Home > Catalog >
Product
Category
ELEVATED PLUS MAZE :
EPM3C - 3 CLICKS ONLY !
(Model: BIO-EPM3C - Software, camera and tripod)
NEW ! A complete (hardware + software), dedicated and automated solution for the Elevated Plus or Zero Maze test, featuring unprecedented simplicity to run these very popular protocols. A user-friendly and innovative solution for your research on anxiety, depression and the screening of anxiolytic drugs.

- More information - - Documents - - Contact Bioseb -
Users
Publications
Technical specifications
Other products / accessory  
  • Faculté de médecine grenoble, France
  • LABORATOIRE DE NEUROPHARMACOLOGIE CHATENAY MALABRY, France
  • MIKROLAB Lublin, Poland
  • LOUISIANA STATE UNIVERSITY Baton-rouge, USA
  • UNIVERSITY OF FLORIDA Gainsville, USA
Download PDF
(Modif.) This page is available in following languages:
! NEW RESEARCH WORK ! A recent publication by I.Mendez-David, JP. Guilloux, M. Papp, L. Tritschler, E. Mocaer, A. Gardier, S. Bretin, D. David in "Frontiers in Pharmacology" highlights the merits of using Bioseb's Elevated Plus Maze : EPM3C - 3 clicks only !: S 47445 Produces Antidepressant- and Anxiolytic Like Effects through Neurogenesis Dependent and Independent Mechanisms

S 47445 Produces Antidepressant- and Anxiolytic Like Effects through Neurogenesis Dependent and Independent Mechanisms
I.Mendez-David, JP. Guilloux, M. Papp, L. Tritschler, E. Mocaer, A. Gardier, S. Bretin, D. David
Institut de Recherches Internationales Servier, Suresnes, France
Published in "Frontiers in Pharmacology" (2017-07-19)


Glutamatergic dysfunctions are observed in the pathophysiology of depression. The glutamatergic synapse as well as the AMPA receptor's (AMPAR) activation may represent new potential targets for therapeutic intervention in the context of major depressive disorders. S 47445 is a novel AMPARs positive allosteric modulator (AMPA-PAM) possessing procognitive, neurotrophic properties and enhancing synaptic plasticity. Here, we investigated the antidepressant/anxiolytic-like effects of S47445 in a mouse model of anxiety/depression based on chronic corticosterone administration (CORT) and in the Chronic Mild Stress (CMS) model in rats. Four doses of S 47445 (0.3 to 10 mg/kg, oral route, 4 and 5 weeks, respectively) were assessed in both models. In mouse, behavioral effects were tested in various anxiety-and depression-related behaviors : the elevated plus maze (EPM), open field (OF), splash test (ST), forced swim test (FST), tail suspension test (TST), fur coat state and novelty suppressed feeding (NSF) as well as on hippocampal neurogenesis and dendritic arborization in comparison to chronic fluoxetine treatment (18 mg/kg, p.o.). In rats, behavioral effects of S 47445 were monitored using sucrose consumption and compared to those of imipramine or venlafaxine (10 mg/kg, i.p.) during the whole treatment period and after withdrawal of treatments. In a mouse model of genetic ablation of hippocampal neurogenesis (GFAP-Tk model), neurogenesis dependent/independent effects of chronic S 47445 treatment were tested, as well as BDNF hippocampal expression. S 47445 reversed CORT-induced depressive-like state by increasing grooming duration and reversing coat state's deterioration. S 47445 also decreased the immobility duration in TST and FST. The highest doses (3 and 10 mg/kg) seem the most effective for antidepressant-like activity in CORT mice. Furthermore, S 47445 significantly reversed the anxiety phenotype observed in OF (at 1 mg/kg) and EPM (from 1 mg/kg). In the CMS rat model, S 47445(from 1 mg/kg) demonstrated a rapid onset of effect on anhedonia compared to venlafaxine and imipramine. In the CORT model, S 47445 demonstrated significant neurogenic effects on proliferation, survival and maturation of hippocampal newborn neurons at doses inducing an antidepressant-like effect. It also corrected CORT-induced deficits of growth and arborization of dendrites. Finally, the antidepressant/anxiolytic-like activities of S 47445 required adult hippocampal neurogenesis in the novelty suppressed feeding test contrary to OF, EPM and ST. The observed increase in hippocampal BDNF levels could be one of the mechanisms of S 47445 responsible for the adult hippocampal neurogenesis increase. Altogether, S 47445 displays robust antidepressant-anxiolytic-like properties after chronic administration through neurogenesis dependent/independent mechanisms and neuroplastic activities. The AMPA-PAM S 47445 could have promising therapeutic potential for the treatment of major depressive disorders or generalized anxiety disorders.
Presentation

Bioseb - EPM3C - Elevated Plus Maze - System overview
EPM3C - System overview
The Elevated Plus-Maze is a commonly used test to assess anxiety-like behavior in laboratory animals (rats/mice). Based on the natural fear that rodents have for height and open spaces, the Elevated Plus Maze is a general research tool in neurobiological anxiety field and usually uses to screen the efficacy of drugs.

The Elevated-Plus-Maze (EPM) is one of the very first tests used by neuroscientists to evaluate anxiety-like behavior in rodents and the most widely used test after the Open Field to evaluate anxiolitic or anxiogenic effects. The EPM (or its variant the Elevated-Zero-Maze) could also be considered among other various other tests for the screening of mice strains. The EPM can also be used to assess side effects of psychiatric disorders treatments.

Bioseb proposes an all-inclusive solution for the Elevated-Plus-Maze (EPM) test with hardware and software components.

Video tracking is a very good way to automate the Elevated-Plus-Maze (EPM) test for rats and mice, which is the the reason why we have designed a dedicated software application, the EPM-3C, to run any EPM/ZERO-M protocols (compatible with hardware from Bioseb or other brands), based on a powerful video tracking system. The zone transition is matched perfectly with the manual scoring by using specific morphologic detection. The tracking zones (open/closed arms, center) are really easy to define and once they are, the software is optimized to be setup easily and starts with just three clicks, in order to assist, speed up and simplify your experiments.

The Bioseb EPM Software gives all the information you need from your EPM experiment and most of the parameters are computed in real-time.

Regarding the hardware, Bioseb has designed its EPM test for mice and rats according to the standard dimensions widely used in the field. The corridors of the Bioseb Elevated-Plus-Maze are made in high quality perpex, so that the material will not retain odors. Their light grey, non-reflective color makes them ideal to combine with video-tracking. Finally, the assembly of the equipment has been made really easy.

Tripod and industrial quality camera are also provided so you can start your experiments rapidly.

Operating principle

Bioseb - EPM3C - Elevated Plus Maze - Close-up
EPM3C - Rat exploring - Close-up
The new EPM-3C solution from BIOSEB features unprecedented simplicity to run ELEVATED + MAZE or ZERO MAZE protocols.

The test setting consists of a plus-shaped apparatus with two open and two enclosed arms, each with an open roof and elevated from the floor. The aversion of the rodents to open spaces leads into a restriction of movement to the enclosed arms.

Anxiety of rodents is directly linked to the proportion of time spent in closed arms versus the time spent in open arms. The more anxious the animals, the more time they spend in the closed arms.

To start the test, the animal is usually placed in the center zone of the maze and the duration of the experiment is generally about 5 minutes. The time spent in the various arms is the main data recorded during this test. The Bioseb software also gives the total number of entries in the various arms (open, closed and center), the global activity of the animal (calculated with the total distance of the animal during the test) and the latency of the first entrance to the open arm.

Your results can then be exported into Excel tables for further analysis.

Supplied with :

The instrument comes with a maze, a camera, a USB cable, a boom stand and a software license.

Domains of application

• Prescreening of newly developed pharmacological agents for treatment of anxiety-related disorders
• Anxiolytic and anxiogenic effects of pharmacological agents, drugs of abuse and hormones
• Study of the effects of reproductive senescence/aging and/or pre-, peri- or postnatal exposure to various stressors
• Model to detect anxiolytic effects of benzodiazepine-related compounds
• Behavioral assay to study the brain sites (e.g., limbic regions, hippocampus, amygdala, dorsal raphe nucleus, etc.) and mechanisms (e.g., GABA, glutamate, serotonin, hypothalamic–pituitary–adrenal axis neuromodulators, etc.) underlying anxiety behavior

Key features

• Easy to set up
• Designed for Rats or Mice
• Hundreds of publication and validation for the EPM test
• The first choice for anxiety
• Modular structure which allows storage in minimum space
• Short-lasting experiment (no more than 5-10 min)
• Exploration-based conflict task
• Based on innate behavioral tendencies (ethological test)


Dedicated software

Here is a table introducing the results available with the Bioseb software and the scientific meaning of each data :

Measured parameter Scientific significance
Absolute time and experiment duration /
Total time per zones (s and %) Total time spent by the animal in open arms is the main indicator to assess anxiety
Latency to first entry per zone Latency to first entry in open arms is another indicator to assess the anxiety of the animal
Visit (and % per zones) Number of visits (or entries) in open arms is another indicator to assess the anxiety of the animal
Distance (cm and % per zones) Distance covered by the animal is a good indicator of the animal activity during the test
Mean time per visits (s) Mean time per visits in open arms can also be used as an indicator for anxiety
Mean speed (cm/s) Speed of the animal is another indicator to assess the locomotor activity of the animal
The data is available for each arm individually, but also for grouped arms. The results can be exported on windows Excel - the software runs under Windows Seven and Eight.

Publications (Click on an article to show details and read the abstract)

CENTRAL NERVOUS SYSTEM (CNS)
- Brain fonctions -
Dissociable Roles for the Basolateral Amygdala and Orbitofrontal Cortex in Decision-Making under Risk of Punishment (2015)
Dissociable Roles for the Basolateral Amygdala and Orbitofrontal Cortex in Decision-Making under Risk of Punishment
Caitlin A. Orsini, Rose T. Trotta, Jennifer L. Bizon and Barry Setlow
University of Florida College of Medicine, Gainesville, Florida
Published in "The Journal of Neuroscience" (2015-01-28)

Several neuropsychiatric disorders are associated with abnormal decision-making involving risk of punishment, but the neural basis of this association remains poorly understood. Altered activity in brain systems including the basolateral amygdala (BLA) and orbitofrontal cortex (OFC) can accompany these same disorders, and these structures are implicated in some forms of decision-making. The current study investigated the role of the BLA and OFC in decision-making under risk of explicit punishment. Rats were trained in the risky decision-making task (RDT), in which they chose between two levers, one that delivered a small safe reward, and the other that delivered a large reward accompanied by varying risks of footshock punishment. Following training, they received sham or neurotoxic lesions of BLA or OFC, followed by RDT retesting. BLA lesions increased choice of the large risky reward (greater risk-taking) compared to both prelesion performance and sham controls. When reward magnitudes were equated, both BLA lesion and control groups shifted their choice to the safe (no shock) reward lever, indicating that the lesions did not impair punishment sensitivity. In contrast to BLA lesions, OFC lesions significantly decreased risk-taking compared with sham controls, but did not impair discrimination between different reward magnitudes or alter baseline levels of anxiety. Finally, neither lesion significantly affected food-motivated lever pressing under various fixed ratio schedules, indicating that lesion-induced alterations in risk-taking were not secondary to changes in appetitive motivation. Together, these findings indicate distinct roles for the BLA and OFC in decision-making under risk of explicit punishment.

- Ischemic Strokes -
Positive effects of the traditional Chinese medicine MLC901 in cognitive tasks (2015)
Positive effects of the traditional Chinese medicine MLC901 in cognitive tasks
Lorivel T, Gandin C, Veyssière J, Lazdunski M, Heurteaux C
Institut de Pharmacologie Moléculaire et Cellulaire (CNRS UMR7275), Université de Nice Sophia Antipolis, Valbonne, France.
Published in "J Neurosci Res." (2015-11-01)

MLC901 (NurAiDII) is used as a treatment for stroke patients. It has been shown that MLC901 improves motor and cognitive recovery in ischemic and traumatic brain-injured rodents. The present study seeks to delineate cognitive effects induced by MLC901 in normal, noninjured mice. To this end, the behaviors of vehicle- and MLC901-treated C57BL/6 mice in hippocampus-dependent (passive avoidance, Morris water maze) and hippocampus-independent (novel object recognition) cognitive tasks are compared. The potential influence of the compound on the anxiety level and nycthemeral rhythm of mice is also assessed. In addition, the long-term effects of MLC901 on hippocampal neurogenesis are measured. The results clearly demonstrate that MLC901 promotes extinction in passive avoidance and reversal learning in the Morris water maze and improves the performance of mice in novel object recognition. In parallel, this study shows the long-term proneurogenesis effects of MLC901 that result in the increase in the number of mature neurons in the hippocampus. If these observations can be extended to humans, then MLC901 could represent a promising therapeutic strategy. © 2015 The Authors. Journal of Neuroscience Research Published by Wiley Periodicals, Inc.

MOOD DISORDERS
- Anxiety -
5-HT4 Receptor Subtype, ?-Arrestin Level, and Rapid-Onset Effects of Antidepressant Drugs (2014)
5-HT4 Receptor Subtype, ?-Arrestin Level, and Rapid-Onset Effects of Antidepressant Drugs
Indira Mendez-David, Denis Joseph David, Jean-Philippe Guilloux, René Hen, Alain Michel Gardier
Universität zu Köln
Published in "Neuromethods Volume 95" (2014-11-19)

Understanding the pathophysiology of affective disorders and their treatment relies on the availability of experimental models that accurately mimic aspects of the disease. The use of exogenously administered corticosterone (CORT model) can mimic the effects of a chronic stress and has been validated as an animal model to study disease states displaying some hallmark characteristics of anxiety and depression observed in patients. Recently, we have adapted the CORT model protocol to screen for rapid-onset drugs to treat anxiety/depression disorders. In spite of the fact that selective serotonin reuptake inhibitors (SSRIs) are the most commonly prescribed drugs for the treatment of depression and several anxiety disorders, the onset of action of SSRIs is often delayed by 3–6 weeks. The existence of this delayed action combined with the fact that one-third of patients do not respond to treatment emphasizes the need for faster acting and more effective antidepressants. This chapter gives laboratory protocols including step-by-step recommendations to explain how the CORT model in mice can be used to screen for candidate drugs. For this purpose we examined the behavioral and cellular effects of a 5-HT4 receptor ligand, RS67333, and compared it with the SSRI, fluoxetine. Likewise, we emphasize that mononuclear cells (PBMCs) isolated from whole blood in corticosterone-treated mice could serve as a marker of treatment response(s) and fast onset of drug action in the mouse CORT model.

- Depression -
S 47445 Produces Antidepressant- and Anxiolytic Like Effects through Neurogenesis Dependent and Independent Mechanisms (2017)
S 47445 Produces Antidepressant- and Anxiolytic Like Effects through Neurogenesis Dependent and Independent Mechanisms
I.Mendez-David, JP. Guilloux, M. Papp, L. Tritschler, E. Mocaer, A. Gardier, S. Bretin, D. David
Institut de Recherches Internationales Servier, Suresnes, France
Published in "Frontiers in Pharmacology" (2017-07-19)

Glutamatergic dysfunctions are observed in the pathophysiology of depression. The glutamatergic synapse as well as the AMPA receptor's (AMPAR) activation may represent new potential targets for therapeutic intervention in the context of major depressive disorders. S 47445 is a novel AMPARs positive allosteric modulator (AMPA-PAM) possessing procognitive, neurotrophic properties and enhancing synaptic plasticity. Here, we investigated the antidepressant/anxiolytic-like effects of S47445 in a mouse model of anxiety/depression based on chronic corticosterone administration (CORT) and in the Chronic Mild Stress (CMS) model in rats. Four doses of S 47445 (0.3 to 10 mg/kg, oral route, 4 and 5 weeks, respectively) were assessed in both models. In mouse, behavioral effects were tested in various anxiety-and depression-related behaviors : the elevated plus maze (EPM), open field (OF), splash test (ST), forced swim test (FST), tail suspension test (TST), fur coat state and novelty suppressed feeding (NSF) as well as on hippocampal neurogenesis and dendritic arborization in comparison to chronic fluoxetine treatment (18 mg/kg, p.o.). In rats, behavioral effects of S 47445 were monitored using sucrose consumption and compared to those of imipramine or venlafaxine (10 mg/kg, i.p.) during the whole treatment period and after withdrawal of treatments. In a mouse model of genetic ablation of hippocampal neurogenesis (GFAP-Tk model), neurogenesis dependent/independent effects of chronic S 47445 treatment were tested, as well as BDNF hippocampal expression. S 47445 reversed CORT-induced depressive-like state by increasing grooming duration and reversing coat state's deterioration. S 47445 also decreased the immobility duration in TST and FST. The highest doses (3 and 10 mg/kg) seem the most effective for antidepressant-like activity in CORT mice. Furthermore, S 47445 significantly reversed the anxiety phenotype observed in OF (at 1 mg/kg) and EPM (from 1 mg/kg). In the CMS rat model, S 47445(from 1 mg/kg) demonstrated a rapid onset of effect on anhedonia compared to venlafaxine and imipramine. In the CORT model, S 47445 demonstrated significant neurogenic effects on proliferation, survival and maturation of hippocampal newborn neurons at doses inducing an antidepressant-like effect. It also corrected CORT-induced deficits of growth and arborization of dendrites. Finally, the antidepressant/anxiolytic-like activities of S 47445 required adult hippocampal neurogenesis in the novelty suppressed feeding test contrary to OF, EPM and ST. The observed increase in hippocampal BDNF levels could be one of the mechanisms of S 47445 responsible for the adult hippocampal neurogenesis increase. Altogether, S 47445 displays robust antidepressant-anxiolytic-like properties after chronic administration through neurogenesis dependent/independent mechanisms and neuroplastic activities. The AMPA-PAM S 47445 could have promising therapeutic potential for the treatment of major depressive disorders or generalized anxiety disorders.

5-HT4 Receptor Subtype, ?-Arrestin Level, and Rapid-Onset Effects of Antidepressant Drugs (2014)
5-HT4 Receptor Subtype, ?-Arrestin Level, and Rapid-Onset Effects of Antidepressant Drugs
Indira Mendez-David, Denis Joseph David, Jean-Philippe Guilloux, René Hen, Alain Michel Gardier
Universität zu Köln
Published in "Neuromethods Volume 95" (2014-11-19)

Understanding the pathophysiology of affective disorders and their treatment relies on the availability of experimental models that accurately mimic aspects of the disease. The use of exogenously administered corticosterone (CORT model) can mimic the effects of a chronic stress and has been validated as an animal model to study disease states displaying some hallmark characteristics of anxiety and depression observed in patients. Recently, we have adapted the CORT model protocol to screen for rapid-onset drugs to treat anxiety/depression disorders. In spite of the fact that selective serotonin reuptake inhibitors (SSRIs) are the most commonly prescribed drugs for the treatment of depression and several anxiety disorders, the onset of action of SSRIs is often delayed by 3–6 weeks. The existence of this delayed action combined with the fact that one-third of patients do not respond to treatment emphasizes the need for faster acting and more effective antidepressants. This chapter gives laboratory protocols including step-by-step recommendations to explain how the CORT model in mice can be used to screen for candidate drugs. For this purpose we examined the behavioral and cellular effects of a 5-HT4 receptor ligand, RS67333, and compared it with the SSRI, fluoxetine. Likewise, we emphasize that mononuclear cells (PBMCs) isolated from whole blood in corticosterone-treated mice could serve as a marker of treatment response(s) and fast onset of drug action in the mouse CORT model.

Long-term deficiency of circulating and hippocampal insulin-like growth factor I induces depressive behavior in adult mice: a potential model of geriatric depression. (2011)
Long-term deficiency of circulating and hippocampal insulin-like growth factor I induces depressive behavior in adult mice: a potential model of geriatric depression.
M. Mitschelen, H. Yan, J.A. Farley, J.P. Warrington, S. Han et al.
The University of Oklahoma Health Sciences Center, Reynolds Oklahoma Center on Aging, Oklahoma City, USA.
Published in "Neuroscience" (2011-06-30)

Numerous studies support the hypothesis that deficiency of insulin-like growth factor I (IGF-1) in adults contributes to depression, but direct evidence is limited. Many psychological and pro-cognitive effects have been attributed to IGF-1, but appropriate animal models of adult-onset IGF-1 deficiency are lacking. In this study, we use a viral-mediated Cre-loxP system to knockout the Igf1 gene in either the liver, neurons of the CA1 region of the hippocampus, or both. Knockout of liver Igf1 reduced serum IGF-1 levels by 40% and hippocampal IGF-1 levels by 26%. Knockout of Igf1 in CA1 reduced hippocampal IGF-1 levels by 13%. The most severe reduction in hippocampal IGF-1 occurred in the group with knockouts in both liver and CA1 (36% reduction), and was associated with a 3.5-fold increase in immobility in the forced swim test. Reduction of either circulating or hippocampal IGF-1 levels did not alter anxiety measured in an open field and elevated plus maze, nor locomotion in the open field. Furthermore, local compensation for deficiencies in circulating IGF-1 did not occur in the hippocampus, nor were serum levels of IGF-1 upregulated in response to the moderate decline of hippocampal IGF-1 caused by the knockouts in CA1. We conclude that adult-onset IGF-1 deficiency alone is sufficient to induce a depressive phenotype in mice. Furthermore, our results suggest that individuals with low brain levels of IGF-1 are at increased risk for depression and these behavioral effects are not ameliorated by increased local IGF-1 production or transport. Our study supports the hypothesis that the natural IGF-1 decline in aging humans may contribute to geriatric depression.



THE INFORMATION IN THIS WEB SITE AND IN LINKED PAGES AND DOCUMENTS IS PROVIDED "AS IS" AND DOES NOT CREATE ANY EXPRESS OR IMPLIED WARRANTY ABOUT BIOSEB OR ITS PRODUCTS OR SERVICES.

Information published on this Web Site as well as services, product specifications, availability and prices are subject to change without notice. BIOSEB may also make improvements and/or changes in the products and/or the programs described in this Web Site at any time without notice.

BIOSEB has made reasonable efforts to verify that the information in this Web site was accurate when first published. Such information may contain errors or omissions, however, and it is subject to change without notice. Bioseb does not undertake to update this information to include any such changes or to correct errors or omissions. Bioseb assumes no responsibility for any use of the information in this Web site or for any infringement of patents or other rights of third parties that may result. Certain information may be country-specific and may not apply in all countries.

Technology Color tracking
Supported OS Microsoft Windows SEVEN or EIGHT
Analysis Real-time from camera flow or video file
Dimensions For mice in cm : L x l x h : 77 x 77 x 51
For rats in cm : L x l x h : 112 x 112 x 71
Weight For mice : 7.5 kg
For rats : 26.5 kg
Material High-quality perpex in non-reflective grey, suitable for video-tracking
Reférences BIO-EPM3C (Software, Camera and Tripod)
BIO-EPM-M for mice (labyrinth only)
BIO-EPM-R for rats (labyrinth only)
Camera - included HD USB based
Resolution : 744x480 pixel
Sampling rate : 76 fps
Maze - included Grey PVC, to be chosen between 2 versions: rats and mice
Stand - included Boom stand

Model:
BIO-EPM3C
Elevated Plus Maze : EPM3C - 3 clicks only ! (Modif.)
Software, camera and tripod Contact us

Accessories :
BIO-EPM-R
Elevated plus-maze (Modif.)
for rats Contact us
BIO-EPM-M
Elevated plus-maze (Modif.)
for mice Contact us
Print version

Bioseb - In Vivo Research Instruments
Phone worldwide : +33 442 344 360 - USA/Canada : (727) 521-1808
e-Mail : Worldwide: info@bioseb.com - USA/Canada: sales@eb-instruments.com