scholarly journals Validation of the Wistar-kyoto Rat Kept in Solitary Housing as an Animal Model for Endogenous Depression Using Voxel-based Morphometry

2021 ◽  
Author(s):  
Takanobu Yoshii ◽  
Naoya Oishi ◽  
Yasutaka Sotozono ◽  
Anri Watanabe ◽  
Yuki Sakai ◽  
...  
Keyword(s):  
Animal Model ◽  
Cerebellar Nuclei ◽  
Endogenous Depression ◽  
Lateral Septum ◽  
Cerebellar Vermis ◽  
Mild Stress ◽  
Voxel Based Morphometry ◽  
Wky Rats ◽  
Study Results ◽  
Wistar Kyoto

Abstract Major depressive disorder is a common psychiatric condition that is often resistant to medication. The Wistar-Kyoto (WKY) rat has been suggested as an animal model of endogenous depression; however, it is challenging to translate results obtained in animal models into humans. Solitary housing is a mild stress paradigm that could simulate the environment of depressive patients with limited social activity due to symptoms. We used voxel-based morphometry to directly compare the solitary-housed WKY rat model with data from previous human studies, and validated our results with behavioural studies and correlation analyses. Atrophy in WKY rats was detected in the ventral hippocampus, caudate putamen, lateral septum, cerebellar vermis, and cerebellar nuclei (p < 0.05, corrected for family-wise error rate). Further, locomotor behaviour was negatively correlated with hippocampal atrophy and positively correlated with atrophy of the cerebellar vermis. The regions of brain atrophy validate WKY rats as an animal model for endogenous depression and can aid the translation of study results to humans. Our study also reveals the possibility of a cerebellar contribution to depression.

scholarly journals Monoamines, BDNF, Dehydroepiandrosterone, DHEA-Sulfate, and Childhood Depression—An Animal Model Study

2009 ◽  
Vol 2009 ◽  
pp. 1-11 ◽  
Author(s):  
O. Malkesman ◽  
T. Asaf ◽  
L. Shbiro ◽  
A. Goldstein ◽  
R. Maayan ◽  
...  
Keyword(s):  
Animal Model ◽  
Childhood Depression ◽  
Forced Swim Test ◽  
Dehydroepiandrosterone Sulfate ◽  
Brain Regions ◽  
Second Phase ◽  
Wky Rats ◽  
Model Study ◽  
Animal Model Study ◽  
Wistar Kyoto

Basal levels of monoamines and DHEA in four main limbic brain regions were measured in prepubertal Wistar Kyoto (WKY) rats (a putative animal model of childhood depression). Basal levels of “Brain-Derived Neurotrophic Factor (BDNF)” were also determined in two regions in the hippocampus, compared with Wistar strain controls. In the second phase, we examined the responsiveness of prepubertal WKY rats to different types of chronic antidepressant treatments: Fluoxetine, Desipramine, and dehydroepiandrosterone sulfate (DHEAS). WKY prepubertal rats exhibited different monoamine levels in the limbic system, reduced DHEA levels in the VTA and lower levels of BDNF in the hippocampus CA3 region compared to controls. In prepubertal WKY rats, only treatment with DHEAS produced a statistically significant decrease in immobility, compared to saline-administered controls in the forced swim test. Wistar controls were not affected by any antidepressant. The results imply that DHEA(S) and BDNF may be involved in the pathophysiology and pharmacotherapy of childhood depression.

scholarly journals AMPA receptors mediate the pro-cognitive effects of electrical and optogenetic stimulation of the medial prefrontal cortex in antidepressant non-responsive Wistar–Kyoto rats

2020 ◽  
Vol 34 (12) ◽  
pp. 1418-1430
Author(s):  
Mariusz Papp ◽  
Piotr Gruca ◽  
Magdalena Lason ◽  
Ewa Litwa ◽  
Wojciech Solecki ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Ampa Receptor ◽  
Ampa Receptors ◽  
Antidepressant Drugs ◽  
Mild Stress ◽  
Sucrose Intake ◽  
Wky Rats ◽  
Optogenetic Stimulation ◽  
Wistar Kyoto

Background: The chronic mild stress (CMS) procedure is a widely used animal model of depression, and its application in Wistar–Kyoto (WKY) rats has been validated as a model of antidepressant-refractory depression. While not responding to chronic treatment with antidepressant drugs, WKY rats do respond to acute deep brain stimulation (DBS) of the medial prefrontal cortex (mPFC). In antidepressant-responsive strains there is evidence suggesting a role for AMPA subtype of glutamate receptor in the action mechanism of both antidepressants and DBS. Methods: Animals were subjected to CMS for 6 to 8 weeks; sucrose intake was monitored weekly and novel object recognition (NOR) test was conducted following recovery from CMS. Wistars were treated chronically with venlafaxine (VEN), while WKY were treated acutely with either DBS, optogenetic stimulation (OGS) of virally-transduced (AAV5-hSyn-ChR2-EYFP) mPFC or ventral hippocampus, or acute intra-mPFC injection of the AMPA receptor positive allosteric modulator CX-516. The AMPA receptor antagonist NBQX was administered, at identical sites in mPFC, immediately following the exposure trial in the NOR. Results: Sucrose intake and NOR were suppressed by CMS, and restored by VEN in Wistars and by DBS, OGS, or CX-516 in WKY. However, OGS of the ventral hippocampal afferents to mPFC was ineffective. A low dose of NBQX selectively blocked the procognitive effect of VEN, DBS and OGS. Conclusions: These results suggest that activation of AMPA receptors in the mPFC represents a common pathway for the antidepressant effects of both conventional (VEN) and novel (DBS, OGS) antidepressant modalities, in both antidepressant responsive (Wistar) and antidepressant-resistant (WKY) rats.

Validation of chronic mild stress in the Wistar-Kyoto rat as an animal model of treatment-resistant depression

2019 ◽  
Vol 30 ◽  
pp. 239-250 ◽  
Author(s):  
Paul Willner ◽  
Piotr Gruca ◽  
Magdalena Lason ◽  
Katarzyna Tota-Glowczyk ◽  
Ewa Litwa ◽  
...  
Keyword(s):  
Animal Model ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Treatment Resistant Depression ◽  
Treatment Resistant ◽  
Wistar Kyoto Rat ◽  
Resistant Depression ◽  
Wistar Kyoto

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.

scholarly journals Strain Differences in the Chronic Mild Stress Animal Model of Depression and Anxiety in Mice

2014 ◽  
Vol 22 (5) ◽  
pp. 453-459 ◽  
Author(s):  
Yang-Hee Jung ◽  
Sa-Ik Hong ◽  
Shi-Xun Ma ◽  
Ji-Young Hwang ◽  
Jun-Sup Kim ◽  
...  
Keyword(s):  
Animal Model ◽  
Strain Differences ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Depression And Anxiety ◽  
Animal Model Of Depression

A metabolomics-based approach for ranking the depressive level in a chronic unpredictable mild stress rat model

RSC Advances ◽  
2016 ◽  
Vol 6 (31) ◽  
pp. 25751-25765 ◽  
Author(s):  
Xinyu Yu ◽  
Shanlei Qiao ◽  
Di Wang ◽  
Jiayong Dai ◽  
Jun Wang ◽  
...  
Keyword(s):  
Animal Model ◽  
Major Depressive Disorder ◽  
Prefrontal Cortex ◽  
Depressive Disorder ◽  
Rat Model ◽  
Untargeted Metabolomics ◽  
Mild Stress ◽  
Chronic Unpredictable Mild Stress ◽  
Major Depressive ◽  
Metabolomics Study

An untargeted metabolomics study to investigate the metabolome change in plasma, hippocampus and prefrontal cortex (PFC) in an animal model with a major depressive disorder (MDD) had been conducted.

scholarly journals Localization of the novel angiotensin peptide, angiotensin-(1-12), in heart and kidney of hypertensive and normotensive rats

2008 ◽  
Vol 294 (6) ◽  
pp. H2614-H2618 ◽  
Author(s):  
Jewell A. Jessup ◽  
Aaron J. Trask ◽  
Mark C. Chappell ◽  
Sayaka Nagata ◽  
Johji Kato ◽  
...  
Keyword(s):  
Ventricular Myocytes ◽  
Renal Tubules ◽  
Uptake Mechanism ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Angiotensin Peptide ◽  
Wistar Kyoto ◽  
Renal Tubular ◽  
Alternate Substrate ◽  
First Time

A low expression of angiotensinogen in the heart has been construed as indicating a circulating uptake mechanism to explain the local effects of angiotensin II on tissues. The recent identification of angiotensin-(1-12) in an array of rat organs suggests this propeptide may be an alternate substrate for local angiotensin production. To test this hypothesis, tissues from 11-wk-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats ( n = 14) were stained with purified antibodies directed to the COOH terminus of angiotensin-(1-12). Robust angiotensin-(1-12) staining was predominantly found in ventricular myocytes with less staining found in the medial layer of intracoronary arteries and vascular endothelium. In addition, angiotensin-(1-12) immunoreactivity was present in the proximal, distal, and collecting renal tubules within the deep cortical and outer medullary zones in both strains. Preadsorption of the antibody with angiotensin-(1-12) abolished staining in both tissues. Corresponding tissue measurements by radioimmunoassay showed 47% higher levels of angiotensin-(1-12) in the heart of SHR compared with WKY rats ( P < 0.05). In contrast, renal angiotensin-(1-12) levels were 16.5% lower in SHR compared with the WKY rats ( P < 0.05). This study shows for first time the localization of angiotensin-(1-12) in both cardiac myocytes and renal tubular components of WKY and SHR. In addition, we show that increased cardiac angiotensin-(1-12) concentrations in SHR is associated with a small, but statistically significant, reduction in renal angiotensin-(1-12) levels.

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