Evaluation of antidepressant and memory-improving efficacy of aripiprazole and fluoxetine in alcohol-preferring rats

2013 ◽  
Vol 26 (2) ◽  
pp. 112-119 ◽  
Author(s):  
Kinga Burda-Malarz ◽  
Krzysztof Kus ◽  
Piotr Ratajczak ◽  
Anna Czubak ◽  
Elżbieta Nowakowska ◽  
...  
Keyword(s):  
Spatial Memory ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Combined Therapy ◽  
Morris Water Maze Test ◽  
Antidepressant Effect ◽  
Combined Administration ◽  
Swimming Test ◽  
Behavioural Tests ◽  
Design And Methods ◽  
Memory Deterioration

Introduction and aimsDependence on ethanol increases the risk of depression in patients and leads to a damage and deficiencies of brain function, which manifest in cognitive functions impairment. Aripiprazole (ARI) is an atypical antipsychotic drug, which has also been shown to have a beneficial effect on cognitive function. Results of many studies show that, for ARI's antidepressant effect to manifest itself, it is necessary to use a combined therapy with a drug from the group of selective serotonin reuptake inhibitors (SSRIs). The aim of this paper was to assess the antidepressant and impact of ARI on spatial memory in alcohol-preferring rats (EtNPRs).Design and methodsIn our study, we used Porsolt's forced swimming test (antidepressant effect) and Morris water maze test. The tests have been conducted upon administration of ARI (6 mg/kg i.p.), fluoxetine (FLX; 5 mg/kg p.o.) and combined administration of both drugs in alcohol-dependent rats.ResultsThe results of behavioural tests carried out have shown a lack of antidepressant and procognitive effects of either ARI or FLX in EtPRs after acute and chronic treatment. Combined administration of both drugs would lead to spatial memory deterioration in the study animals.Discussion and conclusionsOur results suggest that ARI applied in the experiment had no antidepressant effect and failed to improve spatial memory in study rats. Potential antidepressant and procognitive properties of this drug resulting from its mechanism of action encourage attempts (design) of further research aimed at developing a dose, which will show such effects in alcohol-preferring animals.

Long-term combined administration of Bifidobacterium bifidum TMC3115 and Lactobacillus plantarum 45 alleviates spatial memory impairment and gut dysbiosis in APP/PS1 mice

2020 ◽  
Vol 367 (7) ◽  
Author(s):  
Feng Wang ◽  
Tong Xu ◽  
Yujie Zhang ◽  
Tingting Zheng ◽  
Yunling He ◽  
...  
Keyword(s):  
Spatial Memory ◽  
Lactobacillus Plantarum ◽  
Memory Impairment ◽  
Bifidobacterium Bifidum ◽  
Morris Water Maze Test ◽  
Gut Dysbiosis ◽  
Combined Use ◽  
Combined Administration ◽  
Group 1

ABSTRACT This study aimed to determine the effects of Bifidobacterium bifidum TMC3115, Lactobacillus plantarum 45 (LP45) and their combined use on cognitive performance and gut microbiota in APP/PS1 mice. The APP/PS1 mice were randomly divided into four groups: Alzheimer's disease (AD) model group, TMC3115 group [1 × 109 colony forming unit (CFU)], LP45 group (1 × 109 CFU) and a mixture group of TMC3115 (5 × 108 CFU) and LP45 (5 × 108 CFU). The wild-type littermates were chosen as normal control. The mice were sacrificed at the end of 22 weeks after behavioral evaluation. Collected cecum content was analyzed using 16S rRNA sequencing. Combined use of TMC3115 and LP45 significantly increased the times across the platform, time spent in the target quadrant compared with the AD, TMC3115 and LP45 groups in Morris water maze test. Microbiota analysis showed that combined TMC3115 and LP45 supplementation significantly increased observed species and beta diversity, and reversed gut dysbiosis by decreasing the abundance of Bacteroides and increasing the abundance of Acetatifactor and Millionella. These results indicate the long-term combined administration of TMC3115 and LP45 can improve spatial memory impairment in APP/PS1 mice and suggest that modifying the gut microbiome may provide potential benefits for AD patients.

Nitric oxide mediates the antidepressant-like effect of modafinil in mouse forced swimming and tail suspension tests

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Hossein Omidi-Ardali ◽  
Abolfazl Ghasemi Badi ◽  
Elham Saghaei ◽  
Hossein Amini-Khoei
Keyword(s):  
Nitric Oxide ◽  
Effective Dose ◽  
Animal Studies ◽  
Tail Suspension Test ◽  
Forced Swimming ◽  
Antidepressant Effect ◽  
Tail Suspension ◽  
Immobility Time ◽  
Swimming Test ◽  
Underlying Mechanisms

AbstractObjectivesPrevious studies have suggested antidepressant properties for modafinil; however, the underlying mechanisms mediating the antidepressant effect of modafinil have not been well recognized in clinical and animal studies. Nitric oxide (NO) is involved in the pathophysiology of depression. We attempted to investigate the possible role of NO in the antidepressant-like effect of modafinil in mouse forced swimming test (FST) and tail suspension test (TST).MethodsThe antidepressant-like effect of modafinil (25, 50 and 75 mg/kg), alone and in combination with l-arginine, l-arg, (100 mg/kg) and NG-l-arginine methyl ester, l-NAME (5 mg/kg), was evaluated using FST and TST. Following behavioral tests, the hippocampi were dissected out to measure nitrite levels.ResultsFindings suggested that administration of modafinil at doses of 50 and 75 mg/kg significantly reduced immobility time in the FST and TST. Furthermore, administration of l-arg and l-NAME increased and decreased, respectively, the immobility time in the FST and TST. We showed that co-administration of a sub-effective dose of modafinil (25 mg/kg) plus l-NAME potentiated the antidepressant-like effect of the sub-effective dose of modafinil. In addition, co-treatment of an effective dose of modafinil (75 mg/kg) with l-arg attenuated the antidepressant-like effect of the effective dose of modafinil. We showed that the antidepressant-like effect of modafinil is associated with decreased nitrite levels in the hippocampus.ConclusionsOur findings for the first time support that the modulation of NO, partially at least, is involved in the antidepressant-like effect of modafinil in mouse FST and TST.

Effect of combined administration of 5-HT1A or 5-HT1B/1D receptor antagonists and antidepressants in the forced swimming test

2004 ◽  
Vol 487 (1-3) ◽  
pp. 133-142 ◽  
Author(s):  
Ewa Tatarczyńska ◽  
Aleksandra Kłodzińska ◽  
Katarzyna Stachowicz ◽  
Ewa Chojnacka-Wójcik
Keyword(s):  
Forced Swimming Test ◽  
Forced Swimming ◽  
Receptor Antagonists ◽  
Combined Administration ◽  
Swimming Test

scholarly journals ANTI-DEPRESSANT EFFECT OF CEFTRIAXONE IN FORCED SWIMMING TEST AND IN TAIL SUSPENSION TEST IN MICE

2016 ◽  
Vol 8 (11) ◽  
pp. 191 ◽  
Author(s):  
Ajoy Borah ◽  
Binita Singha ◽  
Swopna Phukan
Keyword(s):  
Forced Swimming Test ◽  
Antidepressant Activity ◽  
Tail Suspension Test ◽  
Forced Swimming ◽  
Antidepressant Effect ◽  
Tail Suspension ◽  
Neuroprotective Effects ◽  
The Central Nervous System ◽  
Swimming Test ◽  
Suspension Test

Objective: Depression is a major psychiatric disorder affecting nearly 350 million people worldwide and imposes a substantial health burden on the society. Ceftriaxone has demonstrated neuroprotective effects in animals. It has also undergone trials as a treatment option for amyotrophic lateral sclerosis. This study was therefore undertaken to evaluate the antidepressant-like effect of ceftriaxone in mice.Methods: Ceftriaxone was administered at three different doses (0.130, 0.195 and 0.260g/kg) to Swiss albino mice of either sex by intra peritoneal (i. p.) route. The period of immobility in control and drug-treated mice were recorded in forced swimming test (FST) and tail suspension test (TST). The antidepressant effect of ceftriaxone indicated by the decrease in duration of immobility was compared to that of fluoxetine (0.020 g/kg, i. p.).Results: Ceftriaxone decreased the duration of immobility in mice. It showed a significant dose-dependent antidepressant effect. The antidepressant effect of 0.260g/kg of ceftriaxone was comparable to that of fluoxetine in the TST but not in the FST.Conclusion: The results of the present study indicate antidepressant activity of Ceftriaxone. The study shows that ceftriaxone has additional action on the central nervous system other than neuroprotection. Ceftriaxone therapy in cases of encephalomeningitis and in various cases of hemorrhages in the brain can, therefore, prevent the development of depression in future

scholarly journals Effects of Escitalopram and Relearning on Cortical and Subcortical Grey Matter in Healthy Humans

2021 ◽  
Author(s):  
Thomas Vanicek ◽  
Murray Reed ◽  
Rene Seiger ◽  
Mathis Godbersen ◽  
Manfred Kloebl ◽  
...  
Keyword(s):  
Selective Serotonin Reuptake Inhibitors ◽  
Grey Matter ◽  
Antidepressant Effect ◽  
Healthy Humans ◽  
Learning Tasks ◽  
Dendritic Atrophy ◽  
Healthy Participants ◽  
Ssri Treatment ◽  
Subcortical Volumes ◽  
Serotonergic Modulation

The antidepressant effect of selective serotonin reuptake inhibitors (SSRI) is related to increased neuroplasticity during relearning. Stress-induced dendritic atrophy in key brain areas for learning and memory such as the hippocampus and prefrontal cortex is reversed by SSRI treatment. This finding is accompanied by behavioral stabilization. The aim of this study was to investigated serotonergic modulation effects on structural neuroplasticity (cortical thickness, subcortical volumes) during relearning in healthy subjects. Participants performed daily associative learning tasks over 3 weeks followed by a 3-week relearning phase combined with intake of the SSRI escitalopram or placebo. Evidence suggests that SSRIs promote the brains susceptibility to change on the basis of environment factors. We found no effect of SSRI on grey matter measures during relearning. Here, non-findings might be a consequence of the implemented intensity and duration of study interventions. With sparse literature on healthy participants in this field, future studies will have to further elucidate SSRIs properties on relearning and structural neuroplasticity.

scholarly journals Effect of a single dose of escitalopram on serotonin concentration in the non-human and human primate brain

2013 ◽  
Vol 16 (7) ◽  
pp. 1577-1586 ◽  
Author(s):  
Magdalena Nord ◽  
Sjoerd J. Finnema ◽  
Christer Halldin ◽  
Lars Farde
Keyword(s):  
Single Dose ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Human Subjects ◽  
Temporal Cortex ◽  
Chronic Administration ◽  
Binding Potential ◽  
Antidepressant Effect ◽  
Clinical Effects ◽  
Serotonin Concentration ◽  
Post Dose

AbstractSelective serotonin reuptake inhibitors (SSRIs) are widely prescribed for treatment of psychiatric disorders. The exact mechanism underlying the clinical effects of SSRIs remains unclear, although increased synaptic serotonin concentrations have been hypothesized to be an initial step. [11C]AZ10419369 is a novel 5-HT1B receptor selective radioligand, which is sensitive to changes in endogenous serotonin concentrations. To assess whether a single dose of the SSRI escitalopram affects endogenous serotonin concentrations in serotonergic projection areas and in the raphe nuclei (RN), three cynomolgus monkeys and nine human subjects underwent PET examinations with [11C]AZ10419369 at baseline conditions and after escitalopram administration. In monkeys, the binding potential (BPND) was significantly lower post dose compared to baseline in dorsolateral prefrontal cortex, occipital cortex, thalamus, midbrain and RN (p < 0.05). In humans, the BPND tended to decrease in RN post dose (p = 0.08). In all serotonergic projection areas, the BPND was conversely higher post dose compared to baseline. The increase was significant in a combined region of all projection areas (p = 0.01) and in occipital and temporal cortex (p < 0.05). SSRIs are generally assumed to elevate endogenous serotonin concentrations in projection areas, evoking the antidepressant effect. In the present study, a single, clinically relevant, dose of escitalopram was found to decrease serotonin concentrations in serotonergic projection areas in humans. Hypothetically, desensitization of inhibitory serotonergic autoreceptors will cause the serotonin concentration in projection areas to increase over time with chronic administration. Thus, the findings in the present study might aid in understanding the mechanism of SSRIs' delayed onset of clinical effect.

scholarly journals Antidepressant Effect of Dimeric Dipeptide GSB-106, an Original Low-Molecular-Weight Mimetic of BDNF

Acta Naturae ◽  
2013 ◽  
Vol 5 (4) ◽  
pp. 105-109 ◽  
Author(s):  
S. B. Seredenin ◽  
T. A. Voronina ◽  
T. A. Gudasheva ◽  
T. L. Garibova ◽  
G. M. Molodavkin ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Biological Fluids ◽  
Antidepressant Activity ◽  
Tail Suspension Test ◽  
Antidepressant Effect ◽  
Low Molecular Weight ◽  
Water Wheel ◽  
Outbred Mice ◽  
Swimming Test ◽  
The Brain

A large amount of clinical and experimental data suggest the involvement of neurotrophins, in particular the brain-derived neurotrophic factor (BDNF), in depression pathogenesis. However, the therapeutic use of BDNF is limited because of its instability in biological fluids, poor blood-brain barrier (BBB) permeability, and the presence of side effects. A low-molecular-weight mimetic GSB-106, which is a substituted dimeric dipeptide bis(N-monosuccinyl-L-seryl-L-lysine)hexamethylenediamide, was designed and synthesized based on the BDNF fourth loop structure at the V.V. Zakusov Institute of Pharmacology (RAMS). GSB-106 was found to exhibit an antidepressant activity in various models of depressive-like state when administered intraperitoneally to outbred mice and rats. An effect for the substance, when administered daily for 4-5 days, was detected in the Porsolt forced swimming test (0.1 and 1.0 mg/kg) and in the tail suspension test in mice (1.0 and 1.5 mg/ kg). An effect for GSB-106 at doses of 0.1 and 0.5 mg/kg was observed after a single application in experiments on rats in the Nomura water wheel test. The obtained evidence supports the hypothesis on the involvement of BDNF in the pathogenesis of various depression conditions, thus opening prospects for searching for new original antidepressants.

Sign in / Sign up

Export Citation Format

Share Document