The ultrastructure of spinal cord perivascular spaces: Implications for the circulation of cerebrospinal fluid

Lam, Magdalena; Hemley, Sarah J.; Najafi, Elmira; Vella, Nicole; Bilston, Lynne E.; Stoodley, Marcus A.

doi:10.1038/s41598-017-13455-4

Cited by 55 publications

(54 citation statements)

References 46 publications

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“…A detailed analysis of the spinal cord tissue revealed several abnormalities within perivascular spaces and the surrounding spinal cord tissue of animals with PTS compared with controls. In all animals, perivascular spaces were continuous with the extracellular spaces of the surrounding tissue and with the vascular wall basement membranes, consistent with previous data [21]. However, in animals with PTS, the perivascular spaces were strikingly enlarged with a concomitant loss of connective tissue, and often contained activated macrophages.…”

Section: Discussionsupporting

confidence: 90%

“…Perivascular spaces of arterioles and venules in the healthy spinal cord ranged from 264 nm to 1.9 µm in radial width, in line with previous data [21]. At the level of capillaries in healthy spinal cord, the perivascular space was reduced to a thin (50-100 nm) layer of electron-dense extracellular matrix, the basal lamina ( Fig.…”

Section: Enlarged Perivascular Spacessupporting

confidence: 90%

“…The extracellular space was described as the space between parenchymal cells (astrocytes, oligodendrocytes, neurons and their processes) separated from the CSF-filled areas of the subarachnoid and perivascular space by the foot processes of astrocytes. These fluid compartments are not truly separate, as gap junctions exist between astrocytic foot processes that allow extracellular fluid to communicate with perivascular spaces and basal laminae [21].…”

Section: Resultsmentioning

confidence: 99%

“…Twelve weeks after the induction of syringomyelia, to allow sufficient time for the development of an enlarged syrinx, animals were placed under general anesthesia (5% isoflurane in oxygen induction and maintained at 2.5% isoflurane in oxygen). Animals were intracardially perfused with a mixture of paraformaldehyde (3%) and glutaraldehyde (2.5%) in sodium phosphate buffer (0.1 M), and the spinal cord dissected out and processed for electron microscopy, as described previously [21]. In short, 1 mm thick spinal cord segments underwent post-fixation and en bloc staining with osmium tetroxide (1%; 1 h) and uranyl acetate (2%; 30 min) respectively, followed by ethanol dehydration in graded solutions and LR White resin infiltration (ProSciTech, Queensland, Australia).…”

Section: Methodsmentioning

confidence: 99%

“…However, the contribution of perivascular flow to syrinx formation is unclear. A recent electron microscopic study in healthy rats indicated a continuity of flow between the spinal subarachnoid space and the central canal, via a network of perivascular and extracellular spaces in the white and grey matter [21]. Whether the ultrastructure of perivascular spaces and fluid interfaces of the spinal cord is altered in PTS is yet to be determined.…”

Section: Introductionmentioning

confidence: 99%

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Abnormalities in spinal cord ultrastructure in a rat model of post-traumatic syringomyelia

Berliner

Hemley

Najafi

et al. 2020

Fluids Barriers CNS

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Background: Syringomyelia is a serious complication of spinal cord trauma, occurring in approximately 28% of spinal cord injuries. Treatment options are limited and often produce unsatisfactory results. Post-traumatic syringomyelia (PTS) is presumably related to abnormalities of cerebrospinal fluid (CSF) and interstitial fluid hydrodynamics, but the exact mechanisms are unknown.Methods: Transmission electron microscopy (TEM) was used to investigate in detail the interfaces between fluid and tissue in the spinal cords of healthy Sprague-Dawley rats (n = 3) and in a rat model of PTS (n = 3). PTS was induced by computer-controlled impact (75 kDyn) to the spinal cord between C6 and C8, followed by a subarachnoid injection of kaolin to produce focal arachnoiditis. Control animals received a laminectomy only to C6 and C7 vertebrae. Animals were sacrificed 12 weeks post-surgery, and spinal cords were prepared for TEM. Ultra-thin spinal cord sections at the level of the injury were counterstained for structural anatomy. Results:Spinal cords from animals with PTS displayed several abnormalities including enlarged perivascular spaces, extracellular edema, cell death and loss of tissue integrity. Additionally, alterations to endothelial tight junctions and an abundance of pinocytotic vesicles, in tissue adjacent to syrinx, suggested perturbations to blood-spinal cord barrier (BSCB) function. Conclusions:These findings support the hypothesis that perivascular spaces are important pathways for CSF flow into and out of the spinal cord, but also suggest that fluid may enter the cord through vesicular transport and an altered BSCB.

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Section: Discussionsupporting

confidence: 90%

Section: Enlarged Perivascular Spacessupporting

confidence: 90%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Abnormalities in spinal cord ultrastructure in a rat model of post-traumatic syringomyelia

Berliner

Hemley

Najafi

et al. 2020

Fluids Barriers CNS

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Functional consequences of a close encounter between microglia and brain-infiltrating monocytes during CNS pathology and repair

Quarta

Berneman

Ponsaerts

2020

Journal of Leukocyte Biology

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Neuroinflammation is recognized as an important factor contributing to the development and progression of several central nervous system (CNS) disorders. Upon CNS trauma or disease, parenchymal microglia highly proliferate and accumulate in and around the lesion site. In addition, blood‐derived monocytes can infiltrate the inflamed CNS in response to cellular damage and/or a compromised blood–brain barrier. Both microglia and infiltrating monocytes are characterized by multiple functional states and can either display highly proinflammatory properties or promote resolution of inflammation and tissue regeneration. Despite sharing some basic immunologic functions, microglia and monocytes display many distinctive features, which ultimately define their contribution to neuropathology. Understanding how the innate immune system participates to brain disease is imperative to identify novel treatment options for CNS inflammatory disorders. In this context, existing and newly developed in vitro platforms for disease modeling are fundamental tools to investigate and modulate microglia and monocyte immune functions within a specific neuropathologic context. In this review, we first briefly summarize the current knowledge on microglia and monocyte ontogenesis, as well as their complex and interconnected contributions to the development of various CNS pathologies. Following the well‐recognized concept that both microglia and monocytes can either exert neuroprotective functions or exacerbate tissue damage, we provide a comprehensive overview of cellular models currently available for in vitro study of neuroinflammatory responses. In this context, we highlight how simplified single‐cell models may not always correctly recapitulate in vivo biology, hence future research should move toward novel models with higher and multicellular complexity.

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Plasticity of the spinal glymphatic system in male SD rats with painful diabetic neuropathy induced by type 2 diabetes mellitus

Wang

et al. 2022

J of Neuroscience Research

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Painful diabetic neuropathy (PDN) is one of the most common diabetic complications (Iqbal et al., 2018;Schmader, 2002;Schreiber et al., 2015), and is most often described as "burning," "electric," "sharp," and "dull/ache," which, for most, is worse at night time and when tired or stressed (Schmader, 2002). It affects the physical and mental health of patients seriously, leading to sleeping disorders, fatigue, and decreased activity, thus causing substantial interference in the enjoyment of life (Galer et al., 2000;Schmader, 2002).Owing to our limited knowledge of the underlying mechanism of PDN, current treatments are mainly focused on patients' symptoms and the therapeutic effects are unsatisfied (Iqbal et al., 2018;

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The ultrastructure of spinal cord perivascular spaces: Implications for the circulation of cerebrospinal fluid

Cited by 55 publications

References 46 publications

Abnormalities in spinal cord ultrastructure in a rat model of post-traumatic syringomyelia

Abnormalities in spinal cord ultrastructure in a rat model of post-traumatic syringomyelia

Functional consequences of a close encounter between microglia and brain-infiltrating monocytes during CNS pathology and repair

Plasticity of the spinal glymphatic system in male SD rats with painful diabetic neuropathy induced by type 2 diabetes mellitus

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