Astroglial Knockout of Glucocorticoid Receptor Attenuates Morphine Withdrawal Symptoms, but Not Antinociception and Tolerance in Mice.
Astrocytes
Glucocorticoid receptor
Morphine tolerance
Morphine withdrawal
Journal
Cellular and molecular neurobiology
ISSN: 1573-6830
Titre abrégé: Cell Mol Neurobiol
Pays: United States
ID NLM: 8200709
Informations de publication
Date de publication:
Oct 2022
Oct 2022
Historique:
received:
23
12
2020
accepted:
24
03
2021
pubmed:
7
4
2021
medline:
31
8
2022
entrez:
6
4
2021
Statut:
ppublish
Résumé
The development of tolerance and drug dependence limit the clinical application of opioids for the treatment of severe pain. Glucocorticoid receptors (GRs) are among molecular substrates involved in these processes. Most studies focus on the role of neuronal GR, while the involvement of GR on glial cells is not fully understood. To address this issue, we used a transgenic model of conditional GR knockout mice, targeted to connexin 30-expressing astrocytes, treated with repeated doses of morphine. We observed no difference between control mice and astrocytic GR knockouts in the development of antinociceptive tolerance. Nevertheless, when animals were subjected to precipitated withdrawal, knockouts presented some attenuated symptoms, including jumping. Taken together, our data suggest that hippocampal and spinal astrocytic GRs appear to be involved in opioid withdrawal, and drugs targeting the GR may relieve some symptoms of morphine withdrawal without influencing its antinociceptive properties.
Identifiants
pubmed: 33821329
doi: 10.1007/s10571-021-01086-3
pii: 10.1007/s10571-021-01086-3
pmc: PMC9418269
doi:
Substances chimiques
Analgesics, Opioid
0
Receptors, Glucocorticoid
0
Morphine
76I7G6D29C
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
2423-2426Subventions
Organisme : Narodowe Centrum Nauki
ID : 2013/08/A/NZ3/00848
Informations de copyright
© 2021. The Author(s).
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