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SMART 3.0 - VIDEO TRACKING SYSTEM
(Model: SMART30)
New version of the SMART video tracking system: the most flexible and user-friendly solution for automated evaluation of animal behavior just became even better. Ultra-performant, modular, easy-to-use and cost-saving - a must for all your video-based analysis of pre-clinical and neuroscience applications involving rodents (rats and mice).

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! NEW RESEARCH WORK ! A recent publication by A Tripathi, M Spedding, E Schenker, M Didriksen et al in "Translational Psychiatry" highlights the merits of using Bioseb's Smart 3.0 - Video Tracking System: Cognition-and circuit-based dysfunction in a mouse model of 22q11. 2 microdeletion syndrome: effects of stress

Cognition-and circuit-based dysfunction in a mouse model of 22q11. 2 microdeletion syndrome: effects of stress
A Tripathi, M Spedding, E Schenker, M Didriksen et al
Institute of Psychiatry and Neurosciences of Paris (IPNP), INSERM U1266, Pathophysiology of Psychiatric Disorders, Université de Paris, Paris, France
Published in "Translational Psychiatry" (2020-01-28)


Genetic microdeletion at the 22q11 locus is associated with very high risk for schizophrenia. The 22q11.2 microdeletion (Df(h22q11)/+) mouse model shows cognitive deficits observed in this disorder, some of which can be linked to dysfunction of the prefrontal cortex (PFC). We used behavioral (n_=_10 per genotype), electrophysiological (n_=_7 per genotype per group), and neuroanatomical (n_=_5 per genotype) techniques to investigate schizophrenia-related pathology of Df(h22q11)/+ mice, which showed a significant decrease in the total number of parvalbumin positive interneurons in the medial PFC. The Df(h22q11)/+ mice when tested on PFC-dependent behavioral tasks, including gambling tasks, perform significantly worse than control animals while exhibiting normal behavior on hippocampus-dependent tasks. They also show a significant decrease in hippocampus-medial Prefrontal cortex (H-PFC) synaptic plasticity (long-term potentiation, LTP). Acute platform stress almost abolished H-PFC LTP in both wild-type and Df(h22q11)/+ mice. H-PFC LTP was restored to prestress levels by clozapine (3_mg/kg i.p.) in stressed Df(h22q11)/+ mice, but the restoration of stress-induced LTP, while significant, was similar between wild-type and Df(h22q11)/+ mice. A medial PFC dysfunction may underlie the negative and cognitive symptoms in human 22q11 deletion carriers, and these results are relevant to the current debate on the utility of clozapine in such subjects.
Software Overview

Smart 3.0 is the latest release of the SMART video tracking system, featuring the most flexible and easy-to-learn software for the automated evaluation of behavior in the widest range of pre-clinical and neuroscience applications:

ACTIVITY & EXPLORATION:
ANXIETY:
DEPRESSION:
LEARNING & MEMORY:
ADDICTION & REWARD:
SOCIAL INTERACTIONS:
ZEBRAFISH STUDIES:
- Locomotor Activity, Novel Object Test, Cycling Behavior
- Open-Field, Elevated-Plus Maze, O-Maze, Black And White Test
- Forced-Swimming Test, Tail-Suspension Test
- Water Maze, Radial Maze, T And Y Maze, Fear Conditioning, Object Recognition Test
- Conditioned Place Preference, Odor Place Preference
- Resident Test
- Larvae Tracking - Place Preference Test, etc...

Utilizing an advanced image analysis, SMART 3.0 allows the recording of activity, trajectories, events, social interactions, and global activity of laboratory animals (rodents, rats, mice...) - even under extreme conditions (low-lighting, great similarity between the subjects and the scenario, etc.). SMART 3.0 provides users the versatility of a modular system with the capabilities of a broadband package. Our enhanced data analysis includes customizable data reports, with the possibility of creating outstanding reports based on our new advanced 2D and 3D activity map tool, as well as zone transition lists and events list reports with time evolution and distribution of occurrences. The SMART 3.0 system allows you to perform complete advanced calculations for unlimited behavioral paradigms: time/distance/entries in zones, average speed, alternation triplet, Whishaw’s error, mean directionality, parallel index, turning tendency...

SMART 3.0 was developed with the daily experimental process in mind - easy-to-use interface, highly flexible structure fitting the most applications and budgets. Advanced features ensure reliable data and increased productivity, saving valuable time and resources. SMART 3.0 emphasizes flexibility, productivity and simplicity - just add your desired settings, SMART 3.0 will do the rest. Simply powerful.

Smart 3.0 - Video tracking system - Available customization modules A new modular design for fulfilling your needs!

With a new modular structure, SMART 3.0 offers the most flexiblity for our customers. The SMART 3.0 platform is the main core of a great number of standard and advanced features. Save time and money: adapt the system to meet your specific needs, and expand as your research requires!

A few examples of available modules:
• Experiment-targeted Modules (SMART-WM, PM, OF, CPP, TY, FST...)
• Social Interaction Module/Extension (SMART-SI)
• Global Activity Extension (SMART-GA)
• Multiple arena Extension (SMART-MA)
• TriWise Extension (SMART-TW)
• Input-output Extension (SMART-IO)

Besides preset application-specific modules, the SMART customizable module (SMART-CS) provides the most versatile and powerful solution for running fully custom experimental projects:
• Free edition of arenas, zones and associations.
• Access to the full options of the Timing settings.
• Free definition of calculations and data reports.

Contact us for more information about all available modules.

Smart 3.0 - Video tracking system - Screenshots of different modules, including Forced Swimming Tests and Mazes Key features

• More than 15 years of experience in video tracking systems for laboratory animals (mouse, rat, rodent).
• Flexibility, reliability, productivity and simplicity all combined in the same product!
• Modular structure for fitting all experimental needs (basic and advanced) and budgets.
• Designed with the latest in both hardware and software technologies for increased functionality and maximum productivity for your experiments.
• Known as the most user-friendly interface in the market!
• Dedicated Customer Service & Support Dept. for insuring consultancy service & post-sales assistance.

Parameters measured:

• Parameters characterizing the animal trajectory (distance, speed, permanence time in zone etc.)
• Specific calculations for Global activity (spontaneous activity, immobility/low/high movements, 2d and 3D map activity images
• Specific advanced calculations for water maze, open-field, plus-maze, T-Y maze, place preference, forced-swimming test, etc.
• Automated detection of integrated behavior through the TriWise 3-points detection (rearing, rotations...)
• Events visualized by the experimenter (using event recorder)
• Group evolution graph

Components included:

• Built-in RECORDIT video recorder
• USB Flash key with SMART software installer, drivers/codecs and User's Manual
• SMARTRC Remote control to START/STOP the tracking process
• USB extension cord for SMARTRC Remote control


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

CENTRAL NERVOUS SYSTEM (CNS)
- Ischemic Strokes -
Progressive Loss of Dopaminergic Neurons in the Ventral Midbrain of Adult Mice Heterozygote for Engrailed1. (2007)
Progressive Loss of Dopaminergic Neurons in the Ventral Midbrain of Adult Mice Heterozygote for Engrailed1.
L. Sonnier, G. Le Pen, A. Hartmann, J.-C. Bizot, F. Trovero et al.
Centre National de la Recherche Scientifique, Unité Mixte de Recherche 8542, Development and Evolution of the Nervous System, Paris, France.
Published in "The Journal of Neuroscience" (2007-01-31)

Engrailed1 and Engrailed2 (En1 and En2) are two developmental genes of the homeogene family expressed in the developing midbrain. En1 and, to a lesser degree, En2 also are expressed in the adult substantia nigra (SN) and ventral tegmental area (VTA), two dopaminergic (DA) nuclei of the ventral midbrain. In an effort to study En1/2 adult functions, we have analyzed the phenotype of mice lacking one En1 allele in an En2 wild-type context. We show that in this mutant the number of DA neurons decreases slowly between 8 and 24 weeks after birth to reach a stable 38 and 23% reduction in the SN and VTA, respectively, and that neuronal loss can be antagonized by En2 recombinant protein infusions in the midbrain. These loss and gain of function experiments firmly establish that En1/2 is a true survival factor for DA neurons in vivo. Neuronal death in the mutant is paralleled by a 37% decrease in striatal DA, with no change in serotonin content. Using established protocols, we show that, compared with their wild-type littermates, En1+/_ mice have impaired motor skills, an anhedonic-like behavior, and an enhanced resignation phenotype; they perform poorly in social interactions. However, these mice do not differ from their wild-type littermates in anxiety-measuring tests. Together, these results demonstrate that En1/2 genes have important adult physiological functions. They also suggest that mice lacking only one En1 allele could provide a novel model for the study of diseases associated with progressive DA cell death.

NEURODEGENERATION
- General neurodegeneration -
Brain phospholipid precursors administered post-injury reduce tissue damage and improve neurological outcome in experimental traumatic brain injury (2018)
Brain phospholipid precursors administered post-injury reduce tissue damage and improve neurological outcome in experimental traumatic brain injury
O Thau-Zuchman, RN Gomes, SC Dyall, M Davis, JV Priestley, M Groenendij, M DE WILDE, J Lopez-Tremoleda, T. Michael-Titus
Barts and The London School of Medicine and Dentistry Blizard Institute, Neuroscience and Trauma, London, United Kingdom of Great Britain and Northern Ireland
Published in "Journal of Neurotrauma" (2018-05-17)

Traumatic brain injury (TBI) leads to cellular loss, destabilisation of membranes, disruption of synapses and altered brain connectivity, and increased risk of neurodegenerative disease. A significant and long-lasting decrease in phospholipids (PL), essential membrane constituents, has recently been reported in plasma and brain tissue, in human and experimental TBI. We hypothesised that supporting PL synthesis post-injury could improve outcome after TBI. We tested this hypothesis using a multi-nutrient combination designed to support the biosynthesis of phospholipids and available for clinical use. The multi-nutrient Fortasyn® Connect (FC) contains polyunsaturated omega-3 fatty acids, choline, uridine, vitamins, co-factors required for PL biosynthesis, and has been shown to have significant beneficial effects in early Alzheimer's disease. Male C57BL/6 mice received a controlled cortical impact injury and then were fed a control diet or a diet enriched with FC for 70 days. FC led to a significantly improved sensorimotor outcome and cognition, reduced lesion size and oligodendrocyte loss, and it restored myelin. It reversed the loss of the synaptic protein synaptophysin and decreased levels of the axon growth inhibitor Nogo-A, thus creating a permissive environment. It decreased microglia activation and the rise in ß-amyloid precursor protein and restored the depressed neurogenesis. The effects of this medical multi-nutrient suggest that support of PL biosynthesis after TBI, a new treatment paradigm, has significant therapeutic potential in this neurological condition for which there is no satisfactory treatment. The multi-nutrient tested has been used in dementia patients, is safe and well-tolerated, which would enable rapid clinical exploration in TBI.

MOOD DISORDERS
- Stress -
Cognition-and circuit-based dysfunction in a mouse model of 22q11. 2 microdeletion syndrome: effects of stress (2020)
Cognition-and circuit-based dysfunction in a mouse model of 22q11. 2 microdeletion syndrome: effects of stress
A Tripathi, M Spedding, E Schenker, M Didriksen et al
Institute of Psychiatry and Neurosciences of Paris (IPNP), INSERM U1266, Pathophysiology of Psychiatric Disorders, Université de Paris, Paris, France
Published in "Translational Psychiatry" (2020-01-28)

Genetic microdeletion at the 22q11 locus is associated with very high risk for schizophrenia. The 22q11.2 microdeletion (Df(h22q11)/+) mouse model shows cognitive deficits observed in this disorder, some of which can be linked to dysfunction of the prefrontal cortex (PFC). We used behavioral (n_=_10 per genotype), electrophysiological (n_=_7 per genotype per group), and neuroanatomical (n_=_5 per genotype) techniques to investigate schizophrenia-related pathology of Df(h22q11)/+ mice, which showed a significant decrease in the total number of parvalbumin positive interneurons in the medial PFC. The Df(h22q11)/+ mice when tested on PFC-dependent behavioral tasks, including gambling tasks, perform significantly worse than control animals while exhibiting normal behavior on hippocampus-dependent tasks. They also show a significant decrease in hippocampus-medial Prefrontal cortex (H-PFC) synaptic plasticity (long-term potentiation, LTP). Acute platform stress almost abolished H-PFC LTP in both wild-type and Df(h22q11)/+ mice. H-PFC LTP was restored to prestress levels by clozapine (3_mg/kg i.p.) in stressed Df(h22q11)/+ mice, but the restoration of stress-induced LTP, while significant, was similar between wild-type and Df(h22q11)/+ mice. A medial PFC dysfunction may underlie the negative and cognitive symptoms in human 22q11 deletion carriers, and these results are relevant to the current debate on the utility of clozapine in such subjects.

OTHER DISORDERS
- Cognitive performance -
Brain phospholipid precursors administered post-injury reduce tissue damage and improve neurological outcome in experimental traumatic brain injury (2018)
Brain phospholipid precursors administered post-injury reduce tissue damage and improve neurological outcome in experimental traumatic brain injury
O Thau-Zuchman, RN Gomes, SC Dyall, M Davis, JV Priestley, M Groenendij, M DE WILDE, J Lopez-Tremoleda, T. Michael-Titus
Barts and The London School of Medicine and Dentistry Blizard Institute, Neuroscience and Trauma, London, United Kingdom of Great Britain and Northern Ireland
Published in "Journal of Neurotrauma" (2018-05-17)

Traumatic brain injury (TBI) leads to cellular loss, destabilisation of membranes, disruption of synapses and altered brain connectivity, and increased risk of neurodegenerative disease. A significant and long-lasting decrease in phospholipids (PL), essential membrane constituents, has recently been reported in plasma and brain tissue, in human and experimental TBI. We hypothesised that supporting PL synthesis post-injury could improve outcome after TBI. We tested this hypothesis using a multi-nutrient combination designed to support the biosynthesis of phospholipids and available for clinical use. The multi-nutrient Fortasyn® Connect (FC) contains polyunsaturated omega-3 fatty acids, choline, uridine, vitamins, co-factors required for PL biosynthesis, and has been shown to have significant beneficial effects in early Alzheimer's disease. Male C57BL/6 mice received a controlled cortical impact injury and then were fed a control diet or a diet enriched with FC for 70 days. FC led to a significantly improved sensorimotor outcome and cognition, reduced lesion size and oligodendrocyte loss, and it restored myelin. It reversed the loss of the synaptic protein synaptophysin and decreased levels of the axon growth inhibitor Nogo-A, thus creating a permissive environment. It decreased microglia activation and the rise in ß-amyloid precursor protein and restored the depressed neurogenesis. The effects of this medical multi-nutrient suggest that support of PL biosynthesis after TBI, a new treatment paradigm, has significant therapeutic potential in this neurological condition for which there is no satisfactory treatment. The multi-nutrient tested has been used in dementia patients, is safe and well-tolerated, which would enable rapid clinical exploration in TBI.

A hippocampo-cerebellar centred network for the learning and execution of sequence-based navigation (2017)
A hippocampo-cerebellar centred network for the learning and execution of sequence-based navigation
BM. Babayan, A Watilliaux, G Viejo, A-L Paradis, B Girard, L Rondi-Reig
Sorbonne Universités, UPMC Univ Paris 06, INSERM, CNRS, Neurosciences Paris Seine - Institut de Biologie Paris Seine (NPS - IBPS), Cerebellum Navigation and Memory team (CeZaMe), 75005, Paris, France
Published in "Scientific Reports" (2017-12-19)

How do we translate self-motion into goal-directed actions? Here we investigate the cognitive architecture underlying self-motion processing during exploration and goal-directed behaviour. The task, performed in an environment with limited and ambiguous external landmarks, constrained mice to use self-motion based information for sequence-based navigation. The post-behavioural analysis combined brain network characterization based on c-Fos imaging and graph theory analysis as well as computational modelling of the learning process. The study revealed a widespread network centred around the cerebral cortex and basal ganglia during the exploration phase, while a network dominated by hippocampal and cerebellar activity appeared to sustain sequence-based navigation. The learning process could be modelled by an algorithm combining memory of past actions and model-free reinforcement learning, which parameters pointed toward a central role of hippocampal and cerebellar structures for learning to translate self-motion into a sequence of goal-directed actions.

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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.

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Computer requirements
Up to 4 arenas
2 GHz multi-core processor (Intel Core™2 Duo, AMD Phenom X2 or higher - Celeron processor not supported).
Computer requirements
More than 4 arenas
3 GHz multi-core processor (Intel i3, AMD Phenom X3 or higher - Celeron processor not supported).
Computer requirements - RAM SMART is not designed to make use of the RAM memory above the first 4 Gb. The more RAM memory installed in the computer, the longer a data acquisition session can be.
Computer requirements - HD 150 MB of free hard disk space. The more free disk space, the longer the digital video recording can be.
Computer requirements - Graphics 1280 x1024 pixels and 32-bit true color. Screen text size must be set at 96 DPI (100%).
Computer requirements - Operative system Microsoft® Windows® 7 Professional 32/64 bits, already prepared for Microsoft® Windows® 8 Professional 32/64 bits.
Computer requirements - Ports One free USB 2.0 port needed for the software protection key. Additional USB ports are needed when using a webcam or a USB analog-digital converter. PCI port needed when using PCI digitizer cards.
Computer requirements - Chipset Incompatibilities with VIA chipset have been detected so it is extremely recommended to avoid this chipset in the PC’s motherboard.
Image source supported Analogue cameras through the analog-digital video converter (CONVANAUSB), USB standard webcam, USB DV camera, WIA-compatible devices with a DirectShow driver included, Picolo Junior 4, U4, U8 and U8 PCI digitizer cards.

Model:
SMART30
Smart 3.0 - Video Tracking System
Contact us
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Bioseb - In Vivo Research Instruments
Phone worldwide : +33 442 344 360 - USA/Canada : (727) 521-1808
e-Mail : Worldwide: info@bioseb.com - USA/Canada: info-us@bioseb.com