21 results match your criteria Basal ganglia[Journal]

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Evaluating and Managing Sleep Disorders in the Parkinson's Disease Clinic.

Basal Ganglia 2016 Aug 27;6(3):165-172. Epub 2016 May 27.

Johns Hopkins University, School of Medicine, Department of Neurology.

Parkinson's disease is a multi-systems neurodegenerative disorder that is characterized by a combination of motor and non-motor symptoms. Non-motor symptoms of Parkinson's disease comprise a variety of cognitive, neuropsychiatric, autonomic, sensory, and sleep complaints. Although sleep disruption represents one of the most common non-motor symptom complaints among Parkinson's disease patients, recommendations regarding effective evaluation and management strategies for this specific population remain limited. Read More

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http://dx.doi.org/10.1016/j.baga.2016.05.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5089171PMC

Striatal dopamine neurotransmission: regulation of release and uptake.

Basal Ganglia 2016 Aug;6(3):123-148

Depts of Neurosurgery & Neuroscience and Physiology, New York University School of Medicine, New York, NY, USA.

Dopamine (DA) transmission is governed by processes that regulate release from axonal boutons in the forebrain and the somatodendritic compartment in midbrain, and by clearance by the DA transporter, diffusion, and extracellular metabolism. We review how axonal DA release is regulated by neuronal activity and by autoreceptors and heteroreceptors, and address how quantal release events are regulated in size and frequency. In brain regions densely innervated by DA axons, DA clearance is due predominantly to uptake by the DA transporter, whereas in cortex, midbrain, and other regions with relatively sparse DA inputs, the norepinephrine transporter and diffusion are involved. Read More

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http://dx.doi.org/10.1016/j.baga.2016.02.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4850498PMC
August 2016
26 Reads

Lateralization of the Subthalamic Nucleus with Age in Parkinson's Disease.

Basal Ganglia 2016 Apr;6(2):83-88

Department of Neurosurgery, David Geffen School of Medicine, University of California Los Angeles, USA; Department of Bioengineering, David Geffen School of Medicine, University of California Los Angeles, USA; Neuroscience Interdepartmental Program, David Geffen School of Medicine, University of California Los Angeles, USA; Brain Research Institute, David Geffen School of Medicine, University of California Los Angeles, USA.

Age-related changes in subthalamic nucleus (STN) position have not been well characterized in patients with Parkinson's disease (PD). We report a systematic retrospective analysis of age-related changes in radiographic and final deep brain stimulator (DBS) STN coordinates in PD patients. The charts of 134 PD patients (97 males, 28-84 years) representing 255 STN were reviewed. Read More

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http://dx.doi.org/10.1016/j.baga.2016.01.003DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4755314PMC
April 2016
7 Reads

The Vulnerable Ventral Tegmental Area in Parkinson's Disease.

Basal Ganglia 2015 Aug;5(2-3):51-55

Department of Neurology, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, United States.

Introduction: The involvement of dopaminergic neurons in the ventral tegmental area (VTA) in Parkinson's disease (PD) has not been universally recognized by neuroscientists and neurologists. Here, we conduct a review of previous research documenting dopaminergic neuronal loss in both the substantia nigra pars compacta (SNpc) and VTA and add three new post-mortem PD cases to the literature.

Methods: PD and control brains were sectioned, stained for tyrosine hydroxylase, and cells in the SNpc and VTA were counted. Read More

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http://dx.doi.org/10.1016/j.baga.2015.06.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4523275PMC
August 2015
1 Read

Oscillatory Activity in Basal Ganglia and Motor Cortex in an Awake Behaving Rodent Model of Parkinson's Disease.

Basal Ganglia 2014 Apr;3(4):221-227

Neurophysiological Pharmacology Section, National Institute of Neurological Disorders and Stroke National Institutes of Health, Bethesda, MD20892-3702USA.

Exaggerated beta range (15-30 Hz) oscillatory activity is observed in the basal ganglia of Parkinson's disease (PD) patients during implantation of deep brain stimulation electrodes. This activity has been hypothesized to contribute to motor dysfunction in PD patients. However, it remains unclear how these oscillations develop and how motor circuits become entrained into a state of increased synchronization in this frequency range after loss of dopamine. Read More

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http://dx.doi.org/10.1016/j.baga.2013.12.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4319371PMC
April 2014
4 Reads

Potentiated gene regulation by methylphenidate plus fluoxetine treatment: Long-term gene blunting () and behavioral correlates.

Basal Ganglia 2014 Dec;4(3-4):109-116

Department of Cellular and Molecular Pharmacology, The Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064, USA.

Use of psychostimulants such as methylphenidate (Ritalin) in medical treatments and as cognitive enhancers in the healthy is increasing. Methylphenidate produces some addiction-related gene regulation in animal models. Recent findings show that combining selective serotonin reuptake inhibitor (SSRI) antidepressants such as fluoxetine with methylphenidate potentiates methylphenidate-induced gene regulation. Read More

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http://dx.doi.org/10.1016/j.baga.2014.10.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4267118PMC
December 2014
2 Reads
1 Citation

Dissociable effects of dopamine on learning and performance within sensorimotor striatum.

Basal Ganglia 2014 Jun;4(2):43-54

Movement Disorders Program, University of Michigan, Ann Arbor, Michigan 48109 ; Neuroscience Program, University of Michigan, Ann Arbor, Michigan 48109 ; Department of Psychology, University of Michigan, Ann Arbor, Michigan 48109.

Striatal dopamine is an important modulator of current behavior, as seen in the rapid and dramatic effects of dopamine replacement therapy in Parkinson Disease (PD). Yet there is also extensive evidence that dopamine acts as a learning signal, modulating synaptic plasticity within striatum to affect future behavior. Disentangling these "performance" and "learning" functions is important for designing effective, long-term PD treatments. Read More

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http://dx.doi.org/10.1016/j.baga.2013.11.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4058866PMC
June 2014
9 Reads

Abnormal Bursting as a Pathophysiological Mechanism in Parkinson's Disease.

Authors:
Cj Lobb

Basal Ganglia 2014 Apr;3(4):187-195

Dept. of Biology, Emory University, Atlanta GA 30322.

Despite remarkable advances in Parkinson's disease (PD) research, the pathophysiological mechanisms causing motor dysfunction remain unclear, possibly delaying the advent of new and improved therapies. Several such mechanisms have been proposed including changes in neuronal firing rates, the emergence of pathological oscillatory activity, increased neural synchronization, and abnormal bursting. This review focuses specifically on the role of abnormal bursting of basal ganglia neurons in PD, where a burst is a physiologically-relevant, transient increase in neuronal firing over some reference period or activity. Read More

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http://dx.doi.org/10.1016/j.baga.2013.11.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3979569PMC

Review: Modulation of striatal neuron activity by cyclic nucleotide signaling and phosphodiesterase inhibition.

Basal Ganglia 2013 Dec;3(3):137-146

Department of Neuroscience, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Road, North Chicago, IL, 60064, USA.

The cyclic nucleotides cAMP and cGMP are common signaling molecules synthesized in neurons following the activation of adenylyl or guanylyl cyclase. In the striatum, the synthesis and degradation of cAMP and cGMP is highly regulated as these second messengers have potent effects on the activity of striatonigral and striatopallidal neurons. This review will summarize the literature on cyclic nucleotide signaling in the striatum with a particular focus on the impact of cAMP and cGMP on the membrane excitability of striatal medium-sized spiny output neurons (MSNs). Read More

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http://dx.doi.org/10.1016/j.baga.2013.08.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3904398PMC
December 2013
2 Reads

LRRKing up the right trees? On figuring out the effects of mutant LRRK2 and other Parkinson's disease-related genes.

Authors:
Heinz Steiner

Basal Ganglia 2013 Jul;3(2):73-76

Department of Cellular and Molecular Pharmacology, The Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL 60064, USA.

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http://dx.doi.org/10.1016/j.baga.2013.04.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3780441PMC

Cannabinoids and value-based decision making: implications for neurodegenerative disorders.

Basal Ganglia 2012 Sep 28;2(3):131-138. Epub 2012 Jul 28.

Department of Anatomy and Neurosciences, Neuroscience Campus Amsterdam, VU university medical center, Amsterdam, the Netherlands.

In recent years, disturbances in cognitive function have been increasingly recognized as important symptomatic phenomena in neurodegenerative diseases, including Parkinson's Disease (PD). Value-based decision making in particular is an important executive cognitive function that is not only impaired in patients with PD, but also shares neural substrates with PD in basal ganglia structures and the dopamine system. Interestingly, the endogenous cannabinoid system modulates dopamine function and subsequently value-based decision making. Read More

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http://dx.doi.org/10.1016/j.baga.2012.06.005DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3496267PMC
September 2012
1 Read

Corticostriatal dysfunction and glutamate transporter 1 (GLT1) in Huntington's disease: interactions between neurons and astrocytes.

Basal Ganglia 2012 Jul;2(2):57-66

Program in Neuroscience and Department of Psychological and Brain Sciences, Indiana University, Bloomington, Indiana 47405.

Huntington's Disease (HD) is a fatally inherited neurodegenerative disorder caused by an expanded glutamine repeat in the N-terminal region of the huntingtin (HTT) protein. The result is a progressively worsening triad of cognitive, emotional, and motor alterations that typically begin in adulthood and end in death 10-20 years later. Autopsy of HD patients indicates massive cell loss in the striatum and its main source of input, the cerebral cortex. Read More

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http://dx.doi.org/10.1016/j.baga.2012.04.029DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3418680PMC
July 2012
1 Read

The primate thalamostriatal systems: Anatomical organization, functional roles and possible involvement in Parkinson's disease.

Basal Ganglia 2011 Nov;1(4):179-189

Yerkes National Primate Research Center, 954 Gatewood Road NE, Emory University Atlanta, GA 30329, USA; and Department of Neurology, School of Medicine, Emory University, 101 Woodruff Circle, Atlanta GA 30322 USA.

The striatum receives glutamatergic inputs from two main thalamostriatal systems that originate either from the centre median/parafascicular complex (CM/PF-striatal system) or the rostral intralaminar, midline, associative and relay thalamic nuclei (non-CM/PF-striatal system). These dual thalamostriatal systems display striking differences in their anatomical and, most likely, functional organization. The CM/PF-striatal system is topographically organized, and integrated within functionally segregated basal ganglia-thalamostriatal circuits that process sensorimotor, associative and limbic information. Read More

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http://dx.doi.org/10.1016/j.baga.2011.09.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3389803PMC
November 2011
4 Reads

Anatomy of Graft-induced Dyskinesias: Circuit Remodeling in the Parkinsonian Striatum.

Basal Ganglia 2012 Mar 11;2(1):15-30. Epub 2012 Feb 11.

Department of Translational Science and Molecular Medicine, Michigan State University, Grand Rapids, MI 49503.

The goal of researchers and clinicians interested in re-instituting cell based therapies for PD is to develop an effective and safe surgical approach to replace dopamine (DA) in individuals suffering from Parkinson's disease (PD). Worldwide clinical trials involving transplantation of embryonic DA neurons into individuals with PD have been discontinued because of the often devastating post-surgical side-effect known as graft-induced dyskinesia (GID). There have been many review articles published in recent years on this subject. Read More

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http://dx.doi.org/10.1016/j.baga.2012.01.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3375918PMC
March 2012
5 Reads

Regulation of striatal dopamine release by presynaptic auto- and heteroreceptors.

Basal Ganglia 2012 Mar;2(1):5-13

Department of Psychiatry and Neurology, Columbia University, New York.

Striatal dopamine neurotransmission is critical for normal voluntary movement, affect and cognition. Dysfunctions of its regulation are implicated in a broad range of behaviors and disorders including Parkinson's disease, schizophrenia and drug abuse. Extracellular dopamine levels result from a dynamic equilibrium between release and reuptake by dopaminergic terminals. Read More

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http://dx.doi.org/10.1016/j.baga.2011.11.004DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3375990PMC

The mesopontine rostromedial tegmental nucleus: an integrative modulator of the reward system.

Basal Ganglia 2011 Nov;1(4):191-200

Department of Pharmacological and Physiological Science, Saint Louis University School of Medicine, 1402 S. Grand Blvd., Saint Louis, Missouri 63104.

The mesopontine rostromedial tegmental nucleus (RMTg) is a newly discovered brain structure thought to profoundly influence reward-related pathways. The RMTg is prominently GABAergic, receives dense projections from the lateral habenula and projects strongly to the midbrain ventral tegmental area and substantia nigra compacta. It receives additional afferent connections from widespread brain structures and sends additional strong efferent connections to a number of non-dopaminergic brainstem structures and, to a lesser extent, the forebrain. Read More

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http://dx.doi.org/10.1016/j.baga.2011.08.003DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3233474PMC
November 2011

Subsets of Spiny Striosomal Striatal Neurons Revealed in the Gad1-GFP BAC Transgenic Mouse.

Basal Ganglia 2011 Nov;1(4):201-211

Laboratory for Integrative Neuroscience, National Institute of Alcohol Abuse and Alcoholism, Rockville, MD.

OBJECTIVE: To characterize GFP-expressing cells in the striatum of Cb6-Tg(Gad1-EGFP)G42Zjh/J mice, in which the Gad1 (also referred to as GAD67) promoter drives GFP expression (Gad1-GFP mouse). BACKGROUND: GFP-expressing cells of the GAD1-GFP mouse have been described to be a population of parvalbumin-positive basket interneurons residing in the cerebral cortex and the cerebellum. However, the cells in the dorsal striatum of these mice have not been characterized. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S22105336110019
Publisher Site
http://dx.doi.org/10.1016/j.baga.2011.11.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3225898PMC
November 2011
1 Read

Linking cocaine to endoplasmic reticulum in striatal neurons: role of glutamate receptors.

Basal Ganglia 2011 Jul;1(2):59-63

Department of Biological Sciences, Pusan National University, Pusan 609-735, Korea.

The endoplasmic reticulum (ER) controls protein folding. Accumulation of unfolded and misfolded proteins in the ER triggers an ER stress response to accelerate normal protein folding or if failed to cause apoptosis. The ER stress response is a conserved cellular response in mammalian cells and is sensitive to various physiological or pathophysiological stimuli. Read More

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http://dx.doi.org/10.1016/j.baga.2011.05.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3146341PMC

GPR88 - a putative signaling molecule predominantly expressed in the striatum: Cellular localization and developmental regulation.

Basal Ganglia 2011 Jul;1(2):83-89

Department of Cellular and Molecular Pharmacology, Rosalind Franklin University of Medicine and Science/The Chicago Medical School, North Chicago, IL 60064, USA.

GPR88 is a putative G-protein-coupled receptor that is highly and almost exclusively expressed in the striatum. Its function remains unknown. We investigated GPR88 cellular localization and expression levels across development in different functional domains of the striatum in juvenile (P25), adolescent (P40), and adult (P70) rats, by in situ hybridization histochemistry. Read More

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http://dx.doi.org/10.1016/j.baga.2011.04.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3144573PMC
July 2011
1 Read
17 Citations

Deep-Brain Stimulation for Basal Ganglia Disorders.

Basal Ganglia 2011 Jul;1(2):65-77

Dept. Neurology, Emory University, Atlanta, GA.

The realization that medications used to treat movement disorders and psychiatric conditions of basal ganglia origin have significant shortcomings, as well as advances in the understanding of the functional organization of the brain, has led to a renaissance in functional neurosurgery, and particularly the use of deep brain stimulation (DBS). Movement disorders are now routinely being treated with DBS of 'motor' portions of the basal ganglia output nuclei, specifically the subthalamic nucleus and the internal pallidal segment. These procedures are highly effective and generally safe. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S22105336110010
Publisher Site
http://dx.doi.org/10.1016/j.baga.2011.05.001DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3144572PMC
July 2011
4 Reads

The Basal Ganglia as a Substrate for the Multiple Actions of Amphetamines.

Basal Ganglia 2011 Jul;1(2):49-57

Department of Neurosciences University of Toledo College of Medicine Toledo, Ohio 43614.

Amphetamines are psychostimulant drugs with high abuse potential. Acute and chronic doses of amphetamines affect dopamine (DA) neurotransmission in the basal ganglia. The basal ganglia are a group of subcortical nuclei that are anatomically positioned to integrate cognitive, motor and sensorimotor inputs from the cortex. Read More

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http://dx.doi.org/10.1016/j.baga.2011.05.003DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3144568PMC
July 2011
3 Reads
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