N-Methyl-D-Aspartate Receptor Channels Influence Dendritic Calcium Signaling in Nucleus Accumbens Medium Spiny Neurons – A Computational Study

2009 ◽  
pp. 1123-1126
Author(s):  
J. John ◽  
R. Manchanda
Keyword(s):  
Nucleus Accumbens ◽  
Calcium Signaling ◽  
Computational Study ◽  
Medium Spiny Neurons ◽  
Aspartate Receptor ◽  
Spiny Neurons

Cytoarchitectural impairments in the medium spiny neurons of the Nucleus Accumbens core of hyperactive juvenile rats

2010 ◽  
Vol 28 (6) ◽  
pp. 475-480 ◽  
Author(s):  
I. González-Burgos ◽  
S. García-Martínez ◽  
D.A. Velázquez-Zamora ◽  
R. Ponce-Rolón
Keyword(s):  
Nucleus Accumbens ◽  
Medium Spiny Neurons ◽  
Nucleus Accumbens Core ◽  
Juvenile Rats ◽  
Spiny Neurons ◽  
Accumbens Core

scholarly journals Microglial NFκB-TNFα hyperactivation induces obsessive–compulsive behavior in mouse models of progranulin-deficient frontotemporal dementia

2017 ◽  
Vol 114 (19) ◽  
pp. 5029-5034 ◽  
Author(s):  
Grietje Krabbe ◽  
S. Sakura Minami ◽  
Jon I. Etchegaray ◽  
Praveen Taneja ◽  
Biljana Djukic ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Frontotemporal Dementia ◽  
Knockout Mice ◽  
Nuclear Factor Κb ◽  
Medium Spiny Neurons ◽  
Obsessive Compulsive ◽  
Compulsive Disorder ◽  
Spiny Neurons ◽  
Increased Risk ◽  
Excessive Grooming

Frontotemporal dementia (FTD) is the second most common dementia before 65 years of age. Haploinsufficiency in the progranulin (GRN) gene accounts for 10% of all cases of familial FTD. GRN mutation carriers have an increased risk of autoimmune disorders, accompanied by elevated levels of tissue necrosis factor (TNF) α. We examined behavioral alterations related to obsessive–compulsive disorder (OCD) and the role of TNFα and related signaling pathways in FTD patients with GRN mutations and in mice lacking progranulin (PGRN). We found that patients and mice with GRN mutations displayed OCD and self-grooming (an OCD-like behavior in mice), respectively. Furthermore, medium spiny neurons in the nucleus accumbens, an area implicated in development of OCD, display hyperexcitability in PGRN knockout mice. Reducing levels of TNFα in PGRN knockout mice abolished excessive self-grooming and the associated hyperexcitability of medium spiny neurons of the nucleus accumbens. In the brain, PGRN is highly expressed in microglia, which are a major source of TNFα. We therefore deleted PGRN specifically in microglia and found that it was sufficient to induce excessive grooming. Importantly, excessive grooming in these mice was prevented by inactivating nuclear factor κB (NF-κB) in microglia/myeloid cells. Our findings suggest that PGRN deficiency leads to excessive NF-κB activation in microglia and elevated TNFα signaling, which in turn lead to hyperexcitability of medium spiny neurons and OCD-like behavior.

scholarly journals Sex-Specific Role for Egr3 in Nucleus Accumbens D2-Medium Spiny Neurons Following Long-Term Abstinence From Cocaine Self-administration

2020 ◽  
Vol 87 (11) ◽  
pp. 992-1000 ◽  
Author(s):  
Michel Engeln ◽  
Swarup Mitra ◽  
Ramesh Chandra ◽  
Utsav Gyawali ◽  
Megan E. Fox ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Specific Role ◽  
Medium Spiny Neurons ◽  
Self Administration ◽  
Spiny Neurons

scholarly journals Trafficking of calcium-permeable and calcium-impermeable AMPA receptors in nucleus accumbens medium spiny neurons co-cultured with prefrontal cortex neurons

2017 ◽  
Vol 116 ◽  
pp. 224-232 ◽  
Author(s):  
Craig T. Werner ◽  
Conor H. Murray ◽  
Jeremy M. Reimers ◽  
Niravkumar M. Chauhan ◽  
Kenneth K.Y. Woo ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Nucleus Accumbens ◽  
Ampa Receptors ◽  
Medium Spiny Neurons ◽  
Spiny Neurons

scholarly journals Presence of Inhibitory Glycinergic Transmission in Medium Spiny Neurons in the Nucleus Accumbens

2018 ◽  
Vol 11 ◽  
Author(s):  
Braulio Muñoz ◽  
Gonzalo E. Yevenes ◽  
Benjamin Förstera ◽  
David M. Lovinger ◽  
Luis G. Aguayo
Keyword(s):  
Nucleus Accumbens ◽  
Medium Spiny Neurons ◽  
Spiny Neurons

Pitx3 Deficiency in Mice Affects Cholinergic Modulation of GABAergic Synapses in the Nucleus Accumbens

2006 ◽  
Vol 96 (4) ◽  
pp. 2034-2041 ◽  
Author(s):  
Mischa de Rover ◽  
Johannes C. Lodder ◽  
Marten P. Smidt ◽  
Arjen B. Brussaard
Keyword(s):  
Nucleus Accumbens ◽  
Medium Spiny Neurons ◽  
Wild Type ◽  
Cholinergic Modulation ◽  
Firing Patterns ◽  
Neural Adaptations ◽  
Cholinergic Interneurons ◽  
Spiny Neurons ◽  
Gating Mechanism ◽  
Deficient Mice

We investigated to what extent Pitx3 deficiency, causing hyperdopaminergic transmission in the nucleus accumbens microcircuitry, may lead to developmental changes. First, spontaneous firing activity of cholinergic interneurons in the nucleus accumbens was recorded in vitro. Firing patterns in the Pitx3-deficient mice were more variable and intrinsically different from those observed in wild-type mice. Next, to test whether the irregular firing patterns observed in mutant mice affected the endogenous nicotinic modulation of the GABAergic input of medium spiny neurons, we recorded spontaneous GABAergic inputs to these cells before and after the application of the nicotinic receptor blocker mecamylamine. Effects of mecamylamine were found in slices of either genotype, but in a rather inconsistent manner. Possibly this was attributable to heterogeneity in firing of nearby cholinergic interneurons. Thus paired recordings of cholinergic interneurons and medium spiny neurons were performed to more precisely control the experimental conditions of the cholinergic modulation of GABAergic synaptic transmission. We found that controlling action potential firing in cholinergic neurons leads to a conditional increase in GABAergic input frequency in wild-type mice but not in Pitx3-deficient mice. We conclude that Pitx3-deficient mice have neural adaptations at the level of the nucleus accumbens microcircuitry that in turn may have behavioral consequences. It is discussed to what extent dopamine release in the nucleus accumbens may be a long-term gating mechanism leading to alterations in cholinergic transmission in the nucleus accumbens, in line with previously reported neural adaptations found as consequences of repeated drug treatment in rodents.

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