Adolescent stress leads to glutamatergic disturbance through dopaminergic abnormalities in the prefrontal cortex of genetically vulnerable mice

Matsumoto, Yurie; Niwa, Minae; Mouri, Akihiro; Noda, Yukihiro; Fukushima, Takeshi; Ozaki, Norio; Nabeshima, Toshitaka

doi:10.1007/s00213-017-4704-8

Cited by 15 publications

(20 citation statements)

References 128 publications

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“…As shown in our previous report (Matsumoto et al, 2017), juvenile isolation induced social withdrawal in mutDISC1 mice (Figure 2). The time spent in social interaction in isolated mutDISC1 mice was shorter than in group‐housed WT mice (Figure 2).…”

Section: Resultssupporting

confidence: 85%

“…As shown in our previous report (Matsumoto et al, 2017), juvenile isolation induced social withdrawal in mutDISC1 mice (Figure 2).…”

Section: Hispidulin Attenuated Social Withdrawal In Isolated Mutdissupporting

confidence: 85%

“…The microdialysis procedure was conducted in free‐moving chronic PCP‐treated ddY mice as reported previously (Mouri, Noda, Noda, et al, 2007; Niwa et al, 2010; Matsumoto et al, 2017) with modifications. Mice were administered PCP (10 mg·kg −1 , s.c.) or saline once a day for 14 days (Figure 1d).…”

Section: Methodsmentioning

confidence: 99%

“…The mutDISC1 mice, which carry the dominant‐negative mutation of human DISC1 gene (Ishizuka et al, 2006; Tomoda et al, 2016), displayed methamphetamine‐induced hyperlocomotion (MIH; Jaaro‐Peled et al, 2013), PPI disruption (Hikida et al, 2007), depression‐like behaviour (Hikida et al, 2007) and impaired cognitive performance (Shen et al, 2008). Based on the hypothesis that genetic and environmental risk factors work together during critical periods of neuronal development to ultimately lead to schizophrenia (Marenco & Weinberger, 2000), we have successfully developed an animal model mimicking schizophrenia by giving mutDISC1 mice mild isolation stress during the juvenile period (Matsumoto et al, 2017; Niwa et al, 2013). These juvenile isolated mutDISC1 mice displayed significant social withdrawal, impaired PPI and enhanced methamphetamine‐induced hyperlocomotion (Matsumoto et al, 2017; Niwa et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

“…Based on the hypothesis that genetic and environmental risk factors work together during critical periods of neuronal development to ultimately lead to schizophrenia (Marenco & Weinberger, 2000), we have successfully developed an animal model mimicking schizophrenia by giving mutDISC1 mice mild isolation stress during the juvenile period (Matsumoto et al, 2017; Niwa et al, 2013). These juvenile isolated mutDISC1 mice displayed significant social withdrawal, impaired PPI and enhanced methamphetamine‐induced hyperlocomotion (Matsumoto et al, 2017; Niwa et al, 2013). It is possibly that this is due to hypofunction of dopaminergic transmission in the prefrontal cortex (PFC) resulting from a reduction in tyrosine hydroxylase, a dopamine synthesizing enzyme, due to increased DNA methylation in the limbic dopaminergic neurons that project to the prefrontal cortex (Niwa et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

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Hispidulin attenuates the social withdrawal in isolated disrupted‐in‐schizophrenia‐1 mutant and chronic phencyclidine‐treated mice

Mouri

Lee

Mamiya

et al. 2020

British J Pharmacology

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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-inschizophrenia-1 mutant (mutDISC1) mice and chronic phencyclidine (PCP)-treated naïve mice. Key Results: In chronic PCP-treated mice, hispidulin (10 mgÁkg −1 , i.p.) attenuated social withdrawal similar to that observed with dopamine D 1 receptor antagonist (SCH-23390, 0.02 mgÁkg −1 , i.p.) and was mimicked by the selective COMT inhibitor, OR-486 (10 mgÁkg −1 , i.p.). Hispidulin increased extracellular dopamine levels in the PFC of chronic PCP-treated mice. In isolated mutDISC1 mice, hispidulin also reversed social withdrawal. In both models, intra-PFC microinjection of a D 1 agonist (SKF-81297: 10 nmol/mouse/bilateral) reversed the impairment of Ser 897 phosphorylation at the GluN1 subunit of NMDA receptors, suggesting the association between GluN1 Ser 897-phosphorylation and D 1 activation in the PFC exits in both models. Conclusions and Implications: Hispidulin attenuated social withdrawal by activating D 1 receptors indirectly through elevated dopamine levels in the PFC by COMT inhibition. This nature of hispidulin suggests that it a potential novel therapeutic candidate for the treatment of negative symptoms in schizophrenia.

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Section: Resultssupporting

confidence: 85%

“…As shown in our previous report (Matsumoto et al, 2017), juvenile isolation induced social withdrawal in mutDISC1 mice (Figure 2).…”

Section: Hispidulin Attenuated Social Withdrawal In Isolated Mutdissupporting

confidence: 85%