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ARON TEST OR FOUR PLATES TEST
(Model: LE830 - For Mice)
The Four Plates Test is an exclusivity from BIOSEB!
The Aron test allows a quick characterization of putative anxiolytics compounds in naïve animals. A must for studying anxiety, drug screening and phenotyping.


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  • LAB OF NEUROBIO DE L'ANQUIETE ET DEPRESSION NANTES, FRANCE
  • HOFFMANN-LA ROCHE Ltd BASEL
  • LUNDBECK RESEARCH USAParamus, NJ, États-Unis
  • PSYCHOGENICS INC Tarrytown, États-Unis
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! NEW RESEARCH WORK ! A recent publication by A NIEWIADOMSKA-CIMICKA, F Doussau, JB Perot et al in "Molecular Neurodegeneration" highlights the merits of using Bioseb's Aron Test or Four Plates Test: SCA7 mice recapitulate CNS, PNS and retina pathologies and show a transcriptional signature of Purkinje cell dysfunction prevailing in SCA1 and SCA2 mice.

SCA7 mice recapitulate CNS, PNS and retina pathologies and show a transcriptional signature of Purkinje cell dysfunction prevailing in SCA1 and SCA2 mice.
A NIEWIADOMSKA-CIMICKA, F Doussau, JB Perot et al
Institut de Genetique et de Biologie Moleculaire et Cellulaire
Published in "Molecular Neurodegeneration" (2020-05-01)


Here we describe the first SCA7 knock-in mice that combine most cardinal features of SCA7, including retinal, cerebellar, cerebral and peripheral nerves pathologies, which account for progressive impairment of behavior, motor and vision functions. MRI and brain morphometry reveal atrophy of grey and white matter of specific cerebral regions, while peripheral nerves and photoreceptors show functional and morphological alterations. We show that cerebellar pathology is characterized by gene deregulation in all cerebellar cell types and alterations of SAGA-dependent epigenetic marks. Intranuclear accumulation of mutant ATXN7 and gene downregulation precede the onset of PC pacemaker dysfunction. Interestingly, PC show loss of expression of 83 PC-specific genes coding for ion channels, receptors and signaling proteins involved in pacemaker function and long-term depression, which are causal factors of many type of ataxias. Comparison of cerebellar transcriptome with other SCAs reveals a subset of 67 PC-specific genes downregulated in SCA1, SCA2 and SCA7, providing a common signature of early PC dysfunction.
Presentation

The Aron test or four plates test is an animal model of anxiety in which the exploration of the novel surroundings is suppressed by the delivery of a mild electric foot shock.

Basically, the apparatus consists of a cage floored by four identical rectangular metal plates (8×11 cm) separated from one another by a gap of 4 mm. The plates are connected to a shocker unit that can generate electric footshocks.

Shock generator for Aron' test Following habituation period, the animal is subjected to an electric shock when crossing (transition) from one plate to another, i.e. two legs on one plate and two legs on another. Boissier et al. 1968 has described this test first. The number of punished crossings is generally calculated for a period of 60 s. A substance with anxiolytic properties induces an increase in the number of punished passages.

2 publications showing the efficienty of this instrument for your research work are available for download:

Effects of benzodiazepinic and GABAergic ligands on the anxiolytic-like activity of antidepressants in the four-plate test in mice, by Hascoet, Dubois et al.
(Poster presented at the Congrès P2T Physiology, Pharmacology and Thérapeutics in Toulouse, April 2007)
Click here to send a download request for this publication

Triggering factors for the abolishment of benzodiazepines effects in the four-plate test-retest, by B. Petit-Demoulière, M. Hascoet, M. Bourin et al
(Poster presented at the Congrès P2T Physiology, Pharmacology and Thérapeutics in Toulouse, April 2007)
Click here to send a download request for this publication


Key features

• An elegant and economical solution for screening anxiolytic drugs in mice
• Punishment based conflict test
• Shock with adjustable intensity


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

PAIN
- General pain -
The novel inhibitor of the heterotrimeric G-protein complex, BIM-46187, elicits anti-hyperalgesic properties and synergizes with morphine. (2008)
The novel inhibitor of the heterotrimeric G-protein complex, BIM-46187, elicits anti-hyperalgesic properties and synergizes with morphine.
C. Favre-Guilmard, H. Zeroual-Hider, C. Soulard, C. Touvay, P.-E. Chabrier et al.
Ipsen-Institut Henri Beaufour, Les Ulis, France.
Published in "European Journal of Pharmacology" (2008-10-10)

BIM-46187 (7-[2-amino-1-oxo-3-thio-propyl]-8-cyclohexylmethyl-2-phenyl-5,6,7,8-tetrahydro-imidazo-[1,2a]-pyrazine dimer, hydrochloride) is an inhibitor of the heterotrimeric G-protein complex signalling. Since many mediators of pain act through G-protein coupled receptors, the anti-hyperalgesic effects of BIM-46187 were assessed on experimental models of pain. In addition since opioids are widely used in pain management and act through specific G-protein-coupled receptors, the effects of BIM-46187 on the analgesic properties of morphine have also been investigated. BIM-46187 elicited a dose dependent analgesic effect in the models of carrageenan-induced hyperalgesia (0.1–1 mg/kg; i.v.) and chronic constriction injury (0.3–3 mg/kg; i.v.) in rats. BIM-46187, however, up to 10 mg/kg did not modify the paw oedema induced by carrageenan excluding an anti-inflammatory effect. In addition, at these doses, the compound was not sedative as shown by the lack of effect on the motor performance in the rotarod test. The combination of BIM-46187 and morphine (ratio 1/1) resulted in an unexpected synergistic effect in the model of carrageenan-induced hyperalgesia and in the chronic constriction injury model in rats when evaluated by isobolographic analysis. This synergy allowed a reduction of at least 20 fold in the dose of each compound. Conversely, the drug combination did not increase the side effects of morphine as assessed in the rotarod test. In conclusion, BIM-46187 elicits a potent anti-hyperalgesic effect and strongly synergizes with morphine. This work highlights the role of heterotrimeric G-protein complexes in pain and supports further investigations of the use of BIM-46187 alone, or in combination with low doses of morphine, in the management of pain.

- Mechanical allodynia & hyperlagesia -
Different antinociceptive effects of botulinum toxin type A in inflammatory and peripheral polyneuropathic rat models. (2009)
Different antinociceptive effects of botulinum toxin type A in inflammatory and peripheral polyneuropathic rat models.
C. Favre-Guilmard, M. Auguet, P.-E. Chabrier.
Ipsen Innovation 5, Les Ulis, France.
Published in "European Journal of Pharmacology" (2009-09-01)

In addition to inhibition of acetylcholine release in the neuromuscular junction botulinum toxin type A (BoNT-A) also inhibits the release of mediators involved in pain perception. We have investigated the effect of two types of BoNT-A on mechanical hyperalgesia in the rat models of carrageenan-induced hyperalgesia and of paclitaxel-induced peripheral neuropathy. A subplantar (s.p.) injection of BoNT-A in the ipsilateral hindpaw 3 days before carrageenan administration reduced hypersensitivity. Dysport® and Botox® elicited comparable antihyperalgesic effects. Dysport® up to 30 U/kg and Botox® up to 20 U/kg did not impair the rat withdrawal nociceptive reflex or the locomotor performance as assessed by the rotarod test. Intraperitoneal administration of the skeletal muscle relaxant dantrolene produced, in contrast to BoNT-A, more motor impairment than analgesia. Paclitaxel treatment resulted in a peripheral neuropathy that affected the two hindpaws. Injection of 20 U/kg (s.p.) Dysport® produced a significant antihyperalgesic effect in the injected paw of neuropathic animals 3 days after administration. Unexpectedly, a similar analgesic effect was observed in the contralateral paw. The same results were also observed when Botox® was used instead of Dysport®. In contrast, a contralateral administration of Dysport® in the carrageenan test was ineffective. We conclude that BoNT-A elicits antinociceptive effects independent of the effects on muscular relaxation. Our results suggest that different mechanisms of action are responsible for the effect of BoNT-A in inflammatory and peripheral polyneuropathic rat models.

- Inflammatory pain -
Specific involvement of atypical PKC_/PKM_ in spinal persistent nociceptive processing following peripheral inflammation in rat. (2011)
Specific involvement of atypical PKC_/PKM_ in spinal persistent nociceptive processing following peripheral inflammation in rat.
F. Marchand, R. D'Mello, P. Yip, M. Calvo, E. Muller et al
King's College London, Wolfson Centre for Age-related Diseases, Neurorestoration Group, London, United Kingdom.
Published in "Molecular Pain" (2011-11-05)

BACKGROUND: Central sensitization requires the activation of various intracellular signalling pathways within spinal dorsal horn neurons, leading to a lowering of activation threshold and enhanced responsiveness of these cells. Such plasticity contributes to the manifestation of chronic pain states and displays a number of features of long-term potentiation (LTP), a ubiquitous neuronal mechanism of increased synaptic strength. Here we describe the role of a novel pathway involving atypical PKC_/PKM_ in persistent spinal nociceptive processing, previously implicated in the maintenance of late-phase LTP. RESULTS: Using both behavioral tests and in vivo electrophysiology in rats, we show that inhibition of this pathway, via spinal delivery of a myristoylated protein kinase C-_ pseudo-substrate inhibitor, reduces both pain-related behaviors and the activity of deep dorsal horn wide dynamic range neurons (WDRs) following formalin administration. In addition, Complete Freund's Adjuvant (CFA)-induced mechanical and thermal hypersensitivity was also reduced by inhibition of PKC_/PKM_ activity. Importantly, this inhibition did not affect acute pain or locomotor behavior in normal rats and interestingly, did not inhibited mechanical allodynia and hyperalgesia in neuropathic rats. Pain-related behaviors in both inflammatory models coincided with increased phosphorylation of PKC_/PKM_ in dorsal horn neurons, specifically PKM_ phosphorylation in formalin rats. Finally, inhibition of PKC_/PKM_ activity decreased the expression of Fos in response to formalin and CFA in both superficial and deep laminae of the dorsal horn. CONCLUSIONS: These results suggest that PKC_, especially PKM_ isoform, is a significant factor involved in spinal persistent nociceptive processing, specifically, the manifestation of chronic pain states following peripheral inflammation.

- Neuropathic pain -
Mature Purkinje Cells Require the Retinoic Acid-Related Orphan Receptor-α (RORα) to Maintain Climbing Fiber Mono-Innervation and Other Adult Characteristics (2013)
Mature Purkinje Cells Require the Retinoic Acid-Related Orphan Receptor-α (RORα) to Maintain Climbing Fiber Mono-Innervation and Other Adult Characteristics
XR.Chen , N. Heck, AM. Lohof, C. Rochefort, MP. More et al
UPMC Université Paris 06, CNRS, UMR 7102, Paris, France,
Published in "The Journal of Neuroscience" (2013-05-29)

Neuronal maturation during development is a multistep process regulated by transcription factors. The transcription factor RORα (retinoic acid-related orphan receptor α) is necessary for early Purkinje cell (PC) maturation but is also expressed throughout adulthood. To identify the role of RORα in mature PCs, we used Cre-lox mouse genetic tools in vivo that delete it specifically from PCs between postnatal days 10–21. Up to 14 d of age, differences between mutant and control PCs were not detectable: both were mono-innervated by climbing fibers (CFs) extending along their well-developed dendrites with spiny branchlets. By week 4, mutant mice were ataxic, some PCs had died, and remaining PC soma and dendrites were atrophic, with almost complete disappearance of spiny branchlets. The innervation pattern of surviving RORα-deleted PCs was abnormal with several immature characteristics. Notably, multiple functional CF innervation was reestablished on these mature PCs, simultaneously with the relocation of CF contacts to the PC soma and their stem dendrite. This morphological modification of CF contacts could be induced even later, using lentivirus-mediated depletion of rora from adult PCs. These data show that the late postnatal expression of RORα cell-autonomously regulates the maintenance of PC dendritic complexity, and the CF innervation status of the PC (dendritic vs somatic contacts, and mono-innervation vs multi-innervation). Thus, the differentiation state of adult neurons is under the control of transcription factors; and in their absence, adult neurons lose their mature characteristics and acquire some characteristics of an earlier developmental stage.

N-methyl-d-aspartate receptor-mediated modulations of the anti-allodynic effects of 5-HT1B/1D receptor stimulation in a rat model of trigeminal neuropathic pain. (2011)
N-methyl-d-aspartate receptor-mediated modulations of the anti-allodynic effects of 5-HT1B/1D receptor stimulation in a rat model of trigeminal neuropathic pain.
V. Kayser, A. Latrémolière, M. Hamon, S. Bourgoin.
Centre de Psychiatrie et Neurosciences, Neuropsychopharmacology, Paris, France.
Published in "European Journal of Pain" (2011-05-20)

Previous studies showed that triptans and other 5-HT(1B/1D)-receptor agonists attenuate hyper-responsiveness to mechanical stimulation of the face in a rat model of trigeminal neuropathic pain, probably by activating 5-HT(1B/1D)-receptors on primary afferent nociceptive fibers. We now tested whether blockade of post-synaptic receptors for the excitatory amino acid glutamate released by these fibers would increase this action. We thus evaluated whether (±)1-hydroxy-3-aminopyrrolidine-2-one (HA-966), an antagonist at the glycine/D-serine site of N-methyl-D-aspartate (NMDA)-receptors, would potentiate the anti-allodynic action of dihydroergotamine and zolmitriptan in rats with chronic constriction injury to the infraorbital nerve (CCI-ION). Complementary studies were performed with other NMDA-receptor ligands and in rats with chronic constriction injury to the sciatic nerve (CCI-SN) for comparison. Injury was produced by loose ligatures of the nerves. Responsiveness to mechanical stimulation (vibrissae or hindpaw territories) with von Frey filaments was used to evaluate allodynia 2 weeks after nerve ligature. Rats received NMDA-receptor ligands or saline 20 min before dihydroergotamine (25-100 _g/kg, i.v.) or zolmitriptan (25-100 _g/kg, s.c.). HA-966 (2.5mg/kg, s.c.), inactive on its own, enhanced the anti-allodynic effects of dihydroergotamine (eightfold increase) and zolmitriptan (threefold increase) in CCI-ION rats, but these drugs exerted no effects in allodynic CCI-SN rats. NMDA-receptor blockade by memantine (5mg/kg, i.p.) also enhanced, whereas activation at glycine/NMDA site by D-cycloserine (3mg/kg, i.p.) reduced the anti-allodynic properties of zolmitriptan in CCI-ION rats. Combined administration of NMDA-receptor antagonist and 5-HT(1B/1D)-receptor agonist may be a promising approach for alleviating trigeminal neuropathic pain.

CENTRAL NERVOUS SYSTEM (CNS)
- Ischemic Strokes -
Dose-dependent and long-term cerebroprotective effects of intranasal delivery of progesterone after ischemic stroke in male mice (2020)
Dose-dependent and long-term cerebroprotective effects of intranasal delivery of progesterone after ischemic stroke in male mice
M Fréchou, X Zhu, P Liere, A Pianos, M Schumacher et al
U1195 Inserm and University Paris-Sud and University Paris-Saclay, Kremlin-Bicêtre, France
Published in "Neuropharmacology" (2020-03-06)

Intranasal administration is emerging as a very promising route to deliver therapeutics to the brain. We have recently shown that the intranasal delivery of progesterone at 8 mg/kg is neuroprotective after stroke in male mice. To explore the translational potential of intranasal progesterone treatment, we performed a dose-response study and analyzed outcomes at 48 h after middle cerebral artery occlusion (MCAO). The effects on functional outcomes at long-term were examined by using the optimal dose. In the first experiment, male C57BL/6JRj mice were treated with progesterone at 8, 16 or 24 mg/kg, or with placebo at 1, 6 and 24 h post-MCAO. Our results show that the dose of 8 mg/kg was optimal in counteracting the early histopathological impairments as well as in improving functional recovery. Steroid profiling in plasma showed that the dose of 8 mg/kg is the one that leads to sustained high levels of progesterone and its neuroactive metabolites. In the second experiment, the dose of 8 mg/kg was used and analyzes were performed at 2, 7 and 21 days post-MCAO. Progesterone increased survival, glycemia and body weight. Furthermore, progesterone decreased neurological deficits and improved performances of mice on the rotarod and pole as early as 2 days and up to 21 days post-MCAO. These findings show that intranasal administration of progesterone has a significant translational potential as a cerebroprotective treatment after stroke that can be effective to reduce mortality, to limit tissue and cell damage at the acute phase; and to confer a long-term functional recovery.



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Species Mouse
Cage materials White, transparent plastic and stainless steel
Dimensions 18 x 25 x 16 cm
Shock 0-3 mA, timer 0-10 sec, square pulse
Shock delivery Footswitch
Count Manual

Model:
LE830
Aron Test or Four Plates Test
For Mice Contact us

Accessories :
LE 3806 MULTICOUNTER Programmable counter and SEDACOM Software
Print version

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