Hispidulin attenuates the social withdrawal in isolated disrupted-in-schizophrenia-1 mutant and chronic phencyclidine-treated mice.
Journal
British journal of pharmacology
ISSN: 1476-5381
Titre abrégé: Br J Pharmacol
Pays: England
ID NLM: 7502536
Informations de publication
Date de publication:
07 2020
07 2020
Historique:
received:
22
02
2019
revised:
16
12
2019
accepted:
13
02
2020
pubmed:
7
3
2020
medline:
22
6
2021
entrez:
6
3
2020
Statut:
ppublish
Résumé
Hispidulin is a flavonoid isolated from Clerodendrum inerme that was found to inhibit intractable motor tics. Previously, we found that hispidulin attenuates hyperlocomotion and the disrupted prepulse inhibition induced by methamphetamine and N-methyl-d-aspartate (NMDA) receptor antagonists, two phenotypes of schizophrenia resembling positive symptoms. Hispidulin can inhibit COMT, a dopamine-metabolizing enzyme in the prefrontal cortex (PFC) that is important for social interaction. Here, we investigated whether hispidulin would affect social withdrawal, one of the negative symptoms of schizophrenia. We examined whether acute administration of hispidulin would attenuate social withdrawal in two mice models, juvenile isolated disrupted-in-schizophrenia-1 mutant (mutDISC1) mice and chronic phencyclidine (PCP)-treated naïve mice. In chronic PCP-treated mice, hispidulin (10 mg·kg Hispidulin attenuated social withdrawal by activating D
Sections du résumé
BACKGROUND AND PURPOSE
Hispidulin is a flavonoid isolated from Clerodendrum inerme that was found to inhibit intractable motor tics. Previously, we found that hispidulin attenuates hyperlocomotion and the disrupted prepulse inhibition induced by methamphetamine and N-methyl-d-aspartate (NMDA) receptor antagonists, two phenotypes of schizophrenia resembling positive symptoms. Hispidulin can inhibit COMT, a dopamine-metabolizing enzyme in the prefrontal cortex (PFC) that is important for social interaction. Here, we investigated whether hispidulin would affect social withdrawal, one of the negative symptoms of schizophrenia.
EXPERIMENTAL APPROACH
We examined whether acute administration of hispidulin would attenuate social withdrawal in two mice models, juvenile isolated disrupted-in-schizophrenia-1 mutant (mutDISC1) mice and chronic phencyclidine (PCP)-treated naïve mice.
KEY RESULTS
In chronic PCP-treated mice, hispidulin (10 mg·kg
CONCLUSIONS AND IMPLICATIONS
Hispidulin attenuated social withdrawal by activating D
Identifiants
pubmed: 32133633
doi: 10.1111/bph.15043
pmc: PMC7312434
doi:
Substances chimiques
Flavones
0
Receptors, N-Methyl-D-Aspartate
0
Phencyclidine
J1DOI7UV76
hispidulin
N7F61604C2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
3210-3224Subventions
Organisme : National Health Research Institutes, Taiwan
ID : NHRI-EX107-10733NI
Organisme : National Health Research Institutes, Taiwan
ID : NHRI-EX108-10733NI
Organisme : Ministry of Science and Technology, Taiwan
ID : MOST108-2325-B002-029-MY3
Organisme : Ministry of Science and Technology, Taiwan
ID : MOST108-2321-B002-005
Organisme : Ministry of Science and Technology, Taiwan
ID : MOST104-2923-B002-006-MY3
Organisme : Ministry of Science and Technology, Taiwan
ID : MOST104-2325-B002-010
Organisme : Ministry of Science and Technology, Taiwan
ID : MOST103-2325-B002-037
Organisme : Ministry of Science and Technology, Taiwan
ID : NSC102-2325-B002-047
Organisme : Ministry of Science and Technology, Taiwan
ID : NSC101-2325-B002-048
Organisme : Ministry of Science and Technology, Taiwan
ID : NSC100-2325-B002-050
Organisme : Smoking Research Foundation
Organisme : Nakatomi Foundation
Organisme : Takeda Science Foundation
Organisme : Meijo Asian Research Center
Organisme : Private University Research Branding Project from the Ministry of Education, Culture, Sports, Science and Technology of Japan (MEXT)
Organisme : Japan Society for the Promotion of Science
ID : 26460240
Organisme : Japan Society for the Promotion of Science
ID : 15K08218
Organisme : Japan Society for the Promotion of Science
ID : 16K10195
Organisme : Japan Society for the Promotion of Science
ID : 17H04252
Informations de copyright
© 2020 The British Pharmacological Society.
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