scholarly journals Repeated Restraint Stress Led to Cognitive Dysfunction by NMDA Receptor-Mediated Hippocampal CA3 Dendritic Spine Impairments in Juvenile Sprague-Dawley Rats

2020 ◽  
Vol 13 ◽  
Author(s):  
Dong-sheng Sun ◽  
Gang Zhong ◽  
Hong-Xia Cao ◽  
Yu Hu ◽  
Xiao-Yue Hong ◽  
...  
2018 ◽  
Vol 30 (2) ◽  
pp. 265-273
Author(s):  
Rajiv Balyan ◽  
Ma Cai ◽  
Wenhong Zhao ◽  
Zhao Dai ◽  
Yujia Zhai ◽  
...  

Abstract BackgroundSulfotransferases (SULTs) are phase II drug-metabolizing enzymes. SULTs also regulate the biological activities of biological signaling molecules, such as various hormones, bile acids, and monoamine neurotransmitters; therefore, they play critical roles in the endocrine and nervous systems. People are subject to various kinds of physical, chemical, toxicological, physiological, and psychological stresses at one time or another. The study of the effects produced by stress may lead to finding novel remedies for many disease conditions. The effect of repeated restraint stress on rat SULT expression has not been studied. MethodsThis study involves the effect of repeated restraint stress on SULT1A1 expressions. Male Sprague-Dawley rats (n=4) were subjected to repeated restraint stress 2 h/day for 7 days. Protein and RNA expression of SULT1A1 were analyzed by western blot and quantitative real time reverse transcription polymerase chain reaction, respectively, in important tissues. ResultsWe observed that repeated restraint stress increased the expression of SULT1A1 in the liver, adrenal glands, cerebellum, hypothalamus, and cerebral cortex in male rats. Patterns of enhanced expression were observed at both mRNA and protein level, indicating that repeated restraint stress stimulates enzyme expression at the transcriptional level. ConclusionsChanges of SULT1A1 expression in important tissues caused by repeated restraint stress will have a significant effect on drug metabolism and xenobiotics detoxification. The significant changes in endocrine glands and brain sections may also cause disturbances in hormone homeostasis, therefore leading to disease conditions. This report provides clues for the understanding of the effect of stresses on health.


2021 ◽  
pp. 1-9
Author(s):  
Guizhen Liu ◽  
Yuchuan Sun ◽  
Fei Liu

<b><i>Objective:</i></b> The purpose of this study was to explore the role of curcumin (Cur) in isoflurane (ISO)-induced learning and memory dysfunction in Sprague-Dawley rats and further elucidate the mechanism of the protective effect produced by Cur. <b><i>Methods:</i></b> Rat models of cognitive impairment were established by inhaling 3% ISO. The Morris water maze test was used to assess the cognitive function of rats. ELISA and qRT-PCR were used to analyze the protein levels of pro-inflammatory cytokines and expression levels of miR-181a-5p, respectively. <b><i>Results:</i></b> Cur significantly improved the ISO-induced cognitive dysfunction in rats and alleviated the ISO-induced neuroinflammation. miR-181a-5p was overexpressed in ISO-induced rats, while Cur treatment significantly reduced the expression of miR-181a-5p. Overexpression of miR-181a-5p promoted the cognitive impairment and the release of inflammatory cytokines and reversed the neuroprotective effect of Cur. <b><i>Conclusion:</i></b> Cur has a protective effect on ISO-induced cognitive dysfunction, which may be achieved by regulating the expression of miR-181a-5p.


1999 ◽  
Vol 113 (5) ◽  
pp. 902-913 ◽  
Author(s):  
Cheryl D. Conrad ◽  
Ana María Magariños ◽  
Joseph E. LeDoux ◽  
Bruce S. McEwen

ISRN Pain ◽  
2013 ◽  
Vol 2013 ◽  
pp. 1-5
Author(s):  
Claudio Laurido ◽  
José L. Martínez ◽  
Francisco Morales

The NMDA receptor is central in the generation and maintenance of chronic pain. This receptor has several sites of modulation. One is the glutamate recognition site that can be blocked by (±)-3-(2-carboxypiperazin-yl)propyl-1-phosphoric acid or (±)-CPP. We investigated whether the effect of glial inhibition produced by propentophylline (PPF) can be enhanced when combined with (±)-CPP. We used Sprague-Dawley rats with experimental monoarthritis, administering intrathecally the ED30 for both drugs (3.97 μg of (±)-CPP and 1.42 μg of PPF), since this combination produces an antinociceptive supra-additive effect when used in mechanical nociception (Randall-Selitto test). The combination of (±)-PPF and CPP produced an antinociceptive effect which was greater than that each drug alone as tested by both the C reflex and windup. We conclude that the antinociceptive effect of the combination of (±)-PPF and CPP possibly generates a supra additive interaction type in monoarthritic rats.


2006 ◽  
Vol 1077 (1) ◽  
pp. 7-15 ◽  
Author(s):  
Lenka Trnečková ◽  
Antonio Armario ◽  
Sixtus Hynie ◽  
Pavel Šída ◽  
Věra Klenerová

2000 ◽  
Vol 278 (6) ◽  
pp. G924-G929 ◽  
Author(s):  
M. Ali Gülpinar ◽  
Ayhan Bozkurt ◽  
Tamer Coşkun ◽  
Nefise B. Ulusoy ◽  
Berrak Ç. Yeǧen

In addition to its insulinotropic action, exogenously administered glucagon-like peptide (GLP-1) inhibits gastropancreatic motility and secretion via central pathways. The aims of the present study were to evaluate the effects of exogenous GLP-1-(7–36) amide on fecal output and to investigate the role of endogenous GLP-1 on stress-induced colonic activity. With the use of a stereotaxic instrument, adult male Sprague-Dawley rats weighing 200–250 g were fitted with stainless steel cerebroventricular guide cannulas under ketamine anesthesia. A group of rats were placed in Bollman-type cages to induce restraint stress. Fecal output monitored for 2 h was increased significantly by intracerebroventricular GLP-1 to 500, 1,000, and 3,000 pmol/rat ( P < 0.05–0.01), whereas intraperitoneal GLP-1 had no effect. Intracerebroventricular administration of the GLP-1 receptor antagonist exendin-(9–39) (10 nmol/rat) reversed the increases induced by GLP-1 (500 pmol/rat; P < 0.01). Similar results were also observed with the injection of corticotropin-releasing factor receptor antagonist astressin (10 μg/rat icv). The significant increase in fecal pellet output induced by restraint stress was also decreased by both intracerebroventricular exendin (10 nmol/rat) and astressin (10 μg/rat; P < 0.01–0.001). These results suggest that GLP-1 participates in the central, but not peripheral, regulation of colonic motility via its own receptor and that GLP-1 is likely to be a candidate brain-gut peptide that acts as a physiological modulator of stress-induced colonic motility.


2007 ◽  
Vol 293 (3) ◽  
pp. R1022-R1026 ◽  
Author(s):  
Dolores F. Doane ◽  
Marcus A. Lawson ◽  
Jonathan R. Meade ◽  
Catherine M. Kotz ◽  
J. Lee Beverly

Food intake is stimulated following administration of orexin-A into the perifornical region of the lateral hypothalamus (LH/PFA). Orexin neurons originating in the LH/PFA interact with a number of hypothalamic systems known to influence food intake, including glutamatergic neurons. Glutamatergic systems in the LH/PFA were demonstrated to initiate feeding through N-methyl-d-aspartic acid (NMDA) receptors. Male Sprague-Dawley rats fitted with brain guide cannulas to the LH/PFA were used in two experiments. In the first experiment, a combination microdialysis/microinjection probe was used to deliver artificial cerebrospinal fluid (aCSF) or 500 pmol of orexin-A into the LH/PFA. Orexin-A increased interstitial glutamate to 143 ± 12% of baseline ( P < 0.05), which remained elevated over the 120-min collection period. In the second experiment, the NMDA receptor antagonist d-2-amino-5-phosphonopentanoic acid (d-AP5; 10 nmol) was administered before orexin-A. The orexin-induced increase in food intake (from 1.1 ± 0.4 to 3.2 ± 0.5 g, P < 0.05) during the first hour was absent in rats receiving d-AP5 + orexin-A (1.2 ± 0.5 g). There was no effect of d-AP5 alone on food intake. These data support glutamatergic systems in the LH/PFA mediating the feeding response to orexin-A through NMDA receptors.


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