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  • COA 100022

    Document Type:
    Certificate of Analysis
    Product Catalog Number:
    100022

  • The neural stem cell line CTX0E03 promotes behavioral recovery and endogenous neurogenesis after experimental stroke in a dose-dependent fashion. 19633272

    BACKGROUND: This study investigated behavioral recovery in rats following implanting increasing doses of CTX0E03 cells into the putamen ipsilateral to the stroke damage. Postmortem histological analysis investigated possible mechanisms of behavioral recovery. METHODS: . At 4 weeks after middle cerebral artery occlusion (MCAO), rats were treated with 4500, 45,000, or 450,000 CTX0E03 cells or vehicle implanted into the putamen with testing on a battery of tasks preocclusion and postocclusion. Histological examination of brains included assessment of lesion volumes, implant cell survival and differentiation, changes to host brain matrix, angiogenesis, and neurogenesis using immunohistochemical methods. RESULTS: . Statistically significant dose-related recovery in sensorimotor function deficits (bilateral asymmetry test [BAT; P < .0002] in the mid- and high-dose groups and rotameter test after amphetamine exposure [P < .05] in the high-dose group) was found in the CTX0E03 cell implanted groups compared to the vehicle group. In-life functional improvements correlated with cell dose, though did not correlate with survival of CTX0E03 cells measured at postmortem. Surviving CTX0E03 cells differentiated into oligodendroglial and endothelial phenotypes. MCAO-induced reduction of neurogenesis in the subventricular zone (SVZ) was partially restored to that observed in sham operated controls. No adverse CTX0E03 cell-related effects were observed during in-life observations or on tissue histology. CONCLUSIONS: . This study found that the implantation of CTX0E03 human neural stem cells in rats after MCAO stroke promoted significant behavioral recovery depending on cell dose. The authors propose a paracrine trophic mechanism, which is triggered early after CTX0E03 cell implantation, and which in turn targets restoration of neurogenesis in the SVZ of MCAO rats.
    Document Type:
    Reference
    Product Catalog Number:
    Multiple
    Product Catalog Name:
    Multiple

  • Olfactory ensheathing cells exhibit unique migratory, phagocytic, and myelinating properties in the X-irradiated spinal cord not shared by Schwann cells. 18551623

    Although several studies have shown that Schwann cells (SCs) and olfactory ensheathing cells (OECs) interact differently with central nervous system (CNS) cells in vitro, all classes of adult myelin-forming cells show poor survival and migration after transplantation into normal CNS. X-irradiation of the spinal cord, however, selectively facilitates migration of oligodendrocyte progenitor cells (OPCs), but not SCs, revealing differences in in vivo migratory capabilities that are not apparent in intact tissue. To compare the in vivo migratory properties of OECs and SCs and evaluate the potential of migrating cells to participate in subsequent repair, we first transplanted freshly isolated GFP-expressing adult rat olfactory bulb-derived OECs and SCs into normal and X-irradiated spinal cords. Both OECs and SCs showed limited survival and migration in normal spinal cord at 3 weeks. However, OECs, unlike SCs, migrated extensively in both grey and white matter of the X-irradiated spinal cord, and exhibited a phagocytic phenotype with OX-42 staining on their processes. If a X-irradiated and OEC transplanted spinal cord was then subjected to a focal demyelinating lesion 3 weeks after transplantation, OECs moved into the delayed demyelinated lesion and remyelinated host axons with a peripheral-like pattern of myelin. These results revealed a clear difference between the migratory properties of OECs and SCs in the X-irradiated spinal cord and demonstrated that engrafted OECs can participate in repair of subsequent lesions.
    Document Type:
    Reference
    Product Catalog Number:
    MAB344
    Product Catalog Name:
    Anti-O1 Antibody, clone 59

  • Visualizing corticotropin-releasing hormone receptor type 1 expression and neuronal connectivities in the mouse using a novel multifunctional allele. 22886732

    The corticotropin-releasing hormone (CRH) and its type 1 receptor (CRHR1) play a central role in coordinating the endocrine, autonomic, and behavioral responses to stress. A prerequisite to functionally dissect the complexity of the CRH/CRHR1 system is to unravel the identity of CRHR1-expressing neurons and their connectivities. Therefore, we used a knockin approach to genetically label CRHR1-expressing cells with a tau-lacZ (tZ) reporter gene. The distribution of neurons expressing β-galactosidase in the brain and the relative intensity of labeling is in full accordance with previously described Crhr1 mRNA expression. Combining the microtubule-binding properties of TAU with the Cre-loxP system allowed to direct the β-galactosidase to proximal dendrites, and in particular to axons. Thereby, we were able to visualize projections of CRHR1 neurons such as glutamatergic and dopaminergic afferent connections of the striatum and GABAergic CRHR1-expressing neurons located within its patch compartment. In addition, the tZ reporter gene revealed novel details of CRHR1 expression in the spinal cord, skin, and eye. CRHR1 expression in the retina prompted the identification of a new physiological role of CRHR1 related to the visual system. Besides its reporter properties, this novel CRHR1 allele comprises the possibility to conditionally restore or delete CRHR1 via Flp and Cre recombinase, respectively. Finally, the allele is suitable for further manipulations of the CRHR1 locus by recombinase-mediated cassette exchange. Taken together, this novel mouse allele will significantly facilitate the neuroanatomical analysis of CRHR1 circuits and opens up new avenues to address CRHR1 function in more detail.
    Document Type:
    Reference
    Product Catalog Number:
    AB5622
    Product Catalog Name:
    Anti-Microtubule-Associated Protein 2 (MAP2) Antibody

  • Dopaminergic neurons inhibit striatal output through non-canonical release of GABA. 23034651

    The substantia nigra pars compacta and ventral tegmental area contain the two largest populations of dopamine-releasing neurons in the mammalian brain. These neurons extend elaborate projections in the striatum, a large subcortical structure implicated in motor planning and reward-based learning. Phasic activation of dopaminergic neurons in response to salient or reward-predicting stimuli is thought to modulate striatal output through the release of dopamine to promote and reinforce motor action. Here we show that activation of dopamine neurons in striatal slices rapidly inhibits action potential firing in both direct- and indirect-pathway striatal projection neurons through vesicular release of the inhibitory transmitter GABA (γ-aminobutyric acid). GABA is released directly from dopaminergic axons but in a manner that is independent of the vesicular GABA transporter VGAT. Instead, GABA release requires activity of the vesicular monoamine transporter VMAT2, which is the vesicular transporter for dopamine. Furthermore, VMAT2 expression in GABAergic neurons lacking VGAT is sufficient to sustain GABA release. Thus, these findings expand the repertoire of synaptic mechanisms used by dopamine neurons to influence basal ganglia circuits, show a new substrate whose transport is dependent on VMAT2 and demonstrate that GABA can function as a bona fide co-transmitter in monoaminergic neurons.
    Document Type:
    Reference
    Product Catalog Number:
    AB152
    Product Catalog Name:
    Anti-Tyrosine Hydroxylase Antibody

  • Inhibition of calpains improves memory and synaptic transmission in a mouse model of Alzheimer disease. 18596919

    Calpains are calcium-dependent enzymes that determine the fate of proteins through regulated proteolytic activity. Calpains have been linked to the modulation of memory and are key to the pathogenesis of Alzheimer disease (AD). When abnormally activated, calpains can also initiate degradation of proteins essential for neuronal survival. Here we show that calpain inhibition through E64, a cysteine protease inhibitor, and the highly specific calpain inhibitor BDA-410 restored normal synaptic function both in hippocampal cultures and in hippocampal slices from the APP/PS1 mouse, an animal model of AD. Calpain inhibition also improved spatial-working memory and associative fear memory in APP/PS1 mice. These beneficial effects of the calpain inhibitors were associated with restoration of normal phosphorylation levels of the transcription factor CREB and involved redistribution of the synaptic protein synapsin I. Thus, calpain inhibition may prove useful in the alleviation of memory loss in AD.
    Document Type:
    Reference
    Product Catalog Number:
    MAB1622
    Product Catalog Name:
    Anti-Spectrin alpha chain (nonerythroid) Antibody, clone AA6