Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The molecular phenotype of kisspeptin neurons in the medial amygdala of female mice

ABSTRACT: Little is known about how Kiss1 cells in the medial amygdala (MeA) are regulated and what other gene transcripts are produced by MeA Kiss1 neurons. Estradiol upregulates Kiss1 expression in the medial amygdala (MeA), but it remains unknown if estradiol regulates other gene transcripts in MeA Kiss1 cells. The goal of this study is to identify novel gene transcripts produced by MeA Kiss1 cells and to determine how estradiol regulates the expression of these transcripts. We selectively isolated mRNA from Kiss1 cells in the MeA of female mice using Ribotag transgenic mice, immunoprecipitation, and RNA-seq. Over 13,000 gene transcripts produced by MeA Kiss1 cells were identified, but only 45 of these transcripts had expression levels altered by estradiol.

ORGANISM(S): Mus musculus

PROVIDER: GSE224788 | GEO | 2023/02/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression in AVPV kisspeptin cells

Project description:Estrogen stimulates Kiss1 gene expression in AVPV cells in the brain, but whether estrogen regulates other genes in AVPV Kiss1 cells has not been determined. To provide a more detailed profiling of co-expressed genes in AVPV Kiss1 cells and determine how estrogen alters gene expression levels, we selectively isolated mRNAs from murine AVPV Kiss1 cells using transgenic-mediated immunoprecipitation and performed RNA-seq. This identified >13,000 mRNAs co-expressed in AVPV Kiss1 cells, including multiple transcripts that were positively or negatively regulated by estrogen.

2021-05-26 | GSE168134 | 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.

2021-07-07 | PXD026978 | Pride

Translating ribosome affinity purification of Esr1+ neuronal populations to identify sex and estrus-stage differentially expressed genes

Project description:We used translating ribosome affinity purification (TRAPseq) to profile genetically labeled neurons in the bed nucleus of the stria terminalis (BNST), preoptic area (POA), medial amygdala (MeA) and ventromedial hypothalamus (VMH) from adult male mice, and from adult female mice modeled to be in two distinct stages of the estrus cycle (estrus, sexually receptive, FR; and diestrues, sexually unreceptive, FNR).

2022-01-21 | GSE183092 | GEO

Adolescent Social Isolation Reprograms the Medial Amygdala: Transcriptome and Sex Differences in Reward

Project description:Adolescence is a sensitive window for reward- and stress-associated behavior. Although stress during this period causes long-term changes in behavior in males, how females respond is relatively unknown. Here we show that social isolation stress in adolescence, but not adulthood, induces persistent but opposite effects on anxiety- and cocaine-related behaviors in male vs. female mice, and that these effects are reflected in transcriptional profiles within the adult medial amygdala (meA). By integrating differential gene expression with co-expression network analyses, we identified crystallin mu (Crym), a thyroid hormone binding protein, as a key driver of these transcriptional profiles. Manipulation of Crym specifically within adult meA neurons recapitulates the behavioral and transcriptional effects of social isolation and re-opens a window of plasticity that is otherwise closed. Our results establish that meA is essential for sex-specific responses to stressful and rewarding stimuli through transcriptional programming that occurs during adolescence.

2020-11-30 | GSE146472 | GEO

An amygdala circuit that supresses social engagement

Project description:Innate social behaviors, such as mating and fighting, are fundamental to animal reproduction and survival. However, social engagements are associated with risks for the individual, such as pathogenic infection and physical injury. Little is known about the neural mechanism that allows for appropriate risk assessment and the suppression of hazardous social interactions. We have identified the posteromedial nucleus of the cortical amygdala (COApm) as a locus required for the suppression of mating with an unhealthy female and aggressive behaviors towards a dominant male intruder. Using anatomical tracing, functional imaging, and circuit-level epistatic analyses, we show that suppression of social engagements is mediated by the COApm projections onto the glutamatergic population of the medial amygdalar nucleus (MEA). We further show that this projection that governs social engagements is demarcated by expression of both the neuromodulator thyrotropin-releasing hormone (TRH) in the COApm and the TRH-receptor (TRHR) in the postsynaptic MEA glutamatergic neurons. Modulating TRH-expressing neurons as well as infusing TRHR ligand into the MEA phenocopy functional manipulation of the COApm-MEA circuit. We have, therefore, uncovered a novel neural mechanism that endows animals with the ability to modulate innate reproductive and aggressive social interactions according to the health and threat status of reciprocating individuals. Deficits in such a mechanism may lead to the spread of disease, while uncontrolled engagement may lead to pathological conditions, such as social withdrawal and depression.

2021-02-22 | GSE167176 | GEO

Gene expression profiling of high (HAB) vs. low (LAB) anxiety-related behavior mice in seven brain regions.

Project description:Investigating the molecular basis and correlates of anxiety-related and depression-like behaviors, we generated a mouse model consisting of high (HAB) and low (LAB) anxiety-related behavior mice. We utilized the elevated plus-maze for testing the genetic predisposition to anxiety-related behavior and, consequently, used this as selection criterion for the inbreeding of our animals. In depression-related tests, HAB mice display a more passive, depression-like coping strategy than LAB mice, resembling clinical comorbidity of anxiety and depression as observed in psychiatric patients. Using a microarray approach, the hypothalamic paraventricular nucleus (PVN), the basolateral/lateral (BLA), the medial (MeA) and central amygdala (CeA), the nucleus accumbens (NAc), the cingulate cortex (Cg) and the supraoptic nucleus (SON) – centers of the central nervous anxiety and fear circuitries – were investigated and screened for differences between HAB and LAB mice. Analysis was performed from six animals per line (HAB and LAB, respectively) pooled per brain region in ten technical replicates, thereof five with a dye-swapped design giving a total of 70 array slides analyzed. The LAB mouse line is referred to as reference.

2011-08-29 | E-GEOD-28999 | biostudies-arrayexpress

Sexually Dimorphic Control of Parenting Behavior by the Medial Amygdala

Project description:Single-cell RNA sequencing of male and female mouse medial amygdala using Drop-Seq

2019-02-14 | GSE124061 | GEO

Gene expression profiling of high (HAB) vs. low (LAB) anxiety-related behavior mice in seven brain regions.

2011-08-30 | GSE28999 | GEO

Brain transcriptome profiles in mouse model simulating features of post-traumatic stress disorder

Project description:Social stress mouse models were used to simulate human post-traumatic stress disorder (PTSD). C57B/6 mice exposed to SJL aggressor mice exhibited behaviors accepted as PTSD-in-mouse phenotype: 'frozen' motion, aggressor’s barrier avoidance, startled jumping, and retarded locomotion. Transcripts in hippocampus, amygdala, medial prefrontal cortex, ventral striatum (nucleus acumbens), septal region, corpus striatum, hemi-brain, blood, spleen and heart of stressed and control C57B/6 mice were analyzed using Agilent’s mouse genome-wide arrays.

2015-04-20 | GSE45035 | GEO

Rat, male, brain, medial amygdala, LC-MSMS

Project description:Social isolation poses a severe mental and physiological burden on humans. Most animal models that investigate this effect are based on prolonged isolation, which does not mimic the milder conditions experienced by people in the real world. Here we show that in the medial amygdala, a brain structure that is crucial for social memory, acute social isolation causes social memory loss and significant changes in specific mRNAs and proteins.

2021-11-03 | PXD026871 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data