muntean BS; Sutton LP; Orlandi C; Boye SL; Boye SE; Shih CC; Li Y; Xu B; Smith RG; Yasuda R; Martemyanov KA
[Ad] Address:Department of Neuroscience, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL 33458, USA.
[Ti] Title:NF1 Is a Direct G Protein Effector Essential for Opioid Signaling to Ras in the Striatum.
[So] Source:Curr Biol;26(22):2992-3003, 2016 Nov 21.
[Is] ISSN:1879-0445
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:It is well recognized that G-protein-coupled receptors (GPCRs) can activate Ras-regulated kinase pathways to produce lasting changes in neuronal function. Mechanisms by which GPCRs transduce these signals and their relevance to brain disorders are not well understood. Here, we identify a major Ras regulator, neurofibromin 1 (NF1), as a direct effector of GPCR signaling via Gßγ subunits in the striatum. We find that binding of Gßγ to NF1 inhibits its ability to inactivate Ras. Deletion of NF1 in striatal neurons prevents the opioid-receptor-induced activation of Ras and eliminates its coupling to Akt-mTOR-signaling pathway. By acting in the striatal medium spiny neurons of the direct pathway, NF1 regulates opioid-induced changes in Ras activity, thereby sensitizing mice to psychomotor and rewarding effects of morphine. These results delineate a novel mechanism of GPCR signaling to Ras pathways and establish a critical role of NF1 in opioid addiction.
[Mh] MeSH terms primary: Analgesics, Opioid/metabolism
Neurofibromin 1/genetics
Receptors, G-Protein-Coupled/metabolism
Signal Transduction
ras Proteins/metabolism
[Mh] MeSH terms secundary: Animals
Female
Male
Mice
Neostriatum/metabolism
Neurofibromin 1/metabolism
Neurons/metabolism
Protein Binding
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Analgesics, Opioid); 0 (Neurofibromin 1); 0 (Receptors, G-Protein-Coupled); EC 3.6.5.2 (ras Proteins)
[Em] Entry month:1801
[Cu] Class update date: 180112
[Lr] Last revision date:180112
[Js] Journal subset:IM
[Da] Date of entry for processing:161025
[St] Status:MEDLINE

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[PMID]: 29196217
[Au] Autor:Rosas-Arellano A; Tejeda-Guzmán C; Lorca-Ponce E; Palma-Tirado L; Mantellero CA; Rojas P; Missirlis F; Castro MA
[Ad] Address:Instituto de Bioquímica y Microbiología, Facultad de Ciencias, Universidad Austral de Chile, Valdivia, Chile; Center for Interdisciplinary Studies on the Nervous System (CISNe), Universidad Austral de Chile, Valdivia, Chile; Departamento de Fisiología, Biofísica y Neurociencias, Cinvestav del IPN, C
[Ti] Title:Huntington's disease leads to decrease of GABA-A tonic subunits in the D2 neostriatal pathway and their relocalization into the synaptic cleft.
[So] Source:Neurobiol Dis;110:142-153, 2018 Feb.
[Is] ISSN:1095-953X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:GABA is a widely distributed inhibitory neurotransmitter. GABA-A receptors are hetero-pentameric channels assembled in multiple combinations from 19 available subunits; this diversity mediates phasic and tonic inhibitory synaptic potentials. Whereas GABA-A phasic receptors are located within the synaptic cleft, GABA-A tonic receptors are found peri- or extra-synaptically, where they are activated by diffusion of synaptic GABA release. In the neostriatum, GABA-A tonic subunits are present in the D2 medium-size spiny neurons. Since early impairment of these neurons is observed in Huntington's disease, we determined the ultrastructural localization of GABA-A-α5, -ß3, -δ, -ρ2 and, for the first time, of GABA-A-ρ3 subunits, in the D2 pathway of the YAC128 murine model of Huntington's disease at various stages of disease progression. We report mislocalization of all five subunits from peri- and extra-synaptic spaces into the synaptic clefts of YAC128 mice, present in diseased mice as early as 6 months-old. The synaptic localization of GABA-A tonic receptors correlated with increased sensitivity to pharmacologic antagonists during extracellular electrophysiological recordings in neostriatal slices. Finally, the association of GABA-A tonic receptors with the D2 pathway in 6-month-old mice was largely lost at 12 months of age.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 171230
[Lr] Last revision date:171230
[St] Status:In-Data-Review

  5 / 7259 MEDLINE  
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[PMID]: 29177427
[Au] Autor:Colom-Cadena M; Pegueroles J; Herrmann AG; Henstridge CM; Muñoz L; Querol-Vilaseca M; Martín-Paniello CS; Luque-Cabecerans J; Clarimon J; Belbin O; Núñez-Llaves R; Blesa R; Smith C; McKenzie CA; Frosch MP; Roe A; Fortea J; Andilla J; Loza-Alvarez P; Gelpi E; Hyman BT; Spires-Jones TL; Lleó A
[Ad] Address:Memory Unit, Department of Neurology, Institut d'Investigacions Biomèdiques Sant Pau - Hospital de Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain.
[Ti] Title:Synaptic phosphorylated α-synuclein in dementia with Lewy bodies.
[So] Source:Brain;140(12):3204-3214, 2017 Dec 01.
[Is] ISSN:1460-2156
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Dementia with Lewy bodies is characterized by the accumulation of Lewy bodies and Lewy neurites in the CNS, both of which are composed mainly of aggregated α-synuclein phosphorylated at Ser129. Although phosphorylated α-synuclein is believed to exert toxic effects at the synapse in dementia with Lewy bodies and other α-synucleinopathies, direct evidence for the precise synaptic localization has been difficult to achieve due to the lack of adequate optical microscopic resolution to study human synapses. In the present study we applied array tomography, a microscopy technique that combines ultrathin sectioning of tissue with immunofluorescence allowing precise identification of small structures, to quantitatively investigate the synaptic phosphorylated α-synuclein pathology in dementia with Lewy bodies. We performed array tomography on human brain samples from five patients with dementia with Lewy bodies, five patients with Alzheimer's disease and five healthy control subjects to analyse the presence of phosphorylated α-synuclein immunoreactivity at the synapse and their relationship with synapse size. Main analyses were performed in blocks from cingulate cortex and confirmed in blocks from the striatum of cases with dementia with Lewy bodies. A total of 1 318 700 single pre- or postsynaptic terminals were analysed. We found that phosphorylated α-synuclein is present exclusively in dementia with Lewy bodies cases, where it can be identified in the form of Lewy bodies, Lewy neurites and small aggregates (<0.16 µm3). Between 19% and 25% of phosphorylated α-synuclein deposits were found in presynaptic terminals mainly in the form of small aggregates. Synaptic terminals that co-localized with small aggregates of phosphorylated α-synuclein were significantly larger than those that did not. Finally, a gradient of phosphorylated α-synuclein aggregation in synapses (pre > pre + post > postsynaptic) was observed. These results indicate that phosphorylated α-synuclein is found at the presynaptic terminals of dementia with Lewy bodies cases mainly in the form of small phosphorylated α-synuclein aggregates that are associated with changes in synaptic morphology. Overall, our data support the notion that pathological phosphorylated α-synuclein may disrupt the structure and function of the synapse in dementia with Lewy bodies.
[Mh] MeSH terms primary: Gyrus Cinguli/metabolism
Lewy Body Disease/metabolism
Neostriatum/metabolism
Phosphoproteins/metabolism
Synapses/metabolism
alpha-Synuclein/metabolism
[Mh] MeSH terms secundary: Aged
Aged, 80 and over
Alzheimer Disease/metabolism
Brain/metabolism
Case-Control Studies
Female
Fluorescent Antibody Technique
Humans
Image Processing, Computer-Assisted
Immunohistochemistry
Male
Middle Aged
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Phosphoproteins); 0 (alpha-Synuclein)
[Em] Entry month:1712
[Cu] Class update date: 171213
[Lr] Last revision date:171213
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:171128
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awx275

  6 / 7259 MEDLINE  
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[PMID]: 29136290
[Au] Autor:Robles Gómez AA; Vega AV; Gónzalez-Sandoval C; Barral J
[Ad] Address:Neurociencias, UIICSE, FES Iztacala, UNAM, México.
[Ti] Title:The role of Ca -dependent K - channels at the rat corticostriatal synapses revealed by paired pulse stimulation.
[So] Source:Synapse;, 2017 Nov 14.
[Is] ISSN:1098-2396
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Potassium channels play an important role in modulating synaptic activity both at presynaptic and postsynaptic levels. We have shown before that presynaptically located K and K channels modulate the strength of corticostriatal synapses in rat brain, but the role of other types of potassium channels at these synapses remains largely unknown. Here, we show that calcium-dependent potassium channels BK-type but not SK-type channels are located presynaptically in corticostriatal synapses. We stimulated cortical neurons in rat brain slices and recorded postsynaptic excitatory potentials (EPSP) in medium spiny neurons (MSN) in dorsal neostriatum. By using a paired pulse protocol, we induced synaptic facilitation before applying either BK- or SK-specific toxins. Thus, we found that blockage of BK with iberiotoxin (10 nM) reduces synaptic facilitation and increases the amplitude of the EPSP, while exposure to SK-blocker apamin (100 nM) has no effect. Additionally, we induced train action potentials on striatal MSN by current injection before and after the exposure to K toxins. We found that the action potential becomes broader when the MSN is exposed to iberiotoxin, although it has no impact on frequency. In contrast, exposure to apamin results in loss of afterhyperpolarization phase and an increase of spike frequency. Therefore, we concluded that postsynaptic SK channels are involved in afterhyperpolarization and modulation of spike frequency while the BK channels are involved on the late repolarization phase of the action potential. Altogether, our results show that calcium-dependent potassium channels modulate both input towards and output from the striatum.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171122
[Lr] Last revision date:171122
[St] Status:Publisher
[do] DOI:10.1002/syn.22017

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[PMID]: 29107702
[Au] Autor:Wang AL; Fazari B; Chao OY; Nikolaus S; Trossbach SV; Korth C; Sialana FJ; Lubec G; Huston JP; Mattern C; de Souza Silva MA
[Ad] Address:Center for Behavioral Neuroscience, Institute of Experimental Psychology, Heinrich Heine University Düsseldorf, Germany. Electronic address: An-Li.Wang@uni-duesseldorf.de.
[Ti] Title:Intra-nasal dopamine alleviates cognitive deficits in tgDISC1 rats which overexpress the human DISC1 gene.
[So] Source:Neurobiol Learn Mem;146:12-20, 2017 Oct 28.
[Is] ISSN:1095-9564
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The Disrupted-in-Schizophrenia 1 (DISC1) gene has been associated with mental illnesses such as major depression and schizophrenia. The transgenic DISC1 (tgDISC1) rat, which overexpresses the human DISC1 gene, is known to exhibit deficient dopamine (DA) homeostasis. To ascertain whether the DISC1 gene also impacts cognitive functions, 14-15 months old male tgDISC1 rats and wild-type controls were subjected to the novel object preference (NOP) test and the object-based attention test (OBAT) in order to assess short-term memory (1 h), long-term memory (24 h), and attention. RESULTS: The tgDISC1 group exhibited intact short-term memory, but deficient long-term-memory in the NOP test and deficient attention-related behavior in the OBAT. In a different group of tgDISC1 rats, 3 mg/kg intranasally applied dopamine (IN-DA) or its vehicle was applied prior to the NOP or the OBAT test. IN-DA reversed cognitive deficits in both the NOP and OBAT tests. In a further cohort of tgDISC1 rats, post-mortem levels of DA, noradrenaline, serotonin and acetylcholine were determined in a variety of brain regions. The tgDISC1 group had less DA in the neostriatum, hippocampus and amygdala, less acetylcholine in neostriatum, nucleus accumbens, hippocampus, and amygdala, more serotonin in the nucleus accumbens, and less serotonin and noradrenaline in the amygdala. CONCLUSIONS: Our findings show that DISC1 overexpression and misassembly is associated with deficits in long-term memory and attention-related behavior. Since behavioral impairments in tgDISC1 rats were reversed by IN-DA, DA deficiency may be a major cause for the behavioral deficits expressed in this model.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171111
[Lr] Last revision date:171111
[St] Status:Publisher

  8 / 7259 MEDLINE  
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[PMID]: 29069396
[Au] Autor:Cisbani G; Maxan A; Kordower JH; Planel E; Freeman TB; Cicchetti F
[Ad] Address:Centre de Recherche du CHU de Québec-Université Laval, Axe Neurosciences, 2705 Boulevard Laurier, Québec, QC, Canada.
[Ti] Title:Presence of tau pathology within foetal neural allografts in patients with Huntington's and Parkinson's disease.
[So] Source:Brain;140(11):2982-2992, 2017 Nov 01.
[Is] ISSN:1460-2156
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Cell replacement has been explored as a therapeutic strategy to repair the brain in patients with Huntington's and Parkinson's disease. Post-mortem evaluations of healthy grafted tissue in such cases have revealed the development of Huntington- or Parkinson-like pathology including mutant huntingtin aggregates and Lewy bodies. An outstanding question remains if tau pathology can also be seen in patients with Huntington's and Parkinson's disease who had received foetal neural allografts. This was addressed by immunohistochemical/immunofluorescent stainings performed on grafted tissue of two Huntington's disease patients, who came to autopsy 9 and 12 years post-transplantation, and two patients with Parkinson's disease who came to autopsy 18 months and 16 years post-transplantation. We show that grafts also contain tau pathology in both types of transplanted patients. In two patients with Huntington's disease, the grafted tissue showed the presence of hyperphosphorylated tau [both AT8 (phospho-tau Ser202 and Thr205) and CP13 (pSer202) immunohistochemical stainings] pathological inclusions, neurofibrillary tangles and neuropil threads. In patients with Parkinson's disease, the grafted tissue was characterized by hyperphosphorylated tau (AT8; immunofluorescent staining) pathological inclusions, neurofibrillary tangles and neuropil threads but only in the patient who came to autopsy 16 years post-transplantation. Abundant tau-related pathology was observed in the cortex and striatum of all cases studied. While the striatum of the grafted Huntington's disease patient revealed an equal amount of 3-repeat and 4-repeat isoforms of tau, the grafted tissue showed elevated 4-repeat isoforms by western blot. This suggests that transplants may have acquired tau pathology from the host brain, although another possibility is that this was due to acceleration of ageing. This finding not only adds to the recent reports that tau pathology is a feature of these neurodegenerative diseases, but also that tau pathology can manifest in healthy neural tissue transplanted into the brains of patients with two distinct neurodegenerative disorders.
[Mh] MeSH terms primary: Allografts/pathology
Fetal Tissue Transplantation
Huntington Disease/pathology
Neostriatum/transplantation
Parkinson Disease/pathology
Protein Aggregation, Pathological/pathology
tau Proteins/metabolism
[Mh] MeSH terms secundary: Adult
Aged
Allografts/metabolism
Autopsy
Case-Control Studies
Child
Female
Humans
Huntington Disease/metabolism
Huntington Disease/therapy
Male
Middle Aged
Neostriatum/metabolism
Neostriatum/pathology
Parkinson Disease/metabolism
Parkinson Disease/therapy
Protein Aggregation, Pathological/metabolism
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (MAPT protein, human); 0 (tau Proteins)
[Em] Entry month:1711
[Cu] Class update date: 171107
[Lr] Last revision date:171107
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:171026
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awx255

  9 / 7259 MEDLINE  
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[PMID]: 29028815
[Au] Autor:Morales I; Sanchez A; Rodriguez-Sabate C; Rodriguez M
[Ad] Address:Laboratory of Neurobiology and Experimental Neurology, Department of Basic Medical Sciences, Faculty of Medicine, Universidad de La Laguna, La Laguna, Tenerife, Canary Islands, Spain.
[Ti] Title:Striatal astrocytes engulf dopaminergic debris in Parkinson's disease: A study in an animal model.
[So] Source:PLoS One;12(10):e0185989, 2017.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The role of astrocytes in Parkinson's disease is still not well understood. This work studied the astrocytic response to the dopaminergic denervation. Rats were injected in the lateral ventricles with 6-hydroxydopamine (25µg), inducing a dopaminergic denervation of the striatum not accompanied by non-selective tissue damage. The dopaminergic debris were found within spheroids (free-spheroids) which retained some proteins of dopaminergic neurons (e.g., tyrosine hydroxylase, the dopamine transporter protein, and APP) but not others (e.g., α-synuclein). Free-spheroids showed the initial (LC3-autophagosomes) but not the late (Lamp1/Lamp2-lysosomes) components of autophagy (incomplete autophagy), preparing their autophagosomes for an external phagocytosis (accumulation of phosphatidylserine). Free-spheroids were penetrated by astrocyte processes (fenestrated-spheroids) which made them immunoreactive for GFAP and S100ß, and which had some elements needed to continue the debris degradation (Lamp1/Lamp2). Finally, proteins normally found in neurons (TH, DAT and α-synuclein) were observed within astrocytes 2-5 days after the dopaminergic degeneration, suggesting that the intracellular contents of degenerated cells had been transferred to astrocytes. Taken together, present data suggest phagocytosis as a physiological role of striatal astrocytes, a role which could be critical for cleaning striatal debris during the initial stages of Parkinson's disease.
[Mh] MeSH terms primary: Astrocytes/metabolism
Dopamine/metabolism
Neostriatum/pathology
Parkinson Disease/pathology
[Mh] MeSH terms secundary: Animals
Astrocytes/drug effects
Disease Models, Animal
Male
Neostriatum/drug effects
Oxidopamine/pharmacology
Rats
Rats, Sprague-Dawley
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:8HW4YBZ748 (Oxidopamine); VTD58H1Z2X (Dopamine)
[Em] Entry month:1710
[Cu] Class update date: 171031
[Lr] Last revision date:171031
[Js] Journal subset:IM
[Da] Date of entry for processing:171014
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185989

  10 / 7259 MEDLINE  
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[PMID]: 28945119
[Au] Autor:Levitt JJ; Nestor PG; Levin L; Pelavin P; Lin P; Kubicki M; McCarley RW; Shenton ME; Rathi Y
[Ad] Address:From the Department of Psychiatry, Clinical Neuroscience Division, Laboratory of Neuroscience, VA Boston Healthcare System, Brockton Division, Brockton, Mass.; Harvard Medical School, Boston; the Department of Psychiatry, Psychiatry Neuroimaging Laboratory, Brigham and Women's Hospital, Harvard Medi
[Ti] Title:Reduced Structural Connectivity in Frontostriatal White Matter Tracts in the Associative Loop in Schizophrenia.
[So] Source:Am J Psychiatry;174(11):1102-1111, 2017 Nov 01.
[Is] ISSN:1535-7228
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: The striatum receives segregated and integrative white matter tracts from the cortex facilitating information processing in the cortico-basal ganglia network. The authors examined both types of input tracts in the striatal associative loop in chronic schizophrenia patients and healthy control subjects. METHOD: Structural and diffusion MRI scans were acquired on a 3-T system from 26 chronic schizophrenia patients and 26 matched healthy control subjects. Using FreeSurfer, the associative cortex was parcellated into ventrolateral prefrontal cortex and dorsolateral prefrontal cortex subregions. The striatum was manually parcellated into its associative and sensorimotor functional subregions. Fractional anisotropy and normalized streamlines, an estimate of fiber counts, were assessed in four frontostriatal tracts (dorsolateral prefrontal cortex-associative striatum, dorsolateral prefrontal cortex-sensorimotor striatum, ventrolateral prefrontal cortex-associative striatum, and ventrolateral prefrontal cortex-sensorimotor striatum). Furthermore, these measures were correlated with a measure of cognitive control, the Trail-Making Test, Part B. RESULTS: Results showed reduced fractional anisotropy and fewer streamlines in chronic schizophrenia patients for all four tracts, both segregated and integrative. Post hoc t tests showed reduced fractional anisotropy in the left ventrolateral prefrontal cortex-associative striatum and left ventrolateral prefrontal cortex-sensorimotor striatum and fewer normalized streamlines in the right dorsolateral prefrontal cortex-sensorimotor striatum and in the left and right ventrolateral prefrontal cortex-sensorimotor striatum in chronic schizophrenia patients. Furthermore, normalized streamlines in the right dorsolateral prefrontal cortex-sensorimotor striatum negatively correlated with Trail-Making Test, Part B, time spent in healthy control subjects but not in chronic schizophrenia patients. CONCLUSIONS: These findings demonstrated that structural connectivity is reduced in both segregated and integrative tracts in the striatal associative loop in chronic schizophrenia and that reduced normalized streamlines in the right-hemisphere dorsolateral prefrontal cortex-sensorimotor striatum predicted worse cognitive control in healthy control subjects but not in chronic schizophrenia patients, suggesting a loss of a "normal" brain-behavior correlation in chronic schizophrenia.
[Mh] MeSH terms primary: Neostriatum/diagnostic imaging
Prefrontal Cortex/diagnostic imaging
Schizophrenia/diagnostic imaging
White Matter/diagnostic imaging
[Mh] MeSH terms secundary: Adult
Anisotropy
Case-Control Studies
Diffusion Magnetic Resonance Imaging
Frontal Lobe/diagnostic imaging
Humans
Magnetic Resonance Imaging
Male
Middle Aged
Neural Pathways/diagnostic imaging
Trail Making Test
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1711
[Cu] Class update date: 171107
[Lr] Last revision date:171107
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:170926
[St] Status:MEDLINE
[do] DOI:10.1176/appi.ajp.2017.16091046


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