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  4. Dopamine receptor D3 signalling in astrocytes promotes neuroinflammation
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Dopamine receptor D3 signalling in astrocytes promotes neuroinflammation

Journal
Journal of Neuroinflammation
ISSN
1742-2094
Date Issued
2019
Author(s)
Andro Montoya
Daniela Elgueta
Javier Campos
Ornella Chovar
Paulina Falcón
Soledad Matus
ALFARO CORTEZ, IVAN ESTEBAN  
Facultad de Medicina Clínica Alemana Universidad del Desarrollo  
María Rosa Bono
Rodrigo Pacheco
Type
Resource Types::text::journal::journal article
Scopus ID
2-s2.0-85076229759
WoS ID
WOS:000501815500003
DOI
10.1186/s12974-019-1652-8
URL
https://investigadores.udd.cl/handle/123456789/2385
URL Institutional Repository
http://hdl.handle.net/11447/3122
Cite this document
Montoya, A., Elgueta, D., Campos, J., Chovar, O., Falcón, P., Matus, S., Alfaro, I., Bono, M. R., & Pacheco, R. (2019). Dopamine receptor D3 signalling in astrocytes promotes neuroinflammation. Journal of Neuroinflammation, 16(1), 258. https://doi.org/10.1186/s12974-019-1652-8
Subjects
neuroinflammation

; 

astrocytes

; 

microglia

; 

dopamine receptors

; 

animals

; 

astrocytes

; 

cells, cultured

; 

inflammation

; 

inflammation mediators

; 

lipopolysaccharides

; 

male

; 

mice

; 

mice, inbred c57bl

; 

mice, knockout

; 

microglia

; 

parkinsonian disorders

; 

receptors, dopamine d3

; 

signal transduction

; 

cell protein

; 

dopamine 3 receptor

; 

interleukin 1beta

; 

lipopolysaccharide

; 

protein fizz1

; 

tumor necrosis factor

; 

unclassified drug

; 

autacoid

; 

dopamine 3 receptor

; 

lipopolysaccharide

; 

adult

; 

animal cell

; 

animal experiment

; 

animal model

; 

animal tissue

; 

article

; 

astrocyte

; 

cell activation

; 

cell specificity

; 

controlled study

; 

cytokine production

; 

dopaminergic transmission

; 

flow cytometry

; 

glia cell

; 

immunohistochemistry

; 

in vitro study

; 

in vivo study

; 

male

; 

microglia

; 

mouse

; 

nervous system inflammation

; 

neuropathology

; 

newborn

; 

nonhuman

; 

phenotype

; 

protein analysis

; 

protein deficiency

; 

protein expression

; 

animal

; 

astrocyte

; 

c57bl mouse

; 

cell culture

; 

drug effect

; 

genetics

; 

inflammation

; 

knockout mouse

; 

metabolism

; 

parkinsonism

; 

physiology

; 

signal transduction
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