首页> 外文期刊>American Journal of Physiology >Colitis induces CRF expression in hypothalamic magnocellular neurons and blunts CRF gene response to stress in rats.
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Colitis induces CRF expression in hypothalamic magnocellular neurons and blunts CRF gene response to stress in rats.

机译:结肠炎在下丘脑大细胞神经元中诱导CRF表达,并钝化CRF基因对大鼠的应激反应。

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摘要

We investigated hypothalamic neuronal corticotropin-releasing factor (CRF) gene expression changes in response to visceral inflammation induced by 2,4,6-trinitrobenzenesulfonic acid (TNB) and acute stress. Seven days after TNB, rats were subjected to water-avoidance stress (WAS) or restraint for 30 min and euthanized. Hypothalamic CRF primary transcripts (heteronuclear RNA, hnRNA) and CRF and arginine vasopressin (AVP) mRNAs were assessed by in situ hybridization. Antisense (35)S-labeled cRNA probes against CRF mRNA intronic and exonic sequences and an oligonucleotide probe against the AVP mRNA were used. TNB induced macroscopic lesions and a fivefold elevation in myeloperoxidase activity in the colon. Colitis increased CRF hnRNA and mRNA signals in the magnocellular part of the paraventricular nucleus of the hypothalamus (PVN) and supraoptic neurons, whereas AVP mRNA was not altered. Colitis did not modify CRF hnRNA signal in the parvocellular part of the PVN (pPVN), plasma corticosterone, and serum osmolarity levels. However, CRF hnRNA expression in the pPVN and the rise in corticosterone and defecation induced by WAS or restraint were blunted in colitic rats. These data show that colitis upregulates CRF gene synthesis in magnocellular hypothalamic neurons but dampens CRF gene transcription in the pPVN and plasma corticosterone responses to environmental acute stressors.
机译:我们调查了下丘脑神经元促肾上腺皮质激素释放因子(CRF)基因表达变化以响应由2,4,6-三硝基苯磺酸(TNB)和急性应激引起的内脏炎症。 TNB后7天,对大鼠进行避水胁迫(WAS)或约束30分钟,然后实施安乐死。通过原位杂交评估下丘脑CRF初级转录本(异核RNA,hnRNA)以及CRF和精氨酸加压素(AVP)mRNA。使用了针对CRF mRNA内含子和外显子序列的反义(35)S标记cRNA探针和针对AVP mRNA的寡核苷酸探针。 TNB引起肉眼可见的病变,结肠中的过氧化物酶活性增加了五倍。结肠炎会增加下丘脑室旁核(PVN)和视上神经元的大细胞部分的CRF hnRNA和mRNA信号,而AVP mRNA却没有改变。结肠炎并未改变PVN(pPVN)的小细胞部分,血浆皮质酮和血清渗透压水平的CRF hnRNA信号。然而,在结肠炎大鼠中,pPVN中的CRF hnRNA表达以及WAS或约束引起的皮质酮升高和排便减少。这些数据表明,结肠炎会上调下丘脑神经元中CRF基因的合成,但会抑制pPVN中CRF基因的转录以及血浆皮质酮对环境急性应激源的反应。

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