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medium spiny neuron

Meg Waraczynski, Samantha Abbott, Alex V Schultz
Previous work in our laboratory has shown that stimulating D2 dopamine receptors in the central sublenticular extended amygdala (SLEAc) can render medial forebrain bundle (MFB) stimulation less rewarding. One of the many ways in which D2 stimulation could affect the activity status of SLEAc neurons is by indirectly blocking calcium ion (Ca(2+)) influx through CaV1.3 channels. He we directly investigate the effects of blocking CaV1.3 channels on the rewarding effect of MFB stimulation. In experiment one, CaV1...
October 12, 2016: Behavioural Brain Research
Daniel Enterría-Morales, Ivette López-López, José López-Barneo, Xavier d'Anglemont de Tassigny
Gender difference in Parkinson's disease (PD) suggests that female sex steroids may promote dopaminergic neuron survival and protect them from degeneration. The glial cell line-derived neurotrophic factor (GDNF) is believed to be dopaminotrophic; thus it is considered as a potential therapeutic target in PD. Additionally, GDNF is endogenously synthetized in the caudate/putamen of humans and striatum in rodents. A neuroprotective role of estrogens on the nigrostriatal pathway via the stimulation of GDNF has been proposed...
2016: PloS One
Yoshiro Tomimatsu, Diana Cash, Motohisa Suzuki, Kazunori Suzuki, Michel Bernanos, Camilla Simmons, Steven C R Williams, Haruhide Kimura
TAK-063 is a selective phosphodiesterase 10A (PDE10A) inhibitor that produces potent antipsychotic-like and pro-cognitive effects at 0.3mg/kg (26% PDE10A occupancy in rats) or higher in rodents through the balanced activation of the direct and indirect pathways of striatal medium spiny neurons (MSNs). In this study, we evaluated the specific binding of TAK-063 using in vitro autoradiography (ARG) and the modulation of brain activity using pharmacological magnetic resonance imaging (phMRI) and electroencephalography (EEG)...
October 8, 2016: Neuroscience
Wen-Juan Huang, Wei-Wei Chen, Xia Zhang
Huntington's disease (HD) is a frequent and incurable hereditary neurodegenerative disorder that impairs motor and cognitive functions. Mutations in huntingtin (HTT) protein, which is essential for neuronal development, lead to the development of HD. An increase in the number of CAG repeats within the HTT gene, which lead to an expansion of polyglutamine tract in the resulting mutated HTT protein, which is toxic, is the causative factor of HD. Although the molecular basis of HD is known, there is no known cure for this disease other than symptomatic relief treatment approaches...
October 2016: Experimental and Therapeutic Medicine
Paola C Bello-Medina, Gonzalo Flores, Gina L Quirarte, James L McGaugh, Roberto A Prado Alcalá
A growing body of evidence indicates that treatments that typically impair memory consolidation become ineffective when animals are given intense training. This effect has been obtained by treatments interfering with the neural activity of several brain structures, including the dorsal striatum. The mechanisms that mediate this phenomenon are unknown. One possibility is that intense training promotes the transfer of information derived from the enhanced training to a wider neuronal network. We now report that inhibitory avoidance (IA) induces mushroom spinogenesis in the medium spiny neurons (MSNs) of the dorsal striatum in rats, which is dependent upon the intensity of the foot-shock used for training; that is, the effect is seen only when high-intensity foot-shock is used in training...
October 3, 2016: Proceedings of the National Academy of Sciences of the United States of America
Tina Zimmermann, Floortje Remmers, Beat Lutz, Julia Leschik
Huntington's disease (HD) is characterized by fatal motoric failures induced by loss of striatal medium spiny neurons. Neuronal cell death has been linked to impaired expression and axonal transport of the neurotrophin BDNF (brain-derived neurotrophic factor). By transplanting embryonic stem cell-derived neural progenitors overexpressing BDNF, we combined cell replacement and BDNF supply as a potential HD therapy approach. Transplantation of purified neural progenitors was analyzed in a quinolinic acid (QA) chemical and two genetic HD mouse models (R6/2 and N171-82Q) on the basis of distinct behavioral parameters, including CatWalk gait analysis...
October 11, 2016: Stem Cell Reports
Allison M Keeler, Ellen Sapp, Kathryn Chase, Emily Sottosanti, Eric Danielson, Edith Pfister, Lorelei Stoica, Marian DiFiglia, Neil Aronin, Miguel Sena-Esteves
BACKGROUND: The genetic mutation in Huntington's disease (HD) is a CAG repeat expansion in the coding region of the huntingtin (Htt) gene. RNAi strategies have proven effective in substantially down-regulating Htt mRNA in the striatum through delivery of siRNAs or viral vectors based on whole tissue assays, but the extent of htt mRNA lowering in individual neurons is unknown. OBJECTIVE: Here we characterize the effect of an AAV9-GFP-miRHtt vector on Htt mRNA levels in striatal neurons of Q140/Q140 knock-in mice...
October 1, 2016: Journal of Huntington's Disease
Geetika Kharkwal, Daniela Radl, Robert Lewis, Emiliana Borrelli
The psychomotor effects of cocaine are mediated by dopamine (DA) through stimulation of striatal circuits. Gabaergic striatal medium spiny neurons (MSNs) are the only output of this pivotal structure in the control of movements. The majority of MSNs express either the DA D1 or D2 receptors (D1R, D2R). Studies have shown that the motor effect of cocaine depends on the DA-mediated stimulation of D1R-expressing MSNs (dMSNs), which is mirrored at the cellular level by stimulation of signaling pathways leading to phosphorylation of ERKs and induction of c-fos Nevertheless, activation of dMSNs by cocaine is necessary but not sufficient, and D2R signaling is required for the behavioral and cellular effects of cocaine...
October 11, 2016: Proceedings of the National Academy of Sciences of the United States of America
Meaghan Creed, Niels R Ntamati, Ramesh Chandra, Mary Kay Lobo, Christian Lüscher
Addiction is a disorder of behavioral symptoms including enhanced incentive salience of drug-associated cues, but also a negative affective state. Cocaine-evoked synaptic plasticity in the reward system, particularly the nucleus accumbens (NAc), drives drug-adaptive behavior. However, how information is integrated downstream of the NAc remains unclear. Here, we identify the ventral pallidum (VP) as a site of convergence of medium spiny neurons expressing dopamine (DA) receptor type 1 (D1-MSNs) and type 2 (D2-MSNs) of the NAc...
October 5, 2016: Neuron
Maarten Ooms, Bala Attili, Sofie Celen, Michel Koole, Alfons Verbruggen, Koen Van Laere, Guy Bormans
Phosphodiesterase 10A (PDE10A) is a key regulator of medium spiny neuron excitability. Therefore, it plays an important role in the regulation of motor, reward and cognitive processes. Despite the interest in PDE10A as a drug and PET imaging target, little is known about the regulation of PDE10A enzymatic activity. This study aimed to further investigate the role of cAMP in the regulation of PDE10A activity and PDE10A PET imaging. Using [(18) F]JNJ42259152 as radioligand, we investigated alterations in PDE10A binding secondary to changes in cAMP levels...
September 24, 2016: Journal of Neurochemistry
Tanuja Bordia, Danhui Zhang, Xiomara A Perez, Maryka Quik
Tardive dyskinesia (TD) is a drug-induced movement disorder that arises with antipsychotics. These drugs are the mainstay of treatment for schizophrenia and bipolar disorder, and are also prescribed for major depression, autism, attention deficit hyperactivity, obsessive compulsive and post-traumatic stress disorder. There is thus a need for therapies to reduce TD. The present studies and our previous work show that nicotine administration decreases haloperidol-induced vacuous chewing movements (VCMs) in rodent TD models, suggesting a role for the nicotinic cholinergic system...
September 19, 2016: Experimental Neurology
Kellie S Gross, Dieter D Brandner, Luis A Martinez, M Foster Olive, Robert L Meisel, Paul G Mermelstein
The group I metabotropic glutamate receptors (mGluR1a and mGluR5) are important modulators of neuronal structure and function. Although these receptors share common signaling pathways, they are capable of having distinct effects on cellular plasticity. We investigated the individual effects of mGluR1a or mGluR5 activation on dendritic spine density in medium spiny neurons in the nucleus accumbens (NAc), which has become relevant with the potential use of group I mGluR based therapeutics in the treatment of drug addiction...
2016: PloS One
Luz M Suarez, Oscar Solis, Carolina Aguado, Rafael Lujan, Rosario Moratalla
Dopamine depletion in Parkinson's disease (PD) produces dendritic spine loss in striatal medium spiny neurons (MSNs) and increases their excitability. However, the synaptic changes that occur in MSNs in PD, in particular those induced by chronic L-3,4-dihydroxyphenylalanine (L-DOPA) treatment, are still poorly understood. We exposed BAC-transgenic D1-tomato and D2-eGFP mice to PD and dyskinesia model paradigms, enabling cell type-specific assessment of changes in synaptic physiology and morphology. The distinct fluorescence markers allowed us to identify D1 and D2 MSNs for analysis using intracellular sharp electrode recordings, electron microscopy, and 3D reconstructions with single-cell Lucifer Yellow injections...
September 9, 2016: Cerebral Cortex
Sophie V Precious, Claire M Kelly, Nicholas D Allen, Anne E Rosser
There is preliminary evidence that implantation of primary fetal striatal cells provides functional benefit in patients with Huntington's disease, a neurodegenerative condition resulting in loss of medium-sized spiny neurons (MSN) of the striatum. Scarcity of primary fetal tissue means it is important to identify a renewable source of cells from which to derive donor MSNs. Embryonic stem (ES) cells, which predominantly default to telencephalic-like precursors in chemically defined medium (CDM), offer a potentially inexhaustible supply of cells capable of generating the desired neurons...
2016: Neurogenesis (Austin, Tex.)
Roy S Song, Rosa Tolentino, Eric A Sobie, Susana R Neves-Zaph
Dopamine (DA), a key striatal neuromodulator, increases synaptic strength by promoting membrane insertion and/or retention of α-amino-3-hydroxy- 5-methyl- 4-isoxazolepropionic acid receptors (AMPARs). This process is mediated by GluA1-AMPAR subunit phosphorylation by cyclic nucleotide signaling, making cyclic nucleotide phosphodiesterases (PDEs) potential regulators of synaptic strength. In the current study we examined the role of phosphodiesterase-2 (PDE2), a medium spiny neurons (MSNs)-enriched and cGMP-activated PDE, in AMPAR trafficking...
September 7, 2016: Journal of Biological Chemistry
Samira Ztaou, Nicolas Maurice, Jeremy Camon, Gaëlle Guiraudie-Capraz, Lydia Kerkerian-Le Goff, Corinne Beurrier, Martine Liberge, Marianne Amalric
UNLABELLED: Over the last decade, striatal cholinergic interneurons (ChIs) have reemerged as key actors in the pathophysiology of basal-ganglia-related movement disorders. However, the mechanisms involved are still unclear. In this study, we address the role of ChI activity in the expression of parkinsonian-like motor deficits in a unilateral nigrostriatal 6-hydroxydopamine (6-OHDA) lesion model using optogenetic and pharmacological approaches. Dorsal striatal photoinhibition of ChIs in lesioned ChAT(cre/cre) mice expressing halorhodopsin in ChIs reduces akinesia, bradykinesia, and sensorimotor neglect...
August 31, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Aura Carole Meirsman, Anne Robé, Alban de Kerchove d'Exaerde, Brigitte Lina Kieffer
GPR88 is an orphan G-protein-coupled receptor highly expressed in striatal dopamine D1 (receptor) R- and D2R-expressing medium spiny neurons. This receptor is involved in activity and motor responses, and we previously showed that this receptor also regulates anxiety-like behaviors. To determine whether GPR88 in D2R-expressing neurons contributes to this emotional phenotype, we generated conditional Gpr88 knock-out mice using adenosine A2AR (A2AR)-Cre-driven recombination, and compared anxiety-related responses in both total and A2AR-Gpr88 KO mice...
July 2016: ENeuro
Ravit Hadar, Mareike Voget, Valentina Vengeliene, Jens K Haumesser, Christoph van Riesen, Yosef Avchalumov, Rainer Spanagel, Christine Winter
Alcohol use disorder (AUD) is a severe chronic condition characterized by compulsive alcohol use, cravings and high relapse rates even after long periods of abstinence. It is suggested that alterations in neuronal network activity, especially in the reward pathway accompany or even mediate relapse behavior. Here we used a DSM-based rat model to map in a first set of experiments neurochemical alterations in the reward pathway during alcohol relapse. Compared to the abstinence condition, we found specific elevation of dopamine levels in the nucleus accumbens shell and the medial prefrontal cortex...
January 1, 2017: Behavioural Brain Research
Daniel T Christian, Xiaoting Wang, Eugenia L Chen, Lakshya K Sehgal, Michael N Ghassemlou, Julia J Miao, Derenik Estepanian, Cameron H Araghi, Grace E Stutzmann, Marina E Wolf
Chronic cocaine exposure influences the density and morphology of dendritic spines on medium spiny neurons (MSNs) in the nucleus accumbens (NAc), a critical brain region for cocaine craving. However, the relationship between spine plasticity and craving remains unclear. To study this relationship, we trained rats to self-administer cocaine using an extended-access regimen (6 h/day, 10 days); controls self-administered saline. Previously, a time-dependent intensification (incubation) of cue-induced cocaine craving has been demonstrated after withdrawal from this regimen; furthermore, Ca(2+)-permeable AMPA receptors (CP-AMPARs) increase in the NAc core after ~1 month of withdrawal and thereafter mediate the expression of incubated craving...
August 24, 2016: Neuropsychopharmacology: Official Publication of the American College of Neuropsychopharmacology
Magdalena Czeredys, Filip Maciąg, Axel Methner, Jacek Kuźnicki
Huntington's disease (HD) is a hereditary neurodegenerative disease caused by a polyglutamine expansion within the huntingtin (HTT) gene. One of the cellular functions that is dysregulated in HD is store-operated calcium entry (SOCE), a process in which the depletion of Ca(2+) from the endoplasmic reticulum (ER) induces Ca(2+) influx from the extracellular space. We detected an enhanced activity of SOC channels in medium spiny neurons (MSNs) from YAC128 mice, a transgenic model of HD, and investigated whether this could be reverted by tetrahydrocarbazoles...
August 20, 2016: Biochemical and Biophysical Research Communications
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