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Effects of(-)stepholidine in animal models for schizophrenia

Acta Pharmacologica Sinica 2006年第9期27卷 1111-1118页

作者： bart A ellenbroek 6500 HB Nijmegen Department of Cognitive Neurosciences Section Molecular Neurobiology The Netherlands University of Nijmegen

Aim:(-)Stepholidine(SPD)is an active ingredient of the Chinese herb Stephaniaintermedia,which binds to the dopamine D1and D2like ***,electrophysiological and behavioural experiments have provided strong evidencethat SPD is both a D1and a D2antagonist,which could make SPD a uniqueantipsychotic *** present study aimed to investigate the antipsychoticproperties of SPD in two animal models for ***:The effectsof SPD,clozapine and haloperidol in increasing forelimb and hindlimb retractiontime in the paw test and in reversing the apomorphine and MK801-induced dis-ruption of prepulse inhibition was ***:In the paw test,clozapineand SPD increased the hindlimb retraction time,with only a marginal effect on theforelimb retraction time,whereas haloperidol potently increased *** theprepulse inhibition paradigm,all three drugs reverse the apomorphine-induceddisruption in prepulse inhibition,while none of the drugs could reverse the MK801-induced *** even slightly,but significantly,potentiated the effectsof ***:The data show that SPD showed antipsychotic-like ef-fects in both the prepulse inhibition paradigm and in the paw ***,theresults of the paw test suggest that SPD has an atypical character with a relativelysmall potency to induce extrapyramidal side effects.

关键词： acoustic startle response antipsyehotics apomorphine dopamine D1 receptor dopamine D2 receptor MK801 paw test prepulse inhibition clozapine haloperidol

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The Changes of Histone Methylation Induced by Adolescent Social Stress Regulate the Resting-State Activity in mPFC

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Research 2024年第3期2023卷 273-283页

作者： Jiesi Wang Wei Zhang Hang Xu bart ellenbroek Jiajie Dai Li Wang Chaogan Yan Weiwen Wang CAS Key Laboratory of Mental Health Institute of PsychologyChinese Academy of SciencesBeijing.China Department of Psychology University of Chinese Academy of SciencesBeijingChina School of Psychology Victoria University of WellingtonKelburnWellington 6012New Zealand CAS Key Laboratory of Behavioral Science Institute of PsychologyChinese Academy of SciencesBeijingChina.

Early-life stress can lead to sustained alterations in regional resting-state brain functions, but the underlying molecular mechanism remains unclear. Stress can also induce sustained changes in epigenetic modifications across brain regions, which are not limited to a few genes;rather, they often tend to produce global levels of change. The functional implication of these changes also remains to be elucidated. We hypothesize that global epigenetic changes may partly modulate the resting-state functions of brain regions to influence behavior. To test this hypothesis, we used an adolescent social stress (ASS) model in mice and examined the relationship between epigenetic modifications and regional resting-state brain activity using resting-state functional magnetic resonance imaging (rs-fMRI). The results showed that, compared to the control mice, the stressed mice showed increased anxiety and social avoidance behaviors and greater levels of dimethylation of histone H3 at lysine 9 (H3K9me2) in the medial prefrontal cortex (mPFC). In addition, the resting-state activity represented by the amplitude of low-frequency fluctuation (ALFF) was significantly lower in the mPFC of stressed mice. To verify the relationship of H3K9me2 and ALFF, the specific inhibition of H3Kme2 was performed by using the drug UNC0642, which reversed the anxiety behavior induced by ASS and significantly increase the ALFF value of mPFC in both normal and ASS animals. Our study is the first to report an association between histone modifications and rs-fMRI findings, providing a new perspective for understanding of the significance of regional brain epigenetic changes and a possible molecular explanation for rs-fMRI findings.

关键词： sustained mPFC alterations

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Effects of adolescent social stress and antidepressant treatment on cognitive inflexibility and Bdnf epigenetic modifications in the mPFC of adult mice

Effects of adolescent social stress and antidepressant treat...

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第二十一届全国心理学学术会议

作者： Hang Xu Jiesi Wang Ke Zhang Mei Zhao bart ellenbroek Feng Shao Weiwen Wang CAS Key Laboratory of Mental Health Institute of Psychology The University of Chinese Academy of Sciences School of Psychology Victoria University of Wellington School of Psychological and Cognitive Sciences Beijing Key Laboratory of Behavior and Mental Health Peking University

Adolescent social stress(ASS) can increase susceptibility to depression in adulthood. However, the underlying psychological and neural mechanisms remain unclear. Cortically mediated cognitive dysfunctions are increasingly recognized as an independent and important risk factor of depression. Using social defeat stress, a classical animal model of depression, our previous studies found that mice subjected to this form of stress during early adolescence displayed cognitive inflexibility(CI) in adulthood. This change was accompanied by a down-regulation of Bdnf gene expression in the medial prefrontal cortex(mPFC);this gene encodes a key molecule involved in depression and antidepressant action. In the present paper, we identified epigenetic modification of Bdnf as a possible mechanism underlying the behavioral and molecular changes. ASS induced a set of depressive phenotypes, including increased social avoidance and CI, as well as reduced levels of total Bdnf and isoform IV but not isoform I or VI transcripts in the mPFC. In parallel with changes in Bdnf gene expression, previously stressed adult mice showed increased levels of dimethylation of histone H3 at lysine K9(H3K9me2) immediately downstream of the Bdnf IV promoter. On the other hand, no differences were found in trimethylation of histone H3 at lysine K4(H3K4me3) or in acetylation of histone H3 at lysine K9(H3K9ac) or at K4(H3K4ac) in the Bdnf IV promoter. Likewise, no alterations were found in DNA methylation of the Bdnf IV promoter. Additionally, treatment with the chronic antidepressant tranylcypromine reversed Bdnf epigenetic changes and related gene transcription while also reversing CI, but not social avoidance, in previously stressed adult mice. These results suggest that epigenetic changes to the Bdnf gene in the mPFC after adolescent social adversity may be involved in the regulation of cognitive dysfunction in depression and antidepressant action in adulthood.

关键词： Adolescent Social stress Cognitive inflexibility Brain-derived neurotrophic factor(BDNF) Epigenetic mechanism

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