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Insulin hypoactivity caused by Synaptotagmin-7 deficits contributes to depression-like behaviors and diurnal behavioral fluctuation

ABSTRACT: Insulin hypoactivity caused by Synaptotagmin-7 deficits contributes to depression-like behaviors and diurnal behavioral fluctuation

PROVIDER: PRJNA1190907 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31519330.fastq.gz	Fastqsanger.gz
	SRR31519331.fastq.gz	Fastqsanger.gz
	SRR31519332.fastq.gz	Fastqsanger.gz
	SRR31519333.fastq.gz	Fastqsanger.gz
	SRR31519334.fastq.gz	Fastqsanger.gz

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Insulin hypoactivity caused by Synaptotagmin-7 deficits contributes to depression-like behaviors and diurnal behavioral fluctuation

Project description:Synaptotagmin-7 (Syt7) KO mice show diurnal fluctuations of mania- and depression-like behavioral abnormalities. Although GluN2B-NMDAR hypoactivity has been shown to be involved in the induction of mania-like behaviors of the Syt7 KO mice in the dark phase, the reasons for the depression-like behaviors in the light phase and behavioral fluctuation remain unknown. Here, we show that bipolar I disorder (BDI) patient induced pluripotent stem cell (iPSC)-derived islet-like organoids exhibited Syt7-dependent insulin secretion defects; moreover, Syt7 deficiency-induced insulin hyposecretion generated depression-like behaviors in Syt7 KO mice in the light phase. Furthermore, pancreatic insulin secretion and neuronal activity showed opposite diurnal patterns, in which the Syt7 deficiency-induced disequilibrium induced periodic antagonistic shifts in the mania- and depression-like behaviors. Finally, using RNA-seq analysis, we explored downstream pathways that might underlie the diurnal fluctuation of behaviors. Therefore, Syt7 deficiency-induced insulin hypoactivity contributed to light-phase depression-like behaviors and diurnal behavioral fluctuations in the mice.

2025-05-14 | GSE282863 | GEO

Disturbed rhythm of pancreatic insulin secretion induces circadian-based bipolar swings of behaviors

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2024-12-01 | GSE283118 | GEO

Sex-specific social behavior and amygdala proteomic deficits in Foxp2+/- mutant mice

Project description:In humans, mutations in the transcription factor encoding gene, FOXP2, are associated with language and Autism Spectrum (ASD) Disorders, the latter characterized by deficits in social interactions. However, little is known regarding the function of Foxp2 in male or female social behavior. Our previous studies in mice revealed high expression of Foxp2 within the medial subnucleus of the amygdala (MeA), a limbic brain region highly implicated in innate social behaviors such as mating, aggression, and parental care. Here, using a comprehensive panel of behavioral tests in male and female Foxp2+/- heterozygous mice, we investigated the role Foxp2 plays in MeA-linked innate social behaviors. We reveal significant deficits in olfactory processing, social interaction, mating, aggressive and parental behaviors. Interestingly, some of these deficits displayed in a sex-specific manner. To examine the consequences of Foxp2 loss of function specifically in the MeA, we conducted a proteomic analysis of microdissected MeA tissue and found sex differences in a host of proteins implicated in neuronal communication, connectivity and dopamine signaling. Consistent with this, we discovered that MeA Foxp2-lineage cells were responsive to dopamine with differences between males and females. Thus, our findings reveal a central and sex-specific role for Foxp2 in social behavior and MeA function.

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The basolateral amygdala-anterior cingulate pathway contributes to depression-like behaviors and comorbidity with chronic pain behaviors in male mice

Project description:While depression and chronic pain are frequently comorbid, underlying neuronal circuits, and their relevance for the understanding of psychopathology, remain poorly defined. Here we show in mice that hyperactivity of the neuronal pathway linking the basolateral amygdala to the anterior cingulate cortex is essential for chronic pain-induced depression. In naive male mice, we demonstrate that activation of this pathway is sufficient to trigger depressive-like behaviors, as well as transcriptomic alterations that recapitulate core molecular features of depression in the human brain. These alterations notably impact gene modules related to myelination and the oligodendrocyte lineage. Among these, we show that Sema4a, a hub gene significantly upregulated in both male mice and humans in the context of altered mood, is necessary for the emergence of depressive-like behaviors. Overall, these results place the BLA-ACC pathway at the core of pain and depression comorbidity, and unravel the role of impaired myelination and Sema4a in mood control.

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2021-02-12 | GSE166634 | GEO

The interplay between oxidative stress and inflammation supports autistic-related behaviors in Cntnap2 mutant mice

Project description:Autism Spectrum Disorder (ASD) is a highly prevalent neurodevelopmental condition characterized by social communication deficits and repetitive/restricted behaviors. Several studies showed that inflammation may contribute to ASD. Here we used RT-qPCR, RNA sequencing, immunohistochemistry, and flow cytometry to show that pro-inflammatory molecules were increased in the cerebellum and periphery of mice lackingCntnap2(Cntnap2-/-), a robust model of ASD. In parallel, oxidative stress was present in the cerebellum of mutant animals. Systemic treatment with N-acetyl-cysteine (NAC) rescued cerebellar oxidative stress and inflammation as well as motor and social impairments inCntnap2-/-mice. This was accompanied by improved function of microglia cells in NAC-treated mutant animals. Intriguingly, social deficits, cerebellar inflammation and microglia dysfunction were induced by NAC inCntnap2+/+animals. Our findings therefore suggest that the interplay between oxidative stress and inflammation may support ASD-related behaviors in mice.

2024-05-15 | GSE267182 | GEO

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Project description:Microdeletions of the MEF2C gene are linked to a syndromic form of autism termed MEF2C haploinsufficiency syndrome (MCHS). Here, we show that MCHS-associated missense mutations cluster in the conserved DNA binding domain and disrupt MEF2C DNA binding. DNA binding-deficient global Mef2c heterozygous mice (Mef2c-Het) display numerous MCHS-like behaviors, including autism-related behaviors, as well as deficits in cortical excitatory synaptic transmission. We find that hundreds of genes are dysregulated in Mef2c-Het cortex, including significant enrichments of autism risk and excitatory neuron genes. In addition, we observe an enrichment of upregulated microglial genes, but not due to neuroinflammation in the Mef2c-Het cortex. Importantly, conditional Mef2c heterozygosity in forebrain excitatory neurons reproduces a subset of the Mef2c-Het phenotypes, while conditional Mef2c heterozygosity in microglia reproduces social deficits and repetitive behavior. Together our findings suggest that MEF2C regulates typical brain development and function through multiple cell types, including excitatory neuronal and neuroimmune populations.

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