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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Filename: controllers/Detail.php
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Hypoglycemia-associated autonomic failure (HAAF) is a well-established complication of diabetes. Although HAAF has serious outcomes such as recurrent morbidity, coma, and death, the mechanisms of HAAF and its pathological components are largely unknown. Our previous studies have revealed that hypoglycemia is associated with the upregulation of an immediate early gene - FOS. In addition, it is documented that glucose deprivation activates neuronal autophagic activities. Therefore, the present study aimed to identify the role of FOS and one of the core components of the autophagy pathway, Beclin-1 (encoded by the BECN1 gene), in the regulation of autophagic mechanisms in embryonic hypothalamic neurons in response to hypoglycemic conditions. Embryonic Mouse Hypothalamic Cell Line N39 (mHypoE-N39 or N39) was cultured in reduced concentrations of glucose (2000, 900, 500, and 200 mg/L). Gene and protein expression, as well as immunofluorescence studies on autophagy were conducted under different reduced glucose concentrations in N39 hypothalamic neurons with and without FOS and BECN1 gene knockdowns (KD). The outcomes of the present study have demonstrated a significant increase in autophagosome formation and subsequent lysosomal degradation in the hypothalamic neurons in response to reduced glucose concentrations. This hypoglycemic response appears to be lowered to a similar extent in the FOS KD and BECN1 KD cells, albeit insignificantly from the negative control, is indicative of the involvement of FOS in the autophagic response of hypothalamic neurons to hypoglycemia. Moreover, the KD cells exhibited a change in morphology and reduced cell viability compared with the control cells. Our findings suggest that reduced FOS expression could potentially be associated with impaired autophagic activities that are dependent on BECN1, which could lead to decreased or blunted hypothalamic activation in response to hypoglycemia, and this, in turn, may contribute to the development of HAAF.
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http://dx.doi.org/10.1111/cts.13749 | DOI Listing |
Front Neurosci
December 2024
Department of Behavioral and Molecular Neurobiology, University of Regensburg, Regensburg, Germany.
Introduction: The development of stress-related psychopathologies, often associated with socio-emotional dysfunctions, is crucially determined by genetic and environmental factors, which shape the individual vulnerability or resilience to stress. Especially early adolescence is considered a vulnerable time for the development of psychopathologies. Various mouse strains are known to age-dependently differ in social, emotional, and endocrine stress responses based on genetic and epigenetic differences.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
December 2024
Medical Research Center, Affiliated Hospital 2 of Nantong University, Nantong, China.
Objective: Energy homeostasis is modulated by the hypothalamic is essential for obesity progression, however, the gene expression profiling remains to be fully understood.
Methods: GEO datasets were downloaded from the GEO website and analyzed by the R packages to obtain the DEGs. And, the WGCNA analysis and PPI networks of co-expressed DEGs were designed using STRING to get key genes.
Pain
November 2024
Center for Neuroscience, Indian Institute of Science, Bengaluru, Karnataka, India.
The neural mechanisms of the affective-motivational symptoms of chronic pain are poorly understood. In chronic pain, our innate coping mechanisms fail to provide relief. Hence, these behaviors are manifested at higher frequencies.
View Article and Find Full Text PDFVasopressin (AVP), a nonapeptide synthesized predominantly by magnocellular hypothalamic neurons, is conveyed to the posterior pituitary the pituitary stalk, where AVP is secreted into the circulation. Known to regulate blood pressure and water homeostasis, it also modulates diverse social behaviors, such as pair-bonding, social recognition and cognition in mammals including humans. Importantly, AVP modulates social behaviors in a gender-specific manner, perhaps, due to gender differences in the distribution in the brain of AVP and its main receptor AVPR1a.
View Article and Find Full Text PDFCaloric depletion leads to behavioral changes that help an animal find food and restore its homeostatic balance. Hunger increases exploration and risk-taking behavior, allowing an animal to forage for food despite risks; however, the neural circuitry underlying this change is unknown. Here, we characterize how hunger restructures an animal's spontaneous behavior as well as its directed exploration of a novel object.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!