Characteristic features of a nerve primo-vessel suspended in rabbit brain ventricle and central canal.

Bonghan theory was proposed by Bonghan Kim to illustrate the anatomy and physiology of the acupuncture meridian system. One of his astonishing claims was the physical presence of the nerve primo-vessel, which can be involved with a regenerating system of nerves. Our previous work has shown that there is a nerve primo-vessel in brain ventricles and the central canal of the spine of a rabbit. In this study, confocal laser scanning microscopy, transmission electron microscopy, and high voltage electron microscopy demonstrated that a nerve primo-vessel comprised DNA particles, other microparticles, and rod-shaped nuclei encircled by helix-shaped actins. The nerve primo-vessel had acridine orange-stained DNA particles that varied in size and were in parallel. These characteristics of the nerve primo-vessel are crucial for a comprehensive understanding of their function in the central nervous system, which may be associated with nerve regeneration.

Pathomechanism of ligamentum flavum hypertrophy: a multidisciplinary investigation based on clinical, biomechanical, histologic, and biologic assessments.

STUDY DESIGN: A multidisciplinary study involving clinical, histologic, biomechanical, biologic, and immunohistologic approaches. OBJECTIVE.: To clarify the pathomechanism of hypertrophy of the ligamentum flavum. SUMMARY OF BACKGROUND DATA: The most common spinal disorder in elderly patients is lumbar spinal canal stenosis, causing low back and leg pain, and paresis. Canal narrowing, in part, results from hypertrophy of the ligamentum flavum. Although histologic and biologic literature on this topic is available, the pathomechanism of ligamentum flavum hypertrophy is still unknown. METHODS: The thickness of 308 ligamenta flava at L2/3, L3/4, L4/5, and L5/S1 levels of 77 patients was measured using magnetic resonance imaging. The relationships between thickness, age, and level were evaluated. Histologic evaluation was performed on 20 ligamentum flavum samples, which were collected during surgery. Trichrome and Verhoeff-van Gieson elastic stains were performed for each ligamentum flavum to understand the degree of fibrosis and elastic fiber status, respectively. To understand the mechanical stresses in various layers of ligamentum flavum, a 3-dimensional finite element model was used. Von Mises stresses were computed, and values between dural and dorsal layers were compared. There were 10 ligamenta flava collected for biologic assessment. Using real-time reverse transcriptase polymerase chain reaction, transforming growth factor (TGF)-beta messenger ribonucleic acid expression was quantitatively measured. The cellular location of TGF-beta was also confirmed from 18 ligamenta flava using immunohistologic techniques. RESULTS: The ligamentum flavum thickness increased with age, however, the increment at L4/5 and L3/4 levels was larger than at L2/3 and L5/S1 levels. Histology showed that as the ligamentum flavum thickness increased, fibrosis increased and elastic fibers decreased. This tendency was more predominant along the dorsal side. Von Misses stresses revealed that the dorsal fibers of ligamentum flavum were subjected to higher stress than the dural fibers. This was most remarkably observed at L4/5. The largest increase in ratio observed between the dorsal and dural layer was approximately 5-fold in flexion at L4/5 in flexion. Expression of TGF-beta was observed in all ligamenta flava, however, the expression decreased as the ligamentum flavum thickness increased. Immunohistochemistry showed that TGF-beta was released by the endothelial cells, not by fibroblasts. CONCLUSIONS: Fibrosis is the main cause of ligamentum flavum hypertrophy, and fibrosis is caused by the accumulation of mechanical stress with the aging process, especially along the dorsal aspect of the ligamentum flavum. TGF-beta released by the endothelial cells may stimulate fibrosis, especially during the early phase of hypertrophy.

Immunocytochemical localization of zinc transporter 3 in the ependyma of the mouse spinal cord.

We report, for the first time, the light microscopical and ultrastructural appearance of ZnT3-immunoreactivities in the ependymal cells of the central canal of the mouse spinal cord. Light microscopy revealed the presence of ZnT3-immunoreactive (Ir) ependymal cells in 1 microm thick epon sections stained by the ABC method. The ZnT3-Ir cells were observed at all levels of the spinal cord, but were a little more numerous in lumbosacral segments than in cervicothoracic segments. The ZnT3-Ir cells had large, ovoid nuclei with abundant cytoplasm, and protruded into the lumen of the central canal. Our ultrastructural findings suggest that the ZnT3-Ir ependymal cells possess secretory activity directed towards the central canal. We propose that they may play a role in the trans-ependymal mechanism responsible for zinc homeostasis between cerebrospinal fluid and the central area of the gray matter.

Neuronal progenitor-like cells expressing polysialylated neural cell adhesion molecule are present on the ventricular surface of the adult rat brain and spinal cord.

In the adult rodent brain, it is now well established that neurons are continuously generated from proliferating neuronal progenitor cells located in the subventricular zone of the lateral ventricle (SVZ) and the dentate gyrus of the hippocampus. Recently, it has been shown that neurons can also be generated in vitro from various regions of the adult brain and spinal cord ventricular neuroaxis. As the highly polysialylated neural cell adhesion molecule (PSA-NCAM) has been shown to be specifically expressed by neuronal progenitor cells of the SVZ and the hippocampus, the present study was designed to determine whether cells expressing this molecule could be detected in the vicinity of the ventricular system of the adult rat brain and spinal cord. After double or triple immunostaining for different neuronal and glial markers, confocal microscopy was used to examine the surface of the ventricular neuroaxis in either 40- to 50-microm-thick transverse vibratome sections cut through different brain regions, or in 200- to 300-microm-thick tissue slices including the intact surface of the brain ventricles or of the spinal cord central canal. In untreated rats, PSA-NCAM, microtubule associated protein 2 (MAP2) and class III-beta-tubulin were found to be associated with a number of neuron-like cells located on the surface of the third and fourth ventricles and of the spinal cord central canal. The proliferation of the PSA-NCAM-immunoreactive (IR) neuron-like cells detected on the surface of the third and fourth ventricles was not affected by injection of epidermal growth factor (EGF) or basic fibroblast growth factor (bFGF) into these ventricles, but was stimulated by the combined injection of EGF + bFGF. These data indicate that cells exhibiting features of neuronal progenitors are present on the ependymal surface of the adult rat brain and spinal cord ventricular axis.

The ventriculus terminalis and filum terminale of the human spinal cord.

Serial sections of the conus medullaris and the filum terminale of 23 randomly selected human spinal cords were studied by light and electron microscopy, and following immunoperoxidase staining for glial fibrillary acidic protein (GFAP), vimentin, neuron-specific enolase (NSE), amyloid beta protein, and S-100 protein. The intradural portion of the filum contains bundles of GFAP-positive glial fibers, scattered silver- and NSE-positive neurons, segments of peripheral nerve, blood vessels, fibrous connective tissue, and fat. Glial cell clusters varying from five to 100 cell layers thick at times constitute the bulk of the filum. The periependymal glial cells possess moderate amounts of eosinophilic cytoplasm and relatively uniform round to ovoid nuclei containing evenly distributed chromatin. They are distributed diffusely with no specific pattern of organization, although some of them showed a tendency to form acinar structures. A minority of the glial cells showed GFAP immunoreactivity, and some were immunoreactive for vimentin. Electron microscopy demonstrated the presence of periependymal cells showing cilia, microvilli, and the formation of intercellular junctional complexes, as well as cells containing bundles of glial filaments within the cytoplasm. Degenerated NSE-positive neurons and degenerated neurites resembling neuritic plaques were also demonstrated. However, immunoperoxidase staining for amyloid beta protein was negative in these structures. Thus, the filum terminale is endowed with an abundance of glial cells and neurons and is not simply a fibrovascular tag. Periependymal glial cells in the filum terminale should not be mistaken for neoplasm. The presence of neuropil with profuse astroglial and neuronal components within the filum terminale suggests a possible functional role for these structures.