Dopamine and noradrenaline activate spinal astrocyte endfeet via D1-like receptors

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Astrocytes, the most abundant glial cells in the central nervous system, respond to a wide variety of neurotransmitters binding to metabotropic receptors. Here, we investigated the intracellular calcium responses of spinal cord astrocytes to dopamine and noradrenaline, two catecholamines released by specific descending pathways. In a slice preparation from the spinal cord of neonatal mice, puff application of dopamine resulted in intracellular calcium responses that remained in the endfeet. Noradrenaline induced stronger responses that also started in the endfeet but spread to neighbouring compartments. The intracellular calcium responses were unaffected by blocking neuronal activity or inhibiting various neurotransmitter receptors, suggesting a direct effect of dopamine and noradrenaline on astrocytes. The intracellular calcium responses induced by noradrenaline and dopamine were inhibited by the D1 receptor antagonist SCH 23390. We assessed the functional consequences of these astrocytic responses by examining changes in arteriole diameter. Puff application of dopamine or noradrenaline resulted in vasoconstriction of spinal arterioles. However, blocking D1 receptors or manipulating astrocytic intracellular calcium levels did not abolish the vasoconstrictions, indicating that the observed intracellular calcium responses in astrocyte endfeet were not responsible for the vascular changes. Our findings demonstrate a compartmentalized response of spinal cord astrocytes to catecholamines and expand our understanding of astrocyte–neurotransmitter interactions and their potential roles in the physiology of the central nervous system.
OriginalsprogEngelsk
TidsskriftEuropean Journal of Neuroscience
Vol/bind59
Udgave nummer6
Sider (fra-til)1278-1295
Antal sider18
ISSN0953-816X
DOI
StatusUdgivet - 2024

Bibliografisk note

Funding Information:
The project was funded by the Danish Research Council (Danmarks Frie Forskningsfond [J. F. P.]); Grant 9039‐00072B), Agnes og Poul Friis fond (J. F. P.), and Novo Nordisk Foundation Laureate Program (NNF15OC0016016) (O. K.). A. M. was financed by a PhD stipend from the Faculty of Health and Medical Sciences (UCPH). The authors wish to thank Professor Frank Kirchhoff (University of Saarland, Germany) for providing the transgenic mouse lines and Dr Barbara Lykke Lind for her comments on a previous version of the manuscript.

Publisher Copyright:
© 2023 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.

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