<i>De Novo</i> Expression of Dopamine D2 Receptors on Microglia after Stroke

Huck, Jojanneke H.J.; Freyer, Dorette; Böttcher, Chotima; Mladinov, Mihovil; Muselmann-Genschow, Claudia; Thielke, M; Gladow, Nadine; Bloomquist, Dana; Mergenthaler, Philipp; Priller, Josef

doi:10.1038/jcbfm.2015.128

Cited by 85 publications

(66 citation statements)

References 32 publications

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“…Microglia express all DA receptor subtypes. Presence of D1, D2, D3, D4, and D5 receptor protein and/or mRNA was first demonstrated in cultured microglia, where DA modulates K + current and attenuates NO release through the D1 and D2 receptor (Färber et al ., ; Mastroeni et al ., ; Huck et al ., ; Yoshioka et al ., ). Interestingly, when microglia were investigated in vivo for D2 receptor expression, no expression was detected in unstimulated cells, while an upregulation of D2 receptor mRNA was found in activated microglia after experimental stroke (Huck et al ., ).…”

Section: Non‐neuronal Mechanisms Of Lid: Microgliamentioning

confidence: 98%

l‐DOPA‐induced dyskinesia and neuroinflammation: do microglia and astrocytes play a role?

Carta

Mulas

Bortolanza

et al. 2016

Eur J of Neuroscience

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In Parkinson's disease (PD), L-DOPA therapy leads to the emergence of motor complications including L-DOPA-induced dyskinesia (LID). LID relies on a sequence of pre-and postsynaptic neuronal events, leading to abnormal corticostriatal neurotransmission and maladaptive changes in striatal projection neurons. In recent years, additional non-neuronal mechanisms have been proposed to contribute to LID. Among these mechanisms, considerable attention has been focused on L-DOPA-induced inflammatory responses. Microglia and astrocytes are the main actors in neuroinflammatory responses, and their double role at the interface between immune and neurophysiological responses is starting to be elucidated. Both microglia and astrocytes express a multitude of neurotransmitter receptors and via the release of several soluble molecules modulate synaptic function in neuronal networks. Here we review preclinical and clinical evidence of glial overactivation by L-DOPA, supporting a role of microglia and astrocytes in the development of LID. We propose that in PD, chronically and abnormally activated microglia and astrocytes lead to an aberrant neuron-glia communication, which affect synaptic activity and neuroplasticity contributing to the development of LID.

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Section: Non‐neuronal Mechanisms Of Lid: Microgliamentioning

confidence: 98%

l‐DOPA‐induced dyskinesia and neuroinflammation: do microglia and astrocytes play a role?

Carta

Mulas

Bortolanza

et al. 2016

Eur J of Neuroscience

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“…In this regard, dopaminergic signaling has been reported to modulate different microglial functions, including their inflammatory activity (Yan et al, 2015;Dominguez-Meijide et al, 2017;Elgueta et al, 2017), migration (Farber et al, 2005), and cell adhesion (Fan et al, 2018). Accordingly, microglial cells express both dopamine D1-like and D2-like receptors (Farber et al, 2005;Huck et al, 2015). However, under inflammatory conditions the expression of dopamine receptors might strongly change (Huck et al, 2015).…”

Section: Dopaminergic Regulation Of Microglial Cellsmentioning

confidence: 99%

The Cross-Talk Between the Dopaminergic and the Immune System Involved in Schizophrenia

Vidal

Pacheco

2020

Front. Pharmacol.

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Dopamine is one of the neurotransmitters whose transmission is altered in a number of neural pathways in the brain of schizophrenic patients. Current evidence indicates that these alterations involve hyperactive dopaminergic transmission in mesolimbic areas, striatum, and hippocampus, whereas hypoactive dopaminergic transmission has been reported in the prefrontal cortex of schizophrenic patients. Consequently, schizophrenia is associated with several cognitive and behavioral alterations. Of note, the immune system has been found to collaborate with the central nervous system in a number of cognitive and behavioral functions, which are dysregulated in schizophrenia. Moreover, emerging evidence has associated schizophrenia and inflammation. Importantly, different lines of evidence have shown dopamine as a major regulator of inflammation. In this regard, dopamine might exert strong regulation in the activity, migration, differentiation, and proliferation of immune cells that have been shown to contribute to cognitive functions, including T-cells, microglial cells, and peripheral monocytes. Thereby, alterations in dopamine levels associated to schizophrenia might affect inflammatory response of immune cells and consequently some behavioral functions, including reference memory, learning, social behavior, and stress resilience. Altogether these findings support the involvement of an active cross-talk between the dopaminergic and immune systems in the physiopathology of schizophrenia. In this review we summarize, integrate, and discuss the current evidence indicating the involvement of an altered dopaminergic regulation of immunity in schizophrenia.

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“…[58] Microglia express receptors that respond to various stimuli that may as a consequence result in there activation. [59] A large number of studies indicate that microglia expresses different proteins and cytokines that display different role to express different function. [60] Activated microglia have two phenotypes: classically activated (M1) and alternatively activated (M2).…”

Section: Microglia and Neuroinflammationmentioning

confidence: 99%

Role of neuroinflammation in ischemic stroke

Li¹,

Pan²,

Tang³

et al. 2017

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Ischemic stroke causes the depletion of energy and induce excitotoxicity and neuroinflammation in the brain that results from thrombotic blockage. Neuroinflammation occurs initially depending on activated resident microglia that has the same function as the macrophage. Activated microglia participates in the neuroinflammatory process by phagocytosing the injured brain cells and producing the pro-and anti-inflammatory mediators. In this review, the authors present an overview of the role of microglia in mediating neuroinflammation in ischemic stroke. Key words:Microglia, ischemic stroke, neuroinflammation ABSTRACT Topic: StrokeThis is an open access article distributed under the terms of the Creative Commons AttributionNonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

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De Novo Expression of Dopamine D2 Receptors on Microglia after Stroke

Cited by 85 publications

References 32 publications

l‐DOPA‐induced dyskinesia and neuroinflammation: do microglia and astrocytes play a role?

l‐DOPA‐induced dyskinesia and neuroinflammation: do microglia and astrocytes play a role?

The Cross-Talk Between the Dopaminergic and the Immune System Involved in Schizophrenia

Role of neuroinflammation in ischemic stroke

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