c-fos pThr232 antibody Ab
- Known as:
- c-fos pThr232 (anti-) Antibody
- Catalog number:
- 1488188
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Acris antibodies
- Gene target:
- c-fos pThr232 antibody
Related products to: c-fos pThr232 antibody Ab
Related articles to: c-fos pThr232 antibody Ab
- Environmental enrichment (EE) paradigms in rodents have long demonstrated that enhanced sensory, cognitive, social, and motor stimulation positively impacts brain function, improving learning, memory, and neuroplasticity. These effects have significant implications for understanding cognitive development and mitigating cognitive decline and brain aging. While numerous transcriptomic studies have explored EE-induced molecular changes, a unified view of the genes and pathways consistently modulated remains lacking. To address this gap, we performed a systematic review and meta-analysis. We conducted a comprehensive PubMed search for all studies published up to February 2025 that matched all the following inclusion criteria: (1) employed EE paradigms; (2) were conducted on rodents; (3) utilized genome-wide transcriptomic methods; (4) examined brain regions or neuronal populations. The 323 retrieved articles were manually screened for relevance to the study aims and data availability. Datasets from 20 eligible RNA-seq reports were reprocessed using a unified analysis pipeline and subjected to a meta-analysis with three complementary statistical methods. Despite considerable heterogeneity across studies, our integrative analysis identified consistent gene expression signatures linked to synaptic function, plasticity and their transcriptional regulation. In particular, our findings highlight the upregulation of the activity-dependent transcriptional program, including Fos and Jun family members. These molecular insights advance our understanding of how EE impacts on neuronal and behavioral outcomes, and may inform therapeutic strategies aimed at replicating or enhancing EE benefits. To promote open science and foster further research, we developed an accessible web application, mEEtaBrain, that enables the neuroscience community to navigate and interrogate our meta-analysis results. Substantial methodological heterogeneity across source studies increased variability in the meta-analysis outcomes. The use of stressors or disease models, particularly in rat studies, introduced a major confounding factor and limited reliable interspecies comparison. Overall, the studies exhibited a low to moderate risk of bias. - Source: PubMed
Publication date: 2026/08/26
Kurowska MarcelinaMiozzo FedericoSchroeder RobertMachnicka Magdalena APérez-González RocíoMerienne KarineFischer AndréBarco AngelBoutillier Anne-LaurenceWilczyński Bartek - Chronic intermittent hypoxia (CIH), a hallmark of obstructive sleep apnea, gives rise to cognitive deficits and sleep disruption. To investigate the role of the medial prefrontal cortex (mPFC), male mice were subjected to CIH for 4 weeks (8 h/day). Brain-wide Fos B screening revealed specific hyperactivation in the infralimbic (IL) subregion of the mPFC. Following chemogenetic virus injection into the mPFC, cognitive function was assessed using novel object/location recognition and the Morris water maze, sleep architecture was recorded via EEG/EMG, and synaptic markers were examined by western blotting and immunofluorescence. The results showed that CIH impaired cognitive function and reduced the density of both excitatory and inhibitory synaptic proteins in the mPFC-IL. Chemogenetic inhibition of mPFC-IL neurons attenuated these cognitive deficits and elevated synaptic protein levels, but failed to ameliorate the CIH-induced reduction in REM sleep and increased sleep-state transitions. In conclusion, the mPFC is a critical hub for CIH-induced cognitive impairment, and its targeted inhibition can restore cognitive and synaptic function. However, sleep architecture disruptions are governed by distinct mechanisms, indicating a dissociation between CIH-mediated cognitive and sleep pathologies. Obstructive sleep apnea often causes cognitive impairment, yet the brain mechanisms remain unclear. We found that chronic intermittent hypoxia triggers hyperactivation in a specific subregion of the medial prefrontal cortex, which critically drives cognitive deficits. Suppressing this region restored cognitive function but did not improve accompanying sleep disturbances. This dissociation reveals that cognitive and sleep impairments arise from distinct neural circuits, offering a new target for treating cognitive dysfunction in sleep apnea. - Source: PubMed
Publication date: 2026/08/24
Pei GuoLi XinyueWang YuanyuanSun Yan-YunWu ShuqingRen BixinMa Quan-HongChen Rui - Adaptive social behavior requires balancing self-interest with the welfare of others, a core axiom of social decision-making that determines whether actions are selfish or prosocial. Although the medial prefrontal cortex (mPFC) has been implicated in prosocial behavior, the broader cortical-subcortical networks that arbitrate between selfish and prosocial actions remain poorly understood. Moreover, most studies of social decision-making (at both the single-region and circuit levels) have focused on inbred C57BL/6 mice, leaving unclear whether similar neural mechanisms operate across genetically diverse populations. Here, we combined a social decision-making task with c-Fos mapping to examine activity across distributed cortical and subcortical regions in inbred C57BL/6 and outbred CD1 male mice during prosocial and selfish choices. We found that CD1 mice exhibited a stronger bias toward selfish behavior, whereas C57BL/6 mice were more prosocial. This behavioral divergence was associated with elevated c-Fos activity in the mPFC and nucleus accumbens core (NAcC) in CD1 mice compared with C57BL/6 mice, with mPFC activity positively correlating with selfish choices. At the network level, social decision-making selectively recruited coordinated activity among the distinct mPFC subregions, ventral tegmental area (VTA), and NAcC. Importantly, prosocial and selfish individuals exhibited distinct prefrontal-subcortical network configurations during social decision-making. Together, these findings identify distributed cortical-subcortical network dynamics underlying social choice bias and suggest that differences in the neural architecture associated with prosocial and selfish behavior are influenced by strain in male mice. - Source: PubMed
Publication date: 2026/08/24
Illescas-Huerta ElizabethVillamizar AndreaCum MeghanPadilla-Coreano Nancy - Genome-wide association studies on patients with depression have identified FYN and FYB, an FYN-binding protein, as being linked to depression. We have reported that experimental manipulations in gene expression in the medial prefrontal cortex (mPFC) alter stress-induced object recognition impairments in animals. Therefore, we examined the impact of alterations in FYN and FYB expression in the mPFC of adult male rats on resistance to stress-induced impairments in object recognition. Animals with virus-mediated knockdown or overexpression of Fyn in the mPFC were subjected to either a brief 20-minute restraint with 20 intermittent tail shocks, which does not induce object recognition impairment, or a prolonged 60-minute restraint with 60 intermittent tail shocks, which does. In an object recognition task, control rats maintained intact object recognition following a brief stress, whereas rats with Fyn knockdown or overexpression in the mPFC showed impaired object recognition. Prolonged stress impaired object recognition in both control rats and rats with Fyn knockdown or overexpression. Additionally, rats with Fyn knockdown in the mPFC exhibited fewer c-Fos-positive cells in the mPFC in response to brief stress, accompanied by a trend toward increased c-Fos in the amygdala compared with control rats. Fyn knockdown also reduced Fyb expression in the mPFC. Furthermore, Fyb knockdown in the mPFC impaired object recognition following brief stress, suggesting that the observed effects are consistent with involvement of a coupled Fyn-Fyb signaling axis rather than Fyn alone. These findings suggest that altered Fyn-related signaling in the mPFC may underlie the resistance to stress-induced object recognition impairments. - Source: PubMed
Publication date: 2026/08/24
Jeon Yong-JaeKim Nam-HeonYoon SujungLyoo In KyoonKim Jae-MinHan Jung-Soo - Burning mouth syndrome (BMS), a heterogeneous idiopathic orofacial pain disorder mainly affecting postmenopausal females, is frequently accompanied by anxiety and sleep disturbances. Existing BMS molecular studies have focused primarily on oral bacterial DNA, whereas systematic human salivary transcriptomic profiling remains poorly explored. This study aimed to characterize salivary mRNA and lncRNA signatures in postmenopausal patients with BMS and uncover the transcriptomic mechanisms underlying the pathogenesis of BMS and associated comorbidities. - Source: PubMed
Publication date: 2026/08/24
Lu DingzhuoSu ZhonghaoWen NaWang JianWang BingQin Zhenxia