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Calcium imaging: A versatile tool to examine Huntington's disease mechanisms and progression.
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- Frontiers in Neuroscience, 2022, v. 16, p. 1, doi. 10.3389/fnins.2022.1040113
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Dissociable effects of oxycodone on behavior, calcium transient activity, and excitability of dorsolateral striatal neurons.
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- Frontiers in Neural Circuits, 2022, v. 16, p. 01, doi. 10.3389/fncir.2022.983323
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Synaptic Dysfunction in Huntington's Disease: Lessons from Genetic Animal Models.
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- Neuroscientist, 2022, v. 28, n. 1, p. 20, doi. 10.1177/1073858420972662
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A bidirectional corticoamygdala circuit for the encoding and retrieval of detailed reward memories.
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- eLife, 2021, p. 1, doi. 10.7554/eLife.68617
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Mechanisms underlying the enhancement of γ‐aminobutyric acid responses in the external globus pallidus of R6/2 Huntington's disease model mice.
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- Journal of Neuroscience Research, 2020, v. 98, n. 11, p. 2349, doi. 10.1002/jnr.24710
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Cortical Network Dynamics Is Altered in Mouse Models of Huntington's Disease.
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- Cerebral Cortex, 2020, v. 30, n. 4, p. 2372, doi. 10.1093/cercor/bhz245
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Paroxysmal Discharges in Tissue Slices From Pediatric Epilepsy Surgery Patients: Critical Role of GABA<sub>B</sub> Receptors in the Generation of Ictal Activity.
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- Frontiers in Cellular Neuroscience, 2020, v. 14, p. 1, doi. 10.3389/fncel.2020.00054
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CYBER SECURITY INSURANCE--MITIGATING COMPLIANCE RISK UNDER THE DFARS AND OTHER FEDERAL REGULATIONS.
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- Contract Management, 2019, v. 59, n. 8, p. 42
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Complete but not partial inhibition of glutamate transporters exacerbates cortical excitability in the R6/2 mouse model of Huntington's disease.
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- CNS Neuroscience & Therapeutics, 2019, v. 25, n. 4, p. 509, doi. 10.1111/cns.13070
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Mutant huntingtin reduction in astrocytes slows disease progression in the BACHD conditional Huntington's disease mouse model.
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- Human Molecular Genetics, 2019, v. 28, n. 3, p. 487, doi. 10.1093/hmg/ddy363
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Striatal GABAergic interneuron dysfunction in the Q175 mouse model of Huntington's disease.
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- European Journal of Neuroscience, 2019, v. 49, n. 1, p. 79, doi. 10.1111/ejn.14283
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Cellular antiseizure mechanisms of everolimus in pediatric tuberous sclerosis complex, cortical dysplasia, and non–mTOR‐mediated etiologies.
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- Epilepsia Open, 2018, v. 3, n. 2, p. 180, doi. 10.1002/epi4.12253
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Neural Deletion of Glucose Transporter Isoform 3 Creates Distinct Postnatal and Adult Neurobehavioral Phenotypes.
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- Journal of Neuroscience, 2018, v. 38, n. 44, p. 9579, doi. 10.1523/JNEUROSCI.0503-18.2018
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Striatal Direct and Indirect Pathway Output Structures Are Differentially Altered in Mouse Models of Huntington's Disease.
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- Journal of Neuroscience, 2018, v. 38, n. 20, p. 4678, doi. 10.1523/JNEUROSCI.0434-18.2018
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Therapeutic effects of stem cells in rodent models of Huntington's disease: Review and electrophysiological findings.
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- CNS Neuroscience & Therapeutics, 2018, v. 24, n. 4, p. 329, doi. 10.1111/cns.12839
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Altered lactate metabolism in Huntington's disease is dependent on GLUT3 expression.
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- CNS Neuroscience & Therapeutics, 2018, v. 24, n. 4, p. 343, doi. 10.1111/cns.12837
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Basolateral Amygdala to Orbitofrontal Cortex Projections Enable Cue-Triggered Reward Expectations.
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- Journal of Neuroscience, 2017, v. 37, n. 35, p. 8374, doi. 10.1523/JNEUROSCI.0486-17.2017
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Quantitative electroencephalographic Biomarkers in Preclinical and Human Studies of Huntington's Disease: Are They Fit-for-Purpose for Treatment Development?
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- Frontiers in Neurology, 2017, v. 8, p. 1, doi. 10.3389/fneur.2017.00091
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Altered membrane properties and firing patterns of external globus pallidus neurons in the R6/2 mouse model of Huntington's disease.
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- Journal of Neuroscience Research, 2016, v. 94, n. 12, p. 1400, doi. 10.1002/jnr.23889
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Cholesterol-loaded nanoparticles ameliorate synaptic and cognitive function in Huntington's disease mice.
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- EMBO Molecular Medicine, 2015, v. 7, n. 12, p. 1547, doi. 10.15252/emmm.201505413
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Forebrain deletion of the dystonia protein torsinA causes dystonic-like movements and loss of striatal cholinergic neurons.
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- eLife, 2015, p. 1, doi. 10.7554/eLife.08352
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Basic Mechanisms of Epileptogenesis in Pediatric Cortical Dysplasia.
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- CNS Neuroscience & Therapeutics, 2015, v. 21, n. 2, p. 92, doi. 10.1111/cns.12345
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In Rasmussen Encephalitis, Hemichannels Associated with Microglial Activation are linked to Cortical Pyramidal Neuron Coupling: A Possible Mechanism for Cellular Hyperexcitability.
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- CNS Neuroscience & Therapeutics, 2015, v. 21, n. 2, p. 152, doi. 10.1111/cns.12352
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Neuronal targets for reducing mutant huntingtin expression to ameliorate disease in a mouse model of Huntington's disease.
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- Nature Medicine, 2014, v. 20, n. 5, p. 536, doi. 10.1038/nm.3514
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Targeted expression of μ-opioid receptors in a subset of striatal direct-pathway neurons restores opiate reward.
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- Nature Neuroscience, 2014, v. 17, n. 2, p. 254, doi. 10.1038/nn.3622
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Differential Synaptic and Extrasynaptic Glutamate-Receptor Alterations in Striatal Medium-Sized Spiny Neurons of Aged YAC128 Huntington's Disease Mice.
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- PLoS Currents, 2014, p. 138, doi. 10.1371/currents.hd.34957c4f8bd7cb1f5ec47381dfc811c3
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White Matter Loss in a Mouse Model of Periventricular Leukomalacia Is Rescued by Trophic Factors.
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- Brain Sciences (2076-3425), 2013, v. 3, n. 4, p. 1461, doi. 10.3390/brainsci3041461
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A failure in energy metabolism and antioxidant uptake precede symptoms of Huntington's disease in mice.
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- Nature Communications, 2013, v. 4, n. 12, p. 2917, doi. 10.1038/ncomms3917
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Drug-primed reinstatement of cocaine seeking in mice: increased excitability of medium-sized spiny neurons in the nucleus accumbens.
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- ASN Neuro (Portland Press Ltd.), 2013, v. 5, n. 4, p. 257, doi. 10.1042/AN20130015
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Drug-primed reinstatement of cocaine seeking in mice: increased excitability of mediumsized spiny neurons in the nucleus accumbens.
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- ASN Neuro (Portland Press Ltd.), 2013, v. 5, n. 4, p. 291, doi. 10.1042/an20130015
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Dopamine imbalance in Huntington's disease: a mechanism for the lack of behavioral flexibility.
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- Frontiers in Neuroscience, 2013, v. 7, p. 1, doi. 10.3389/fnins.2013.00114
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Multiple Sources of Striatal Inhibition Are Differentially Affected in Huntington's Disease Mouse Models.
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- Journal of Neuroscience, 2013, v. 33, n. 17, p. 7393, doi. 10.1523/JNEUROSCI.2137-12.2013
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Effects of the Pimelic Diphenylamide Histone Deacetylase Inhibitor HDACi 4b on the R6/2 and N171-82Q Mouse Models of Huntington's Disease.
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- PLoS Currents, 2013, p. 230, doi. 10.1371/currents.hd.ec3547da1c2a520ba959ee7bf8bdd202
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Dopamine-NMDA Receptor Interactions: Twenty Years Later.
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- Developmental Neuroscience, 2012, v. 34, n. 1, p. 2, doi. 10.1159/000338590
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Elevated tonic extracellular dopamine concentration and altered dopamine modulation of synaptic activity precede dopamine loss in the striatum of mice overexpressing human α-synuclein.
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- Journal of Neuroscience Research, 2011, v. 89, n. 7, p. 1091, doi. 10.1002/jnr.22611
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Differential Electrophysiological Changes in Striatal Output Neurons in Huntington's Disease.
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- Journal of Neuroscience, 2011, v. 31, n. 4, p. 1170, doi. 10.1523/JNEUROSCI.3539-10.2011
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Comparative study of cellular and synaptic abnormalities in brain tissue samples from pediatric tuberous sclerosis complex and cortical dysplasia type II.
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- Epilepsia (Series 4), 2010, v. 51, p. 160, doi. 10.1111/j.1528-1167.2010.02633.x
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Interneurons, GABA currents, and subunit composition of the GABA<sub>A</sub> receptor in type I and type II cortical dysplasia.
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- Epilepsia (Series 4), 2010, v. 51, p. 166, doi. 10.1111/j.1528-1167.2010.02634.x
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Dopamine and Glutamate in Huntington's Disease: A Balancing Act.
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- CNS Neuroscience & Therapeutics, 2010, v. 16, n. 3, p. 163, doi. 10.1111/j.1755-5949.2010.00134.x
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Dopamine modulation of excitatory currents in the striatum is dictated by the expression of D1 or D2 receptors and modified by endocannabinoids.
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- European Journal of Neuroscience, 2010, v. 31, n. 1, p. 14, doi. 10.1111/j.1460-9568.2009.07047.x
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Alterations in Cortical Excitation and Inhibition in Genetic Mouse Models of Huntington's Disease.
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- Journal of Neuroscience, 2009, v. 29, n. 33, p. 10371, doi. 10.1523/JNEUROSCI.1592-09.2009
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Assessment and surgical outcomes for mild type I and severe type II cortical dysplasia: A critical review and the UCLA experience.
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- Epilepsia (Series 4), 2009, v. 50, n. 6, p. 1310, doi. 10.1111/j.1528-1167.2008.01998.x
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Age-Dependent Alterations of Corticostriatal Activity in the YAC128 Mouse Model of Huntington Disease.
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- Journal of Neuroscience, 2009, v. 29, n. 8, p. 2414, doi. 10.1523/JNEUROSCI.5687-08.2009
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Differential Susceptibility to Excitotoxic Stress in YAC128 Mouse Models of Huntington Disease between Initiation and Progression of Disease.
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- Journal of Neuroscience, 2009, v. 29, n. 7, p. 2193, doi. 10.1523/JNEUROSCI.5473-08.2009
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Full-Length Human Mutant Huntingtin with a Stable Polyglutamine Repeat Can Elicit Progressive and Selective Neuropathogenesis in BACHD Mice.
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- Journal of Neuroscience, 2008, v. 28, n. 24, p. 6182, doi. 10.1523/JNEUROSCI.0857-08.2008
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- Article
Age-Dependent Alterations of Corticostriatal Activity in the YAC128 Mouse Model of Huntington Disease.
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- Journal of Neuroscience, 2008, p. 2414, doi. 10.1523/JNEUROSCI.5687-08.2009
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- Article
Differential electrophysiological properties of dopamine D1 and D2 receptor-containing striatal medium-sized spiny neurons.
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- European Journal of Neuroscience, 2008, v. 27, n. 3, p. 671, doi. 10.1111/j.1460-9568.2008.06038.x
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A Hypothesis Regarding the Pathogenesis and Epileptogenesis of Pediatric Cortical Dysplasia and Hemimegalencephaly Based on MRI Cerebral Volumes and NeuN Cortical Cell Densities.
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- Epilepsia (Series 4), 2007, v. 48, p. 74, doi. 10.1111/j.1528-1167.2007.01292.x
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Immature Neurons and GABA Networks May Contribute to Epileptogenesis in Pediatric Cortical Dysplasia.
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- Epilepsia (Series 4), 2007, v. 48, p. 79, doi. 10.1111/j.1528-1167.2007.01293.x
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Pathological cell-cell interactions are necessary for striatal pathogenesis in a conditional mouse model of Huntington's disease.
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- Molecular Neurodegeneration, 2007, v. 2, p. 8, doi. 10.1186/1750-1326-2-8
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