Are you using neuronal densities, synaptic densities or neurochemical densities as your definitive data? there is a better way to go

Oorschot, Dorothy E.

doi:10.1016/0301-0082(94)90040-x

Cited by 135 publications

(114 citation statements)

References 103 publications

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“…mation of the percentage of spared tissue was calculated using the Cavalieri method. The total volume of spared white and lesion area was calculated by summing their individual subvolumes (Oorschot, 1994). Individual subvolumes of lesion area and spared tissue were calculated by multiplying the cross-sectional area ( A) by D, where D represents the distance between sections (200 m).…”

Section: Figure 1 Demyelination After Contusive Sci a Bmentioning

confidence: 99%

Functional Recovery in Traumatic Spinal Cord Injury after Transplantation of Multineurotrophin-Expressing Glial-Restricted Precursor Cells

Cao¹,

Xu²,

DeVries³

et al. 2005

J. Neurosci.

264

220

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Demyelination contributes to the physiological and behavioral deficits after contusive spinal cord injury (SCI). Therefore, remyelination may be an important strategy to facilitate repair after SCI. We show here that rat embryonic day 14 spinal cord-derived glial-restricted precursor cells (GRPs), which differentiate into both oligodendrocytes and astrocytes, formed normal-appearing central myelin around axons of cultured DRG neurons and had enhanced proliferation and survival in the presence of neurotrophin 3 (NT3) and brain-derived neurotrophin factor (BDNF). We infected GRPs with retroviruses expressing the multineurotrophin D15A (with both BDNF and NT3 activities) and then transplanted them into the contused adult thoracic spinal cord at 9 d after injury. Expression of D15A in the injured spinal cord is five times higher in animals receiving D15A-GRP grafts than ones receiving enhanced green fluorescent protein (EGFP)-GRP or DMEM grafts. Six weeks after transplantation, the grafted GRPs differentiated into mature oligodendrocytes expressing both myelin basic protein (MBP) and adenomatus polyposis coli (APC).UltrastructuralanalysisshowedthatthegraftedGRPsformedmorphologicallynormal-appearingmyelinsheathsaroundtheaxonsinthe ventrolateral funiculus (VLF) of spinal cord. Expression of D15A significantly increased the percentage of APC ϩ oligodendrocytes of grafted GRPs (15-30%). Most importantly, 8 of 12 rats receiving grafts of D15A-GRPs recovered transcranial magnetic motor-evoked potential responses, indicating that conduction through the demyelinated VLF axons was restored. Such electrophysiological recovery was not observed in rats receiving grafts of EGFP-GRPs, D15A-NIH3T3 cells, or an injection of an adenovirus expressing D15A. Recovery of hindlimb locomotor function was also significantly enhanced only in the D15A-GRP-grafted animals at 4 and 5 weeks after transplantation. Therefore, combined treatment with neurotrophins and GRP grafts can facilitate functional recovery after traumatic SCI and may prove to be a useful therapeutic strategy to repair the injured spinal cord.

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Section: Figure 1 Demyelination After Contusive Sci a Bmentioning

confidence: 99%

Functional Recovery in Traumatic Spinal Cord Injury after Transplantation of Multineurotrophin-Expressing Glial-Restricted Precursor Cells

Cao¹,

Xu²,

DeVries³

et al. 2005

J. Neurosci.

264

220

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“…Age-related reductions in synaptic numerical densities, however, cannot be unambiguously interpreted as evidence of synapse loss, in that they can result from changes in either the volume of the region, or synapse number or both. Estimating total synapse GEIN1SMAN, GUNDERSON, VAN DER ZEE and WEST number, rather than synaptic numerical density, eliminates the questionable assumption, implicit in comparisons of density data, that the volumes of the regions being compared are the same (Braendgaard & Gundersen, 1986;Swaab & Uylings, 1987;Oorschot, 1994).…”

Section: Estimating Total Synapse Number Rather Than Synaptic Numerimentioning

confidence: 99%

Unbiased stereological estimation of the total number of synapses in a brain region

et al. 1996

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SummaryModern stereological methods have been used to make unbiased estimates of the total number of synapses in the striatum radiatum of the hippocampal CA1 region of five rabbits. The approach used involved a two stage analysis and is generally applicable to all parts of the nervous system. During the first stage of the analysis, the reference volume was estimated by point counting, at the light microscope level, according to the Cavalieri principle. During the second stage, the numerical density of synapses was estimated with disectors at the electron microscopic level. The total number of synapses was calculated as the product of the numerical density and the volume of the region. The sampling with points and disectors was carried out in all three dimensions of the entire CA1 region in a manner that ensured that all parts of the region and all synapses within it had equal probabilities of being sampled. An analysis of the precision of the estimate of total synapse number has been performed in terms of the variances of volume and synaptic numerical density at different levels of sampling, i.e. at the level of points, sections, individual animals and group of animals. Detailed descriptions of the procedures used to estimate the total number of synapses, evaluate the precision of the estimates, and optimize the sampling scheme are provided.

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“…An unbiased estimation of the percentage of spared tissue was calculated using the Cavalieri method 26 . The total volume of spared white and gray matter was calculated by summing their individual subvolumes 27 . Individual subvolumes of spared tissue were calculated by multiplying the cross-sectional area A x d, where d represents the distance between sections (240 µm).…”

Section: Tissue Processing Histology and Lesion Assessmentsmentioning

confidence: 99%

Inhibition of Cytosolic Phospholipase A₂Has Neuroprotective Effects on Motoneuron and Muscle Atrophy after Spinal Cord Injury

Liu

Byers

Lam

et al. 2021

Journal of Neurotrauma

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Surviving motoneurons undergo dendritic atrophy after spinal cord injury (SCI), suggesting an important therapeutic target for neuroprotective strategies to improve recovery of function after SCI. Our previous studies showed that phospholipase A 2 (PLA 2 ) may play an important role in the pathogenesis of SCI. In the present study, we investigated whether blocking cPLA 2 pharmacologically with arachidonyl trifluoromethyl ketone (ATK) or genetically using cPLA 2 knockout (KO) mice attenuates motoneuron atrophy following SCI. C57BL/6 mice received either sham or contusive SCI at the T10 level. At 30 min after SCI, mice were treated with ATK or vehicle. Four weeks later, motoneurons innervating the vastus lateralis muscle of the quadriceps were labeled with cholera toxin-conjugated horseradish peroxidase, and dendritic arbors were reconstructed in three dimensions. Soma volume, motoneuron number, lesion volume, and tissue sparing were also assessed, as were muscle weight, fiber cross-sectional area, and motor endplate size and density. ATK administration reduced percent lesion volume and increased percent volume of spared white matter compared to the vehicle-treated control animals. SCI with or without ATK treatment had no effect on the number or soma volume of quadriceps motoneurons. However, SCI resulted in a decrease in dendritic length of quadriceps motoneurons in untreated animals, and this decrease was completely prevented by treatment with ATK. Similarly, the vastus lateralis muscle weights of untreated SCI animals were smaller than those of sham-surgery controls, and these reductions were prevented by ATK treatment. No effects on fiber cross-sectional areas, motor endplate area or density were observed across treatment groups. Remarkably, genetically deleting cPLA 2 in cPLA 2 KO mice attenuated dendritic atrophy after SCI. These findings suggest that after SCI, cord tissue damage and regressive changes in motoneuron and muscle morphology can be reduced by inhibition of cPLA 2 , further supporting a role for cPLA 2 as a neurotherapeutic target for SCI treatment.

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Are you using neuronal densities, synaptic densities or neurochemical densities as your definitive data? there is a better way to go

Cited by 135 publications

References 103 publications

Functional Recovery in Traumatic Spinal Cord Injury after Transplantation of Multineurotrophin-Expressing Glial-Restricted Precursor Cells

Functional Recovery in Traumatic Spinal Cord Injury after Transplantation of Multineurotrophin-Expressing Glial-Restricted Precursor Cells

Unbiased stereological estimation of the total number of synapses in a brain region

Inhibition of Cytosolic Phospholipase A₂Has Neuroprotective Effects on Motoneuron and Muscle Atrophy after Spinal Cord Injury

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Are you using neuronal densities, synaptic densities or neurochemical densities as your definitive data? there is a better way to go

Cited by 135 publications

References 103 publications

Functional Recovery in Traumatic Spinal Cord Injury after Transplantation of Multineurotrophin-Expressing Glial-Restricted Precursor Cells

Functional Recovery in Traumatic Spinal Cord Injury after Transplantation of Multineurotrophin-Expressing Glial-Restricted Precursor Cells

Unbiased stereological estimation of the total number of synapses in a brain region

Inhibition of Cytosolic Phospholipase A2Has Neuroprotective Effects on Motoneuron and Muscle Atrophy after Spinal Cord Injury

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Inhibition of Cytosolic Phospholipase A₂Has Neuroprotective Effects on Motoneuron and Muscle Atrophy after Spinal Cord Injury