Introducing Black-Gold II, a highly soluble gold phosphate complex with several unique advantages for the histochemical localization of myelin

Schmued, Larry C.; Bowyer, John F.; Cozart, Matthew; Heard, David J.; Binienda, Zbigniew; Paule, Merle G.

doi:10.1016/j.brainres.2008.06.129

Cited by 85 publications

(68 citation statements)

References 9 publications

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“…VGluT2-and ERRβ immunolabeling in the SC was quantified using the same process described here for quantifying CTB density. To visualize RGC axons in layer III of the SC and determine SC volume, we used the myelin marker Black Gold II (Histochem) (31) in serial 50-μm SC sections. For quantifying axons in the optic nerve, segments near the eye (proximal) and optic chiasm (distal) were quantified as described (16,30).…”

Section: Methodsmentioning

confidence: 99%

Distal axonopathy with structural persistence in glaucomatous neurodegeneration

Crish

Sappington

Inman

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

316

482

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An early hallmark of neuronal degeneration is distal transport loss and axon pathology. Glaucoma involves the degeneration of retinal ganglion cell (RGC) neurons and their axons in the optic nerve. Here we show that, like other neurodegenerations, distal axon injury appears early in mouse glaucoma. Where RGC axons terminate in the superior colliculus, reduction of active transport follows a retinotopic pattern resembling glaucomatous vision loss. Like glaucoma, susceptibility to transport deficits increases with age and is not necessarily associated with elevated ocular pressure. Transport deficits progress distal-to-proximal, appearing in the colliculus first followed by more proximal secondary targets and then the optic tract. Transport persists through the optic nerve head before finally failing in the retina. Although axon degeneration also progresses distal-to-proximal, myelinated RGC axons and their presynaptic terminals persist in the colliculus well after transport fails. Thus, distal transport loss is predegenerative and may represent a therapeutic target.axon transport | optic neuropathy | retinal ganglion cell | glaucoma | optic nerve

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Section: Methodsmentioning

confidence: 99%

Distal axonopathy with structural persistence in glaucomatous neurodegeneration

Crish

Sappington

Inman

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

316

482

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“…Coronal sections and transversal sections with a cutting angle of 30° from C57BL6/129SvPas/Thy1-eYFP mice were stained with Nissl Neurotrace stain (Invitrogen) and observed with stereoscopic microscope (Nikon, AZ100M) and with confocal microscope (Zeiss, LSM 710). Coronal sections of C57BL6/129SvPas mice were stained using the gold method66 and counterstained with cresyl violet. For the evaluation of subicular neuronal density, coronal section of Thy1-eYFP mice was immunostained with an NeuN antibody and eYFP-positive cells were quantified using an homemade ImageJ macro.…”

Section: Methodsmentioning

confidence: 99%

Microtubule-associated protein 6 mediates neuronal connectivity through Semaphorin 3E-dependent signalling for axonal growth

et al. 2015

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Structural microtubule associated proteins (MAPs) stabilize microtubules, a property that was thought to be essential for development, maintenance and function of neuronal circuits. However, deletion of the structural MAPs in mice does not lead to major neurodevelopment defects. Here we demonstrate a role for MAP6 in brain wiring that is independent of microtubule binding. We find that MAP6 deletion disrupts brain connectivity and is associated with a lack of post-commissural fornix fibres. MAP6 contributes to fornix development by regulating axonal elongation induced by Semaphorin 3E. We show that MAP6 acts downstream of receptor activation through a mechanism that requires a proline-rich domain distinct from its microtubule-stabilizing domains. We also show that MAP6 directly binds to SH3 domain proteins known to be involved in neurite extension and semaphorin function. We conclude that MAP6 is critical to interface guidance molecules with intracellular signalling effectors during the development of cerebral axon tracts.

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“…Free floating brain sections were stained with Black Gold II myelin staining kit according to the manufacturer instructions (Millipore, Billerica, MA) (Schmued et al, 2008) and scanned at 20× with the Mirax Midi (Zeiss, Göttingen, Germany). A mean optical densitometry was calculated on matching regions of interest with the software Mercator (Explora Nova, La Rochelle, France).…”

Section: Myelin Stainingmentioning

confidence: 99%

In vivo assessment of myelination by phase imaging at high magnetic field

et al. 2012

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The present study evaluated the potential of using the phase of T 2 * weighted MR images to characterize myelination during brain development and pathology in rodents at 9.4 T. Phase contrast correlated with myelin content assessed by histology and suggests that most contrast between white and cortical gray matter is modulated by myelin. Ex vivo experiments showed that gray-white matter phase contrast remains unchanged after iron extraction. In dysmyelinated shiverer mice, phase imaging correlated strongly with myelin staining, showing reduced contrast between white and gray matter when compared to healthy controls. We conclude that highresolution phase images, acquired at high field, allow assessment of myelination and dysmyelination.© 2011 Elsevier Inc. All rights reserved. IntroductionThe assessment of myelination in healthy subjects and following injury in humans and in animal models is one of the ways to determine the degree of cerebral integrity or the degree of injury in case of white matter disease like multiple sclerosis. In newborns, myelination of the posterior limb of the internal capsule, when assessed at term equivalent, has been shown to be a very robust predictor of motor impairment (Cowan and de Vries, 2005). A simple technique that would access the degree of myelination of white matter would be very useful in mature animal models of white matter injury such as multiple sclerosis and in immature animal models of white matter injury such as periventricular leukomalacia as well as in human studies. There are various methods available: one approach consists of quantification of myelin bond and free water fractions by a multiexponential analysis of the T 2 decay (Beaulieu et al., 1998;MacKay et al., 1994;Whittall and MacKay, 1989;Lancaster et al., 2003). This is generally performed using a CarrPurcell-Meiboom-Gill (CPMG) or a Turbo Spin-Echo sequences with multiple echo times (Beaulieu et al., 1998). Due to specific absorption rate (SAR) (especially at high fields) and timing constraints, the T 2 decay curve is often not fully sampled for an accurate quantification. Recently, it has been shown that myelin water fraction can also be measured using a multi-exponential analysis of the T 2 * decay in multislice multiple echo gradient echo sequence (Du et al., 2007;Hwang et al., 2010). The resulting myelin water fractions are highly dependent on the constraints introduced on the multi-exponential fitting procedure (Hwang et al., 2010) and suffer from significant inaccuracies in regions close to air-tissue interfaces. An alternative approach of a multicomponent relaxation analysis using multicomponent driven equilibrium single pulse observation of T1 and T2 (mcDESPOT) (Deoni et al., 2008) was applied successfully on infants from 3 to 11 months to quantify myelination (Deoni et al., 2011). Magnetization transfer represents an alternative approach to quantify myelin with new approaches refining its modelization by characterizing individually the relaxation and exchange rates of the free water and macromolec...

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Introducing Black-Gold II, a highly soluble gold phosphate complex with several unique advantages for the histochemical localization of myelin

Cited by 85 publications

References 9 publications

Distal axonopathy with structural persistence in glaucomatous neurodegeneration

Distal axonopathy with structural persistence in glaucomatous neurodegeneration

Microtubule-associated protein 6 mediates neuronal connectivity through Semaphorin 3E-dependent signalling for axonal growth

In vivo assessment of myelination by phase imaging at high magnetic field

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