Reduced immobility time in the tail suspension test (TST) by chronic immobilization stress. Role of corticosterone and brain serotonergic and adrenergic receptors

1992 ◽  
Vol 7 (5) ◽  
pp. 235-238
Author(s):  
E De Castro-e-Silva ◽  
MF Peres ◽  
P Brito ◽  
C Cobas ◽  
A Saraiva ◽  
...  
Keyword(s):  
Immobilization Stress ◽  
Chronic Administration ◽  
Tail Suspension Test ◽  
Tail Suspension ◽  
Immobility Time ◽  
Adrenoceptor Blocker ◽  
Induced Changes ◽  
Chronic Immobilization Stress ◽  
Suspension Test

SummaryChronically stressed adult male Balb C mice were submitted to the tail suspension test. Chronic immobilization stress (6 h/d for 14 consecutive days) induced a significant reduction in immobility time when compared to non-stressed controls. Pretreatment with LY 53857, a serotonin 5HT2 antagonist, and IPS 339, a selective beta-2 adrenoceptor blocker, reversed immobility time to the levels of non-stressed controls. Chronic administration of corticosterone (100 mg/kg for 7 d) did not modify immobility time as compared to saline treated controls. It is suggested that both serotonergic and adrenergic pathways in the brain may participate in the stress-induced changes occurring in the tail suspension test response and that corticosterone does not appear to play a role in this process.

scholarly journals Evaluation of antidepressant activity of tramadol in comparison with imipramine in Swiss albino mice

2017 ◽  
Vol 6 (3) ◽  
pp. 695
Author(s):  
Chiranjeevi Bonda ◽  
Sudhir Pawar ◽  
Jaisen Lokhande
Keyword(s):  
Forced Swim Test ◽  
Antidepressant Activity ◽  
Tail Suspension Test ◽  
Antidepressant Effect ◽  
Tail Suspension ◽  
Swim Test ◽  
Forced Swim ◽  
Group I ◽  
Immobility Time ◽  
Suspension Test

Background: The aim of the study was to evaluate the antidepressant effect of opioid analgesic tramadol using forced swim test and tail suspension test models.Methods: The antidepressant effect was assessed by recording the immobility time in Forced swim test (FST) and Tail suspension test (TST). The mice were randomly divided into five groups. Mice belonging to group I was given normal saline (0.1ml/kg) which acted as control. Group II received imipramine (15mg/kg) considered as the standard drug tramadol was given in graded dose (10, 20 and 40 mg/kg) to mice of groups III, IV, V respectively. All drugs were administered intraperitoneally for seven successive days; test was done on 7th day.Results: Tramadol and Imipramine showed antidepressant activity when compared to control. There is dose dependent increase in antidepressant activity of tramadol. The antidepressant activity of imipramine was significantly (P<0.05) more than tramadol at dose 10 and 20 mg/kg but antidepressant activity with tramadol 40mg/kg was comparable to imipramine treated mice.Conclusions: The results of this study indicated the presence of antidepressant activity of tramadol at 40mg/kg.

scholarly journals Role of 5-HT1A and 5-HT2A receptors in the antidepressant activity of YM992 in the mouse tail suspension test

1997 ◽  
Vol 73 ◽  
pp. 173
Author(s):  
Hiromi Takcuchi ◽  
Shin-ichi Yatsugi ◽  
Ken-ichi Hatanaka ◽  
Satoshi Hayashihe ◽  
Shin-ichi Tsukamoto ◽  
...  
Keyword(s):  
Antidepressant Activity ◽  
Tail Suspension Test ◽  
Tail Suspension ◽  
Suspension Test

scholarly journals Neurobehavioral and neuroprotective role of captopril in the rotenone model of rat Parkinsonism

2019 ◽  
Vol 10 (4) ◽  
pp. 3523-3534
Author(s):  
Prakash KG ◽  
Bannur BM ◽  
Madhavrao C ◽  
Saniya K ◽  
Sudha M J ◽  
...  
Keyword(s):  
Forced Swim Test ◽  
Tail Suspension Test ◽  
Tail Suspension ◽  
Rotarod Test ◽  
Swim Test ◽  
Board Test ◽  
Hole Board ◽  
Hole Board Test ◽  
Suspension Test

Angiotensin-converting enzymes are increasingly being tested in therapeutics of Parkinsonism. The objective of the present study was to evaluate the behavioral changes and neuroprotective role of captopril in the rotenone model of Parkinsonism in rats. Adult Wistar albino rats were divided into four groups of six each. Parkinsonism was induced with rotenone (3 mg/Kg intraperitoneal) in three groups. The experimental group was treated with captopril (20 mg/kg intraperitoneal). The effects were compared with a standard group treated with levodopa (12 mg/Kg) and Benserazide (3 mg/Kg). Behavioral effects were evaluated by the rotarod test, spontaneous locomotor activity, hole board test, forced swim test, and tail suspension test. Neuroprotection was noted with an estimation of glutathione and lipid peroxidation from rat brain homogenate. Levels of dopamine, serotonin, and GABA were also noted. Haematoxylin and eosin-stained sections of the brain evaluated for any histoarchitectural changes. Rats pre-treated with captopril have shown a significant increase in the duration of stay in the rotarod test, a significant increase in the number of head dipping in hole board test, significant lower duration of immobility in forced swim test and tail suspension test. Captopril has a significant neuroprotective role, as evidenced by a significant decrease in levels of glutathione and a significant increase in lipid peroxidase, myeloperoxidase, catalase, superoxide dismutase, and MAO-B levels. Captopril has significant effects on brain neurotransmitters, as evidenced by dopamine, serotonin, and acetylcholine. Captopril has shown significant neuronal protection by increased expression of Bcl-2 immunohistochemistry in rotenone-induced PD. Captopril has shown significant improvement in motor coordination (as evidenced through rotarod test), exploratory behavior (hole board test), depression (forced swimming test, and tail suspension test). Captopril significantly reduces oxidative stress conditions. Captopril has not shown major histoanatomical changes in the rotenone model. Angiotensin-converting enzyme inhibitors; neuroprotection; dopaminergic neurons; Parkinsonism; rotenone model

scholarly journals Homeostasis Imbalance of Microglia and Astrocytes Leads to Alteration in the Metabolites of the Kynurenine Pathway in LPS-Induced Depressive-Like Mice

2020 ◽  
Vol 21 (4) ◽  
pp. 1460 ◽  
Author(s):  
Xue Tao ◽  
Mingzhu Yan ◽  
Lisha Wang ◽  
Yunfeng Zhou ◽  
Zhi Wang ◽  
...  
Keyword(s):  
Tail Suspension Test ◽  
Treated Group ◽  
Dose Effect ◽  
Tail Suspension ◽  
Linear Dose ◽  
Immobility Time ◽  
Non Linear ◽  
Dose Dependent ◽  
The Brain ◽  
Suspension Test

In the pathology-oriented study of depression, inflammation hypothesis has received increasing attention for recent years. To mimic the depressive state caused by inflammation, rodents injected intraperitoneally with lipopolysaccharide (LPS) are usually used to stimulate an immune response. However, the dose of LPS that causes depressive-like behavior varies widely across many literatures. Previous study has uncovered the non-linearity in the dose-effect relationship for the depressive-like behavior induced by LPS administration, while the reason for this is still unclear. The present study aims to investigate the underlying mechanisms of this non-linear dose-dependent relationship. Four groups of mice were injected intraperitoneally with different doses of LPS (0, 0.32, 0.8, and 2 mg/kg). The tail suspension test was conducted to evaluate the depressive-like behavior within 23–25 h after the LPS administration. The neuroplasticity was assessed by the levels of related proteins, TrkB and PSD-95, and by the quantification of neurons using Nissl staining. The levels of the two metabolites of the kynurenine (KYN) pathway, 3-hydroxykynurenine (3-HK) and kynurenic acid (KYNA), in the brain were analyzed by LC-MS/MS. Activation of microglia and astrocytes in the brain were also determined by immunohistochemistry and western blotting, respectively. The results showed that, compared with the control group, the mice in the 0.8 mg/kg LPS-treated group exhibited a remarkable increase of immobility time in the tail suspension test. The neuroplasticity of mice in the 0.8 mg/kg LPS-treated group was also significantly reduced. The neurotoxic metabolite, 3-HK, was accumulated significantly in the hippocampus of the 0.8 mg/kg LPS-treated mice. Surprisingly, the 2 mg/kg LPS-treated mice did not exhibit a remarkable change of 3-HK but expressed increased KYNA significantly, which is neuroprotective. Furthermore, the activation of microglia and astrocytes, which were recognized as the primary source of 3-HK and KYNA, respectively, corresponded to the content of these two metabolites of the KYN pathway in each group. Consequently, it was speculated that the homeostasis of different glial cells could lead to a non-linear dose-dependent behavior by regulating the KYN pathway in the LPS-induced depressive-like mice.

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