The role of dopaminergic immune cell signalling in poststroke inflammation
(2018) In Therapeutic Advances in Neurological Disorders 11.- Abstract
Upon ischaemic stroke, brain-resident and peripheral immune cells accumulate in the central nervous system (CNS). Interestingly, these cells express pattern specific to neurotransmitter receptors and, therefore, seem to be susceptible to neurotransmitter stimulation, potentially modulating their properties and functions. One of the principal neurotransmitters in the CNS, dopamine, is involved in the regulation of processes of brain development, motor control and higher brain functions. It is constantly released in the brain and there is experimental and clinical evidence that dopaminergic signalling is involved in recovery of lost neurological function after stroke. Independent studies have revealed specific but different patterns of... (More)
Upon ischaemic stroke, brain-resident and peripheral immune cells accumulate in the central nervous system (CNS). Interestingly, these cells express pattern specific to neurotransmitter receptors and, therefore, seem to be susceptible to neurotransmitter stimulation, potentially modulating their properties and functions. One of the principal neurotransmitters in the CNS, dopamine, is involved in the regulation of processes of brain development, motor control and higher brain functions. It is constantly released in the brain and there is experimental and clinical evidence that dopaminergic signalling is involved in recovery of lost neurological function after stroke. Independent studies have revealed specific but different patterns of dopamine receptor subtypes on different populations of immune cells. Those patterns are dependent on the activation status of cells. Generally, exposure to dopamine or dopamine receptor agonists decreases detrimental actions of immune cells. In contrast, a reduction of dopaminergic inputs perpetuates a pro-inflammatory state associated with increased release of pro-inflammatory molecules. In addition, subsets of immune cells have been identified to synthesize and release dopamine, suggesting autoregulatory mechanisms. Evidence supports that inflammatory processes activated following ischaemic stroke are modulated by dopaminergic signalling.
(Less)
- author
- Talhada, Daniela LU ; Rabenstein, Monika and Ruscher, Karsten LU
- organization
- publishing date
- 2018-05-10
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- dopamine, dopamine receptor, immune cell, immunodepression, inflammation, neurotransmission, stroke recovery
- in
- Therapeutic Advances in Neurological Disorders
- volume
- 11
- publisher
- SAGE Publications
- external identifiers
-
- scopus:85054850501
- pmid:29774058
- ISSN
- 1756-2856
- DOI
- 10.1177/1756286418774225
- language
- English
- LU publication?
- yes
- id
- 7d9a4a8a-2ab2-42c7-b9ac-4cb52f310964
- date added to LUP
- 2018-11-09 08:47:42
- date last changed
- 2024-06-10 21:45:31
@article{7d9a4a8a-2ab2-42c7-b9ac-4cb52f310964,
abstract = {{<p>Upon ischaemic stroke, brain-resident and peripheral immune cells accumulate in the central nervous system (CNS). Interestingly, these cells express pattern specific to neurotransmitter receptors and, therefore, seem to be susceptible to neurotransmitter stimulation, potentially modulating their properties and functions. One of the principal neurotransmitters in the CNS, dopamine, is involved in the regulation of processes of brain development, motor control and higher brain functions. It is constantly released in the brain and there is experimental and clinical evidence that dopaminergic signalling is involved in recovery of lost neurological function after stroke. Independent studies have revealed specific but different patterns of dopamine receptor subtypes on different populations of immune cells. Those patterns are dependent on the activation status of cells. Generally, exposure to dopamine or dopamine receptor agonists decreases detrimental actions of immune cells. In contrast, a reduction of dopaminergic inputs perpetuates a pro-inflammatory state associated with increased release of pro-inflammatory molecules. In addition, subsets of immune cells have been identified to synthesize and release dopamine, suggesting autoregulatory mechanisms. Evidence supports that inflammatory processes activated following ischaemic stroke are modulated by dopaminergic signalling.</p>}},
author = {{Talhada, Daniela and Rabenstein, Monika and Ruscher, Karsten}},
issn = {{1756-2856}},
keywords = {{dopamine; dopamine receptor; immune cell; immunodepression; inflammation; neurotransmission; stroke recovery}},
language = {{eng}},
month = {{05}},
publisher = {{SAGE Publications}},
series = {{Therapeutic Advances in Neurological Disorders}},
title = {{The role of dopaminergic immune cell signalling in poststroke inflammation}},
url = {{http://dx.doi.org/10.1177/1756286418774225}},
doi = {{10.1177/1756286418774225}},
volume = {{11}},
year = {{2018}},
}