Masques d’anesthésie rats et souris pour cadres de stéréotaxie
Masques d’anesthésie pour rat et/ou souris. Ils sont spécialement conçus et usinés pour se monter sur la majorité des cadres stéréotaxiques et permettent d’exposer le museau du sujet expérimental au mélange anesthésique avec un minimum de fuites.
Choisissez votre modèle parmi les configurations du menu déroulant :
Ces différents modèles de masque de maintient en anesthésie sont spécialement conçus pour se monter sur la majorité des cadres stéréotaxiques.
Ils permettent d’exposer le museau du sujet expérimental au mélange anesthésique avec un minimum de fuites. Ils sont fixés directement sur l’adaptateur de gueule.
Le cône s’ouvre vers la partie ouverte du «U». Les incisives de l’animal sont placées sur la barre dans le masque.
Deux types de masque stéréotaxique à structure conique sont disponibles:
Le premier est un masque dit «passif» avec entrée et sortie colinéaires.
VI-68602 masque pour rats évacuation passive
Le deuxième est un masque dit «actif» avec entrée et sortie séparées (non colinéaires) des deux côtés.
VI-68663/65 masque pour souris
Le masque «passif» sera à privilégier lorsque l’évacuation du mélange est passive (gaz poussés) vers une cartouche de charbon actif
et le masque «actif» peut être utilisé lorsque l’installation dispose d’un instrument d’extraction des résidus halogénés.
Les masques sont livrés complet avec tubulures entrée sorties et adaptateurs:
Effect of ischaemic brain injury on sexual function in adult mice
Yaohui Tang et al. Stroke and Vascular Neurology September 2016 – Volume 1 – 3
Objective Priapism refers to a condition with persistent abnormal erection of the penis, which is usually caused by disease or injury in the brain or spinal cord, or obstruction to the outflow of blood through the dorsal vein at the root of the penis, without sexual desires. The effect of cerebral ischaemia on sexual function is unknown. The aim of this study is to explore whether priapism occurs in adult mice. Furthermore, we examined the relationship between priapism and the region of infarct in the brain.
Design Adult male CD-1 mice who underwent permanent middle cerebral artery occlusion (pMCAO) were closely examined from 2 hours to 14 days postoperation.
Results We found that priapism occurs in ∼80% of the mice with pMCAO, which could persist up to 14 days. Further study has demonstrated that the occurrence of priapism is related to the infarct region: priapism is found only in mice with ischaemic injury extending to the hypothalamus and the hippocampus regions.
Conclusion Our result suggested priapism may be used as a deep brain injury marker for evaluating brain injury in mice after pMCAO.
Unilateral hippocampal inactivation or lesion selectively impairs remote contextual fear memory
Contextual fear memory depends on the hippocampus, but the role of unilateral hippocampus in this type of memory remains unclear.
Objectives
Herein, pharmacological inactivation or excitotoxic lesions were used to study the role of unilateral hippocampus in the stages of contextual fear memory.
Results
The pharmacological experiments revealed that compared with the control groups, unilateral hippocampal blockade did not impair 1-day recent memory following learning, whereas bilateral hippocampal blockade significantly impaired this memory. The lesion experiments showed that compared with the control groups, the formed contextual fear memory was retained for 7 days and that 30-day remote memory was markedly reduced in unilateral hippocampal lesion groups.
Conclusions
These results indicate that an intact bilateral hippocampus is required for the formation of remote memory and that unilateral hippocampus is sufficient for recent contextual fear memory.
Adeno-associated virus 9–mediated Cdk5 inhibitory peptide reverses pathologic changes and behavioral deficits in the Alzheimer’s disease mouse model
Yong Heet al. faseb journal Published Online:18 Apr 2017
Abstract
Cyclin-dependent kinase 5 (Cdk5), which binds to and is activated by p35, phosphorylates multiple substrates and plays an essential role in the development and function of the CNS; however, proteolytic production of p25 from p35 under stress conditions leads to the inappropriate activation of Cdk5 and contributes to hyperphosphorylation of τ and other substrates that are related to the pathogenesis of Alzheimer’s disease. Selective inhibition of aberrant Cdk5 activity viagenetic overexpression of Cdk5 inhibitory peptide (CIP) reduces pathologic changes and prevents brain atrophy and memory loss in p25-transgenic mice. In the present study, we delivered adeno-associated virus 9 carrying green fluorescent protein–CIP (AAV9-GFP-CIP) to brain cells via intracerebroventricular infusion in amyloid precursor protein/presenilin 1 (APP/PS1) double-transgenic 3-mo-old mice after the occurrence of β-amyloid (Aβ) aggregation and the hyperphosphorylation of τ. Three months of treatment of AAV9-GFP-CIP reduced pathologic changes, including τ hyperphosphorylation, (Aβ) deposit, astrocytosis, and microgliosis, which were correlated with the reversal of memory loss and anxiety-like behavior observed in APP/PS1 mice. The neuroprotection effect of AAV9-GFP-CIP lasted an additional 7 mo—the end point of the study. These findings provide a novel strategy to selectively target Cdk5 for the treatment of Alzheimer’s disease.—He, Y., Pan, S., Xu, M., He, R., Huang, W., Song, P., Huang, J., Zhang, H.-T., Hu, Y. Adeno-associated virus 9–mediated Cdk5 inhibitory peptide reverses pathologic changes and behavioral deficits in the Alzheimer’s disease mouse model.
NMDA and D1 receptors are involved in one-trial tolerance to the anxiolytic-like effects of diazepam in the elevated plus maze test in rats
Heng Zhou et al. may 2015 Pharmacology, Biochemistry and Behavior
The elevated plus maze (EPM) test is used to examine anxiety-like behaviors in rodents. One interesting phenomenon in the EPM test is one-trial tolerance (OTT), which refers to the reduction in the anxiolytic-like effects of benzodiazepines when rodents are re-exposed to the EPM. However, the underlying mechanism of OTT is still unclear.Inthisstudy,wereported that OTT occurredwhenre-exposureto theEPM (trial2)only dependedon the
prior experience of the EPM (trial 1) rather than diazepam treatment. This process was memory-dependent, as it was prevented by the N-methyl-D-aspartate (NMDA) receptors antagonist MK-801 1.5 h before trial 2. In addi-
tion, OTT was maintained for at least one week but was partially abolished after an interval of 28 days. Furthermore, the administration of the D1-like receptors agonist SKF38393 to the bilateral dorsal hippocampus largely
prevented OTT, as demonstrated by the ability of the diazepam treatment to produce significant anxiolytic-like effects in trial 2 after a one-day interval. These findings suggest that OTT to the EPM test may occur via the acti-
vation of NMDA receptors and the inactivation of D1-like receptors in certain brain regions, including the hippocampus.
