medial prefrontal cortex
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2022 ◽  
Vol 205 ◽  
pp. 108913
Author(s):  
Hugo Bayer ◽  
Cristina A.J. Stern ◽  
Fernanda Troyner ◽  
Lucas Gazarini ◽  
Francisco S. Guimarães ◽  
...  

2022 ◽  
Vol 14 ◽  
Author(s):  
Miguel Skirzewski ◽  
Stéphane Molotchnikoff ◽  
Luis F. Hernandez ◽  
José Fernando Maya-Vetencourt

In the mammalian brain, information processing in sensory modalities and global mechanisms of multisensory integration facilitate perception. Emerging experimental evidence suggests that the contribution of multisensory integration to sensory perception is far more complex than previously expected. Here we revise how associative areas such as the prefrontal cortex, which receive and integrate inputs from diverse sensory modalities, can affect information processing in unisensory systems via processes of down-stream signaling. We focus our attention on the influence of the medial prefrontal cortex on the processing of information in the visual system and whether this phenomenon can be clinically used to treat higher-order visual dysfunctions. We propose that non-invasive and multisensory stimulation strategies such as environmental enrichment and/or attention-related tasks could be of clinical relevance to fight cerebral visual impairment.


2022 ◽  
Vol 23 (2) ◽  
pp. 955
Author(s):  
Hana Ujcikova ◽  
Dagoberto Robles ◽  
Xu Yue ◽  
Petr Svoboda ◽  
Yeon Sun Lee ◽  
...  

Chronic pain is associated with time-dependent structural and functional reorganization of the prefrontal cortex that may reflect adaptive pain compensatory and/or maladaptive pain-promoting mechanisms. However, the molecular underpinnings of these changes and whether there are time-dependent relationships to pain progression are not well characterized. In this study, we analyzed protein composition in the medial prefrontal cortex (mPFC) of rats at two timepoints after spinal nerve ligation (SNL) using two-dimensional gel electrophoresis (2D-ELFO) and liquid chromatography with tandem mass spectrometry (LC–MS/MS). SNL, but not sham-operated, rats developed persistent tactile allodynia and thermal hyperalgesia, confirming the presence of experimental neuropathic pain. Two weeks after SNL (early timepoint), we identified 11 proteins involved in signal transduction, protein transport, cell homeostasis, metabolism, and apoptosis, as well as heat-shock proteins and chaperones that were upregulated by more than 1.5-fold compared to the sham-operated rats. Interestingly, there were only four significantly altered proteins identified at 8 weeks after SNL (late timepoint). These findings demonstrate extensive time-dependent modifications of protein expression in the rat mPFC under a chronic neuropathic pain state that might underlie the evolution of chronic pain characterized by early pain-compensatory and later aberrant mechanisms.


Author(s):  
Patricia L. Moravec ◽  
Antino Kim ◽  
Alan R. Dennis ◽  
Randall K. Minas

Research shows that consuming ratings influences purchase decisions in e-commerce and also has modest effects on belief in news articles on social media. We find that the act of producing ratings reduces belief in news articles on social media and induces social media users to think more critically. We propose this intervention as a method to encourage users to realize that, unlike in the product rating setting, social media users who submit their ratings for news articles typically lack firsthand knowledge of the events reported in the news, making it difficult for most users to rate news articles accurately. We asked 68 social media users to assess the believability of 42 social media articles and measured their cognitive activity using electroencephalography. We found that asking users to rate articles using a self-referential question induced them to think more critically—as indicated by increased activation in the medial prefrontal cortex and dorsolateral prefrontal cortex—and made them less likely to believe the articles. The effect extended to subsequent articles; after being asked to rate an article, users were less likely to believe other articles that followed it whether they were asked to rate them or not.


2021 ◽  
Author(s):  
TSUYOSHI HATTORI ◽  
Stanislav M Cherepanov ◽  
Ryo Sakaga ◽  
Jureepon Roboon ◽  
Dinh Thi Nguyen ◽  
...  

Social behavior is essential for the health, survival and reproduction of animals, yet the role of astrocytes in social behavior is largely unknown. CD38 is critical for social behaviors by regulating oxytocin release from hypothalamic neurons. On the other hand, CD38 is most abundantly expressed in astrocytes especially in the postnatal cortex, and is important for astroglial development. Here, we demonstrate that astroglial CD38 plays a pivotal role in the social behavior. Selective deletion of CD38 in postnatal astrocytes, but not in adult astrocytes, specifically impaired social memory without any other behavioral abnormalities. Morphological analysis revealed reductions in spine numbers, mature spines and excitatory synapse numbers in the pyramidal neurons of the medial prefrontal cortex (mPFC) due to deletion of astroglial CD38 in the postnatal brain. Astrocyte-conditioned medium (ACM) of CD38 KO astrocytes reduced synaptogenesis of cortical neurons by reducing extracellular SPARCL1, a synaptogenic protein. Finally, the release of SPARCL1 from astrocytes is regulated by CD38/cADPR/calcium signaling. Our data indicate that astroglial CD38 developmentally regulates social memory and neural circuit formation in the developing brain by promoting synaptogenesis through SPARCL1.


2021 ◽  
Vol 15 ◽  
Author(s):  
Taylor Jefferson ◽  
Crystle J. Kelly ◽  
Marco Martina

Chronic pain patients suffer a disrupted quality of life not only from the experience of pain itself, but also from comorbid symptoms such as depression, anxiety, cognitive impairment, and sleep disturbances. The heterogeneity of these symptoms support the idea of a major involvement of the cerebral cortex in the chronic pain condition. Accordingly, abundant evidence shows that in chronic pain the activity of the medial prefrontal cortex (mPFC), a brain region that is critical for executive function and working memory, is severely impaired. Excitability of the mPFC depends on the integrated effects of intrinsic excitability and excitatory and inhibitory inputs. The main extracortical sources of excitatory input to the mPFC originate in the thalamus, hippocampus, and amygdala, which allow the mPFC to integrate multiple information streams necessary for cognitive control of pain including sensory information, context, and emotional salience. Recent techniques, such as optogenetic methods of circuit dissection, have made it possible to tease apart the contributions of individual circuit components. Here we review the synaptic properties of these main glutamatergic inputs to the rodent mPFC, how each is altered in animal models of chronic pain, and how these alterations contribute to pain-associated mPFC deactivation. By understanding the contributions of these individual circuit components, we strive to understand the broad spectrum of chronic pain and comorbid pathologies, how they are generated, and how they might be alleviated.


2021 ◽  
Author(s):  
Cong-Cong Fu ◽  
Xin-Yi Zhang ◽  
Liu Xu ◽  
Hui-Xian Huang ◽  
Shuang Xu ◽  
...  

Abstract ObjectiveEpidemiological studies suggest a bidirectional association between depression and obesity; however, the biological mechanisms that link the development of depression to a metabolic disorder remain unclear. Even though nuclear receptor peroxisome proliferator-activated receptor γ (PPARγ) agonists show anti-depressive effect, and high-fat diet-(HFD)-induced PPARγ dysfunction is involved in the pathogenesis of metabolic disorders, the neuronal PPARg has never been studied in HFD-induced depression. Thus, we aimed to investigate the effect of neuronal PPARγ on depressive-like behaviors in HFD-induced obese mice. MethodsWe fed male C57BL/6J mice with HFD to generate obese mice and conducted a series of behavioral tests to assess the effects of HFD feeding on depression. We generated neuron-specific PPARγ knockout mice (NKO) to determine whether neuronal PPARg deficiency was correlated with depressive-like behaviors. To further prove whether PPARγ in the medial prefrontal cortex (mPFC) neurons is involved in depressive-like behaviors, we applied AAV- CaMKIIa-Cre approach to specifically knockout PPARγ in the mPFC neurons of LoxP mice and used AAV-syn-PPARγ vectors to overexpress PPARγ in the mPFC neurons of NKO mice. ResultsWe observed a low mPFC PPARγ level and an increase in depressive-like behaviors in the HFD-fed mice. Moreover, neuronal-specific PPARγ deficiency in mice induced depressive-like behaviors, which could be abolished by imipramine. Furthermore, overexpressing PPARg in the mPFC reversed the depressive-like behaviors in HFD-fed mice as well as in neuronal-specific PPARγ knockout mice. ConclusionsThese results implicate that dysregulation of neuronal PPARγ in the mPFC may contribute to an increased risk for depression in obese populations.


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