Linkage of stress-induced hypocalcemia, gastric lesions, and emotional behavior in Wistar-Kyoto rats

1994 ◽  
Vol 266 (3) ◽  
pp. R960-R965 ◽  
Author(s):  
J. Ma ◽  
S. Aou ◽  
T. Hori ◽  
J. Ding
Keyword(s):  
Wistar Rats ◽  
Emotional Behavior ◽  
Dependent Manner ◽  
Gastric Lesions ◽  
Blood Calcium ◽  
Wky Rats ◽  
Immobility Time ◽  
Behavioral Responsiveness ◽  
Swimming Test ◽  
Wistar Kyoto

The effects of water-restraint stress on blood calcium levels and gastric pathology and their behavioral relevance were examined in Wistar-Kyoto (WKY) and Wistar rats. The stress induced more severe hypocalcemia (0.32 mM decrease) and gastric lesions (34.6 mm in mean length) in WKY rats than in Wistar rats (0.19 mM and 17.7 mm, respectively). The magnitude of hypocalcemia correlated positively with that of gastric lesions in both strains (WKY, r = 0.59; Wistar, r = 0.69). In the forced-swimming test, WKY rats exhibited a longer immobility time (6.53 min) and a shorter struggling time (0.54 min) than Wistar rats (3.33 and 1.90 min, respectively). The severity of hypocalcemia and gastric lesions correlated positively (r = 0.59 and 0.69, respectively) with the length of immobility time in the WKY rats, while it correlated negatively (r = -0.70 and -0.61, respectively) with the length of struggling time in the Wistar rats. These results suggest that stress-induced hypocalcemia and gastric lesions are closely related and are also influenced by behavioral responsiveness in a strain-dependent manner.

Clinical doses of citalopram or reboxetine differentially modulate passive and active behaviors of female Wistar rats with high or low immobility time in the forced swimming test

2013 ◽  
Vol 110 ◽  
pp. 89-97 ◽  
Author(s):  
Ana Gisela Flores-Serrano ◽  
María Leonor Vila-Luna ◽  
Fernando José Álvarez-Cervera ◽  
Francisco José Heredia-López ◽  
José Luis Góngora-Alfaro ◽  
...  
Keyword(s):  
Wistar Rats ◽  
Forced Swimming Test ◽  
Forced Swimming ◽  
Immobility Time ◽  
Female Wistar Rats ◽  
Swimming Test

Altered hormone levels and circadian rhythm of activity in the WKY rat, a putative animal model of depression

2001 ◽  
Vol 281 (3) ◽  
pp. R786-R794 ◽  
Author(s):  
Leah C. Solberg ◽  
Susan Losee Olson ◽  
Fred W. Turek ◽  
Eva Redei
Keyword(s):  
Circadian Rhythm ◽  
Wistar Rats ◽  
Depressive Disorders ◽  
Rat Plasma ◽  
Thyroid Stimulating Hormone ◽  
Constant Darkness ◽  
Wky Rats ◽  
Animal Model Of Depression ◽  
Wistar Kyoto ◽  
Free Running Period

The Wistar Kyoto (WKY) rat is hyperreactive to stress and exhibits depressive-like behavior in several standard behavioral tests. Because patients with depressive disorders often exhibit disruptions in the circadian rhythm of activity, as well as altered secretory patterns of the hypothalamic-pituitary-adrenal and hypothalamic-pituitary-thyroid hormones, we tested the hypothesis that these phenomena occur in the WKY rat. Plasma ACTH and corticosterone levels remained significantly higher after the diurnal peak for several hours in WKY rats relative to Wistar rats. Also, plasma levels of thyroid-stimulating hormone were significantly higher in WKY relative to Wistar rats across the 24-h period, despite normal or slightly higher levels of 3,5,3′-triiodothyronine. In addition, under constant darkness conditions, WKY rats exhibited a shorter free running period and a decreased response to a phase-delaying light pulse compared with Wistar rats. In several ways these results are similar to those seen in other animal models of depression as well as in depressed humans, suggesting that the WKY rat could be used to investigate the genetic basis for these abnormalities.

Hypothalamic linkage in stress-induced hypocalcemia, gastric damage, and emotional behavior in rats

1994 ◽  
Vol 267 (1) ◽  
pp. R38-R43 ◽  
Author(s):  
S. Aou ◽  
J. Ma ◽  
T. Hori ◽  
N. Tashiro
Keyword(s):  
Restraint Stress ◽  
Opposite Effect ◽  
Forced Swimming Test ◽  
Emotional Behavior ◽  
Gastric Damage ◽  
Ventromedial Nucleus ◽  
Gastric Lesions ◽  
Swim Test ◽  
Swimming Test ◽  
Bilateral Lesions

The effects of hypothalamic lesions on stress-induced hypocalcemia, gastric damage, and swim test-evoked behavior were examined in rats. Bilateral lesions of the ventromedial nucleus in the hypothalamus (VMH) eliminated water-restraint stress-induced hypocalcemia and attenuated any gastric damage compared with those in the sham-operated rats. In contrast, lesions in the paraventricular nucleus (PVN) exacerbated both the stress-induced hypocalcemia and gastric lesions in comparison with those in the control rats. In a forced-swimming test, the VMH-lesioned rats showed a significantly shorter time of immobility as well as a longer duration of struggling than the control rats, respectively, while the PVN-lesioned animals spent a longer time in immobility and a shorter period struggling than the control rats. These results suggest that the VMH has an accelerative action in stress-induced hypocalcemia, gastric lesions, and behavioral despair, while the PVN has an opposite effect.

scholarly journals Antidepressant Effect ofTetragonia tetragonoides (Pall.) KuntzeExtract on Serotonin Turnover

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Hyun Yang ◽  
Hye Jin Kim ◽  
Eui-Ju Hong ◽  
Bo-Jeong Pyun ◽  
Byung-Seob Ko ◽  
...  
Keyword(s):  
Serum Level ◽  
Forced Swimming Test ◽  
Forced Swimming ◽  
Female Rats ◽  
Serotonin Level ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Ovx Rats ◽  
Immobility Time ◽  
Swimming Test

Tetragonia tetragonoides (Pall.) Kuntze(TTK) is a groundcover found along coastal areas of the Korean peninsula. TTK is traditionally used to improve women’s health and treat gastrointestinal diseases. Use of herbal medicines in the treatment of mood disorders has recently been suggested as an alternative therapeutic strategy. In the present study, we determined that consumption of TTK extract ameliorated progression of depressive-like symptoms in ovariectomized (OVX) rats and further examined the mechanisms involved, i.e., synthesis, release, and reuptake(s) of serotonin (also known as 5-HT). We assessed the mRNA expression levels of tryptophan hydroxylases (TPH-1 and TPH-2) and serotonin transporter (SERT) as well as the reuptake activity of serotonin in RBL-2H3 cells. We also determined whether or not TTK extract regulates the serum level of serotonin and improves depressive-like symptoms in 0.5, 1, and 2% TTK-fed OVX female rats in a forced swimming test. Our results show that the mRNA levels of TPH-1 and SERT were significantly reduced, whereas the mRNA level of TPH-2 was dose-dependently elevated by TTK (50 and 100μg/mL) in RBL-2H3 cells. TTK significantly inhibited LPS- (lipopolysaccharide-) induced serotonin uptake in RBL-2H3 cells in a dose-dependent manner. The serum level(s) of serotonin was elevated by 1% and 2% TTK treatment in OVX female rats. Moreover, immobility time in the forced swimming test was reduced by 1% and 2% TTK treatment but not altered by 0.5% TTK treatment in OVX female rats. Taken together, these results indicate that TTK may significantly inhibit depressive-like symptoms due to upregulation of serotonin level(s) and regulation of serotonin reuptake activity. Thus, TTK may exert beneficial effects on depression during pre- or/and postmenopausal periodsviamodulation of serotonin synthesis and metabolism.

Central ANG II-receptor antagonists impair cardiovascular and vasopressin response to hemorrhage in rats

1995 ◽  
Vol 268 (6) ◽  
pp. R1500-R1506 ◽  
Author(s):  
W. J. Lee ◽  
E. K. Yang ◽  
D. K. Ahn ◽  
Y. Y. Park ◽  
J. S. Park ◽  
...  
Keyword(s):  
Wistar Rats ◽  
Physiological Role ◽  
Ang Ii ◽  
Vasopressin Release ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Artificial Cerebrospinal Fluid ◽  
Wistar Kyoto ◽  
Different Strains

The role of brain angiotensin II (ANG II) in mediating cardiovascular, vasopressin, and renin responses to hemorrhage was assessed in conscious spontaneously hypertensive rats (SHR) and in normotensive Wistar-Kyoto (WKY) and Wistar rats. Intracerebroventricular administration of losartan (10 micrograms) and saralasin (1 microgram.microliter-1.min-1) produced a markedly greater fall in blood pressure and a reduced tachycardia during and after hemorrhage (15 ml/kg) compared with the artificial cerebrospinal fluid control in SHR and Wistar rats but not in WKY rats. Vasopressin release after hemorrhage was also impaired, but renin release was enhanced by intracerebroventricular ANG II antagonists in SHR and Wistar rats but not in WKY rats. Losartan and saralasin produced remarkably similar effects on the cardiovascular, vasopressin, and renin responses to hemorrhage. These data suggest that brain ANG II acting through AT1 receptors plays an important physiological role in mediating rapid cardiovascular regulation and vasopressin release in response to hemorrhage. The relative importance of brain angiotensin system may vary in different strains of rate.

Myocardial hypertrophy of normotensive Wistar-Kyoto rats

2004 ◽  
Vol 286 (4) ◽  
pp. H1229-H1235 ◽  
Author(s):  
Ernesto A. Aiello ◽  
María C. Villa-Abrille ◽  
Eduardo M. Escudero ◽  
Enrique L. Portiansky ◽  
Néstor G. Pérez ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Hypertrophy ◽  
Wistar Rats ◽  
Left Ventricular ◽  
Cross Sectional Area ◽  
Sectional Area ◽  
Cross Sectional ◽  
Wky Rats ◽  
Wistar Kyoto ◽  
Cell Capacitance

In our studies with spontaneously hypertensive (SHR), Wistar-Kyoto (WKY), and Wistar rats, we observed normotensive WKY rats with cardiac hypertrophy determined by a greater left ventricular (LV) mass (LVM)-to-body weight (BW) ratio (LVM/BW) than that of normotensive Wistar rats. Thus we compared the following parameters in SHR, WKY, and Wistar rats: LVM/BW, cell capacitance as index of total surface area of the myocytes, length, width, and cross-sectional area of cardiac myocytes, LV collagen volume fraction, and myocardial stiffness. The LVM/BW of WKY (2.41 ± 0.03 mg/g, n = 41) was intermediate between SHR (2.82 ± 0.04 mg/g, n = 47) and Wistar rats (1.98 ± 0.04 mg/g, n = 28). A positive correlation between blood pressure and LVM was found in SHR, whereas no such relationship was observed in WKY or Wistar rats. Cell capacitance and cross-sectional area were not significantly different in SHR and WKY rats; these values were significantly higher than those of Wistar rats. The cell length was smaller but the width was similar in WKY compared with SHR. Papillary muscles isolated from the LV of WKY and SHR were stiffer than those from Wistar rats. Consistently, a greater level of myocardial fibrosis was detected in WKY and SHR compared with Wistar rats. These findings demonstrate blood pressure-independent cardiac hypertrophy in normotensive WKY rats.

scholarly journals Curcumin evokes antidepressant-like effects in mice by regulating miR-124/brain derived neurotrophic factor

2021 ◽  
Vol 18 (3) ◽  
pp. 603-609
Author(s):  
Yanhong Yi ◽  
Jing Li ◽  
Weian Chen
Keyword(s):  
Neurotrophic Factor ◽  
Preference Test ◽  
Brain Derived Neurotrophic Factor ◽  
Mild Stress ◽  
Dependent Manner ◽  
Immobility Time ◽  
Swimming Test ◽  
Sucrose Preference Test ◽  
Loss Of Appetite

Purpose: To investigate the effect and mechanism of curcumin on depression in mice Methods: Mice were subjected to chronic unpredictable mild stress (CUMS), and behavioural changes were evaluated by sucrose preference test (SPT) and forced swimming test (FST). CUMS-treated mice received curcumin at a concentration of 50, 100, or 200 mg/kg. The level of MiR-124 was measured by real-time polymerase chain reaction (RT-PCR). Brain-derived neurotrophic factor (BDNF) levels were evaluated by western blotting. Results: CUMS induced depressive behaviour in mice, with increase in miR-124 and decrease in BDNF. Curcumin inhibited miR-124 expression and promoted BDNF in a dose-dependent manner in CUMS-treated mice. Brain-derived neurotrophic factor was the direct target of miR-124, decreasing the transcription of BDNF, but this was reversed by curcumin in vitro. MicroRNA-124 overexpression aggravated CUMS-induced depressive symptoms including loss of appetite, less sucrose consumption, shorter swimming time, and longer immobility time (p < 0.001). The effects were attenuated by curcumin. Conclusion: Curcumin alleviates CUMS-induced depressive behaviour by regulating miR-124/BDNF, suggesting that curcumin may a viable treatment option for depression.

scholarly journals Aerobic Exercise Prevents Depression via Alleviating Hippocampus Injury in Chronic Stressed Depression Rats

2020 ◽  
Vol 11 (1) ◽  
pp. 9
Author(s):  
Jie Kang ◽  
Di Wang ◽  
Yongchang Duan ◽  
Lin Zhai ◽  
Lin Shi ◽  
...  
Keyword(s):  
Aerobic Exercise ◽  
Mild Stress ◽  
Glutamatergic System ◽  
Sprague Dawley ◽  
Bdnf Expression ◽  
Sprague Dawley Rats ◽  
Immobility Time ◽  
Neurotoxic Effects ◽  
Swimming Test ◽  
Underlying Mechanisms

(1) Background: Depression is one of the overwhelming public health problems. Alleviating hippocampus injury may prevent depression development. Herein, we established the chronic unpredictable mild stress (CUMS) model and aimed to investigate whether aerobic exercise (AE) could alleviate CUMS induced depression-like behaviors and hippocampus injury. (2) Methods: Forty-eight healthy male Sprague-Dawley rats (200 ± 20 g) were randomly divided into 4 groups (control, CUMS, CUMS + 7 days AE, CUMS + 14 days AE). Rats with AE treatments were subjected to 45 min treadmill per day. (3) Results: AE intervention significantly improved CUMS-induced depressive behaviors, e.g., running square numbers and immobility time assessed by the open field and forced swimming test, suppressed hippocampal neuron apoptosis, reduced levels of phosphorylation of NMDA receptor and homocysteine in hippocampus, as well as serum glucocorticoids, compared to the CUMS rats. In contrast, AE upregulated phosphorylation of AMPAR receptor and brain-derived neurotrophic factor (BDNF) hippocampus in CUMS depression rats. The 14 day-AE treatment exhibited better performance than 7 day-AE on the improvement of the hippocampal function. (4) Conclusion: AE might be an efficient strategy for prevention of CUMS-induced depression via ameliorating hippocampus functions. Underlying mechanisms may be related with glutamatergic system, the neurotoxic effects of homocysteine, and/or influences in glucocorticoids-BDNF expression interaction.

Enhanced renal sensitivity of the spontaneously hypertensive rat to urotensin II

2008 ◽  
Vol 295 (4) ◽  
pp. F1239-F1247 ◽  
Author(s):  
Alaa E. S. Abdel-Razik ◽  
Richard J. Balment ◽  
Nick Ashton
Keyword(s):  
Renal Function ◽  
Spontaneously Hypertensive Rat ◽  
Renal Medulla ◽  
Fractional Excretion ◽  
Urotensin Ii ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Hypertensive Rat ◽  
Fractional Excretion Of Sodium ◽  
Wistar Kyoto

Urotensin II (UII) has been implicated widely in cardiovascular disease. The mechanism(s) through which it contributes to elevated blood pressure is unknown, but its emerging role as a regulator of mammalian renal function suggests that the kidney might be involved. The aim of this study was to determine the effect of UII on renal function in the spontaneously hypertensive rat (SHR). UII infusion (6 pmol·min−1·100 g body wt−1) in anesthetized SHR and control Wistar-Kyoto (WKY) rats produced marked reductions in glomerular filtration rate (ΔGFR WKY, n = 7, −0.3 ± 0.1 vs. SHR, n = 7, −0.6 ± 0.1 ml·min−1·100 g body wt−1, P = 0.03), urine flow, and sodium excretion rates, which were greater in SHR by comparison with WKY rats. WKY rats also showed an increase in fractional excretion of sodium (ΔFENa; +0.6 ± 0.1%, P = 0.02) in contrast to SHR in which no such change was observed (ΔFENa −0.6 ± 0.2%). Blockade of the UII receptor (UT), and thus endogenous UII activity, with urantide evoked an increase in GFR which was greater in SHR (+0.3 ± 0.1) compared with WKY rats (+0.1 ± 0.1 ml·min−1·100 g body wt−1, P = 0.04) and was accompanied by a diuresis and natriuresis. UII and UT mRNA expression were greater in the renal medulla than the cortex of both strains; however, expression levels were up to threefold higher in SHR tissue. SHR are more sensitive than WKY to UII, which acts primarily to lower GFR thus favoring salt retention in this model of hypertension.

Sign in / Sign up

Export Citation Format

Share Document