Role of the Serotonin Receptor 7 in Brain Plasticity: From Development to Disease.
brain connectivity
brain development
gut-brain axis
neurodevelopmental diseases
neuronal cytoarchitecture
neuroplasticity
regulatory T cells
serotonin (5-HT)
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
13 Jan 2020
13 Jan 2020
Historique:
received:
06
12
2019
revised:
08
01
2020
accepted:
10
01
2020
entrez:
17
1
2020
pubmed:
17
1
2020
medline:
2
10
2020
Statut:
epublish
Résumé
Our knowledge on the plastic functions of the serotonin (5-HT) receptor subtype 7 (5-HT7R) in the brain physiology and pathology have advanced considerably in recent years. A wealth of data show that 5-HT7R is a key player in the establishment and remodeling of neuronal cytoarchitecture during development and in the mature brain, and its dysfunction is linked to neuropsychiatric and neurodevelopmental diseases. The involvement of this receptor in synaptic plasticity is further demonstrated by data showing that its activation allows the rescue of long-term potentiation (LTP) and long-term depression (LTD) deficits in various animal models of neurodevelopmental diseases. In addition, it is becoming clear that the 5-HT7R is involved in inflammatory intestinal diseases, modulates the function of immune cells, and is likely to play a role in the gut-brain axis. In this review, we will mainly focus on recent findings on this receptor's role in the structural and synaptic plasticity of the mammalian brain, although we will also illustrate novel aspects highlighted in gastrointestinal (GI) tract and immune system.
Identifiants
pubmed: 31941109
pii: ijms21020505
doi: 10.3390/ijms21020505
pmc: PMC7013427
pii:
doi:
Substances chimiques
Receptors, Serotonin
0
serotonin 7 receptor
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Regione Campania
ID : POR Campania FESR 2014/2020
Organisme : Università degli Studi di Napoli Federico II
ID : Finanziamento Ricerca di Ateneo
Déclaration de conflit d'intérêts
The authors declare no conflict of interest.
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