scholarly journals LTP- and LTD-inducing stimulations cause opposite changes in arc/arg3.1 mRNA level in hippocampal area CA1 in vivo

Hippocampus ◽  
2010 ◽  
Vol 21 (12) ◽  
pp. 1290-1301 ◽  
Author(s):  
Eser Yilmaz-Rastoder ◽  
Takeaki Miyamae ◽  
Amy E. Braun ◽  
Edda Thiels
Keyword(s):  
Mrna Level ◽  
Area Ca1 ◽  
Hippocampal Area

scholarly journals Circadian modulation of neurons and astrocytes controls synaptic plasticity in hippocampal area CA1

2019 ◽  
Author(s):  
John P. McCauley ◽  
Maurice A. Petroccione ◽  
Lianna Y. D’Brant ◽  
Gabrielle C. Todd ◽  
Nurat Affinnih ◽  
...  
Keyword(s):  
Cognitive Processing ◽  
Temporal Dynamics ◽  
Rhythmic Activity ◽  
Surface Expression ◽  
Receptor Activation ◽  
Cellular Mechanisms ◽  
Functional Changes ◽  
Area Ca1 ◽  
Hippocampal Area

SummaryMost animal species operate according to a 24-hour period set by the suprachiasmatic nucleus (SCN) of the hypothalamus. The rhythmic activity of the SCN is known to modulate hippocampal-dependent memory processes, but the molecular and cellular mechanisms that account for this effect remain largely unknown. Here, we show that there are cell-type specific structural and functional changes that occur with circadian rhythmicity in neurons and astrocytes in hippocampal area CA1. Pyramidal neurons change the surface expression of NMDA receptors, whereas astrocytes change their proximity to synapses. Together, these phenomena alter glutamate clearance, receptor activation and integration of temporally clustered excitatory synaptic inputs, ultimately shaping hippocampal-dependent learningin vivo. We identify corticosterone as a key contributor to changes in synaptic strength. These findings identify important mechanisms through which neurons and astrocytes modify the molecular composition and structure of the synaptic environment, contribute to the local storage of information in the hippocampus and alter the temporal dynamics of cognitive processing.

scholarly journals The Potential Role of IL1RAP on Tumor Microenvironment-Related Inflammatory Factors in Stomach Adenocarcinoma

2021 ◽  
Vol 20 ◽  
pp. 153303382199528
Author(s):  
Qing Lv ◽  
Qinghua Xia ◽  
Anshu Li ◽  
Zhiyong Wang
Keyword(s):  
Tumor Microenvironment ◽  
Interleukin 1 ◽  
Mrna Level ◽  
Inflammatory Factors ◽  
Stomach Carcinoma ◽  
Downstream Target ◽  
Volume Weight

This study was performed to investigate the role of interleukin-1 receptor accessory protein (IL1RAP) in stomach carcinoma in vitro and in vivo, determine whether IL1RAP knockdown could regulate the development of stomach carcinoma, and elucidate the relationship between IL1RAP knockdown and inflammation by tumor microenvironment-related inflammatory factors in stomach carcinoma. We first used TCGA and GEPIA systems to predict the potential function of IL1RAP. Second, western blot and RT-PCR were used to analyze the expression, or mRNA level, of IL1RAP at different tissue or cell lines. Third, the occurrence and development of stomach carcinoma in vitro and in vivo were observed by using IL1RAP knockdown lentivirus. Finally, the inflammation of stomach carcinoma in vitro and in vivo was observed. Results show that in GEPIA and TCGA systems, IL1RAP expression in STAD tumor tissue was higher than normal, and high expression of IL1RAP in STAD patients had a worse prognostic outcome. Besides, GSEA shown IL1RAP was negative correlation of apopopsis, TLR4 and NF-κB signaling pathway. We also predicted that IL1RAP may related to IL-1 s, IL-33, and IL-36 s in STAD. The IL1RAP expression and mRNA level in tumor, or MGC803, cells were increased. Furthermore, IL1RAP knockdown by lentivirus could inhibit stomach carcinoma development in vitro and in vivo through weakening tumor cell proliferation, migration, invasion, therefore reducing tumor volume, weight, and biomarker levels, and increasing apoptotic level. Finally, we found IL1RAP knockdown could increase inflammation of tumor microenvironment-related inflammatory factors of stomach carcinoma, in vitro and in vivo. Our study demonstrates that IL1RAP is possibly able to regulate inflammation and apoptosis in stomach carcinoma. Furthermore, TLR4, NF-κB, IL-1 s, IL-33, and IL-36 s maybe the downstream target factor of IL1RAP in inflammation. These results may provide a new strategy for stomach carcinoma development by regulating inflammation.

Tri-iodothyronine increases insulin-like growth factor binding protein-4 expression in rat hepatocytes

1997 ◽  
Vol 154 (1) ◽  
pp. 155-165 ◽  
Author(s):  
I Demori ◽  
C Bottazzi ◽  
A Voci ◽  
G Gallo ◽  
J-G Scharf ◽  
...  
Keyword(s):  
Growth Factor ◽  
Binding Protein ◽  
Mrna Level ◽  
Insulin Like Growth Factor ◽  
Cultured Hepatocytes ◽  
Adult Rats ◽  
Direct Role ◽  
Factor Binding ◽  
Rat Thyroid

Abstract Previous in vivo studies demonstrated significant variations in insulin-like growth factor binding protein-1 (IGFBP-1), IGFBP-2 and IGFBP-4 hepatic mRNAs and/or serum levels depending on the rat thyroid status. In this study we employed cultured hepatocytes from adult rats to demonstrate a possible direct regulation of these genes by tri-iodothyronine (T3). Northern blot analysis revealed that IGFBP-1 and -4 messages were clearly expressed, whereas IGFBP-2 signal was barely detectable. No significant effects on IGFBP-1 mRNA level or on peptide secretion were detected in T3-cultured hepatocytes. In contrast, significant increases in IGFBP-4 mRNA steady-state levels as well as in IGFBP-4 secretion were observed in hepatocytes cultured for 12–24 h in the presence of T3. The T3 effect on IGFBP-4 transcript levels appears to consist of enhanced gene transcription and is independent of ongoing protein synthesis. The T3-increased IGFBP-4 expression in cultured hepatocytes is consistent with our in vivo experiments demonstrating an increase in hepatic IGFBP-4 mRNA and serum IGFBP-4 levels in T3-treated rats. Furthermore, significant decreases in hepatic IGFBP-4 message and serum IGFBP-4 levels were observed in hypothyroid rats compared with euthyroid controls. Our data establish an important direct role for thyroid hormone in regulating IGFBP-4 expression and consequently IGF activity. Journal of Endocrinology (1997) 154, 155–165

scholarly journals Sublayer-Specific Coding Dynamics during Spatial Navigation and Learning in Hippocampal Area CA1

Neuron ◽  
2016 ◽  
Vol 91 (3) ◽  
pp. 652-665 ◽  
Author(s):  
Nathan B. Danielson ◽  
Jeffrey D. Zaremba ◽  
Patrick Kaifosh ◽  
John Bowler ◽  
Max Ladow ◽  
...  
Keyword(s):  
Spatial Navigation ◽  
Area Ca1 ◽  
Hippocampal Area
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