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Results for “GANGLIA, SPINAL”

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PubMed1984

Galactose neuropathy: impact of chronic endoneurial edema on nerve blood flow.

Peripheral neuropathy induced by galactose feeding results in endoneurial edema with increased tissue pressure and ultimate demyelination of nerve fibers. To assess the role of ischemia in the pathogenesis of this neuropathy, nerve blood flow was measured 6 months after the start of galactose ingestion, between the onset of edema and nerve fiber changes. Measurement was carried out by a noninvasive technique involving the use of [14C]iodoantipyrine as a radioactive tracer of tissue perfusion. A significant decline in nerve blood flow was found, which correlated positively with increased nerve water content as quantified by a microgravimetric technique. We sought to establish the pathogenic role of nerve edema in the development of schwannopathy and demyelination by morphological examination. It was found that Schwann cells appeared normal in areas of the peripheral nervous system in which edema does not occur, such as spinal ganglia and roots, whereas in regions in which there was edema, massive glycogen accumulation in Schwann cells and demyelination occurred. These findings suggest that edema, rather than hyperactivity in the sorbitol pathway, is responsible for the pathological changes in galactosemic neuropathy and that ischemia resulting from edema and increased endoneurial fluid pressure is the mechanism responsible for fiber injury.

Animals↗

PubMed1994

Immunohistochemical localization of the high-affinity NGF receptor (gp140-trkA) in the adult human dorsal root and sympathetic ganglia and in the nerves and sensory corpuscles supplying digital skin.

BACKGROUND: Nerve growth factor (NGF) is produced in target tissues of sympathetic and neural-crest derived sensory neurons, including skin, to provide them trophic support. The biological effects of NGF on responsive cells are mediated by specific high-affinity receptors. Recently, a protein tyrosine kinase of congruent to 140 kDa molecular weight, encoded by the proto-oncogene trkA, has been identified as the high-affinity NGF receptor (gp140-trkA). The present work was undertaken to study the localization of gp140-trkA-like immunoreactivity (IR) in human peripheral ganglia (sympathetic and dorsal root ganglia), and in glabrous skin. METHODS: Lumbar dorsal root ganglia, para- and prevertebral sympathetic ganglia, and digital glabrous skin were studied immunohistochemically using a rabbit anti-gp140-trkA polyclonal antibody. In order to accurately establish the localization of gp140-trkA IR, the neurofilament proteins and S-100 protein were studied in parallel in: (1) sensory and sympathetic ganglia, to label neuron cell bodies and satellite or supporting cells, respectively; (2) human skin, to label axons, Schwann and related cells within nerves and sensory corpuscles. Moreover, a quantitative study (neuron size, intensity of immunostaining) was carried out on sympathetic and dorsal root ganglia neuron cell bodies. RESULTS: A specific gp140-trkA-like IR was found in: (1) a subpopulation (65%) of primary sensory neuron cell bodies, including most of the large-sized ones but also small- and intermediate-sized ones; (2) most of sympathetic neuron cell bodies (82%); (3) the perineurial cell, Schwann cells, and large axons of the nerve trunks supplying digital skin; (4) the lamellar cells of Meissner corpuscles; (5) the central axon, inner-core, outer-core, and capsule of Pacinian corpuscles. In addition, the occurrence of gp140-trkA-like IR was observed in some non-nervous tissues of the skin, including epidermis (mainly in the basal layer), sweat glands, and arterial blood vessels. CONCLUSIONS: Present results provide evidence for the localization of gp140-trkA-like IR in: (1) nerve cells which are known to be NGF-responsive, and (2) non-nervous cutaneous tissues which are innervated by NGF-dependent peripheral neurons. These findings suggest that, in addition to the well-established role of NGF on sensory and sympathetic neurons, this neurotrophin may be able to regulate some other functions on non-nervous cells which are targets for NGF-dependent peripheral neurons.

Adult↗

PubMed2002

Differentiation and maturation of zebrafish dorsal root and sympathetic ganglion neurons.

The trunk neural crest of vertebrate embryos gives rise to dorsal root ganglion (DRG) sensory neurons and autonomic sympathetic neurons, among other derivatives. We have examined the development of DRG and sympathetic neurons during development in the zebrafish. We found that sensory neurons differentiate rapidly and that their overt neuronal differentiation significantly precedes that of sympathetic neurons in the trunk. Sympathetic neurons in different regions differentiate at different times. The most rostral population, which we call the cervical ganglion, differentiates several days before trunk sympathetic neurons. After undergoing overt neuronal differentiation, sympathetic neurons subsequently express the adrenergic differentiation markers dopamine beta-hydroxylase and tyrosine hydroxylase. A second population of adrenergic nonneuronal cells initially localized with cervical sympathetic neurons appears to represent adrenal chromaffin cells. In more mature fish, these cells were present in clusters within the kidneys. Individual DRG and sympathetic ganglia initially contain few neurons. However, the number of neurons in DRG and sympathetic ganglia increases continuously at least up to 4 weeks of age. Analysis of phosphohistone H3 expression and bromodeoxyuridine incorporation studies suggests that the increases in DRG and sympathetic ganglion neuronal cell number are due wholly or in part to the division of neuronal cells within the ganglia.

Animals↗

PubMed1981

The ratio of preganglionic axons to postganglionic cells in the sympathetic nervous system of the rat.

Previously reported preganglionic-postganglionic ratios for the sympathetic system are a major part of the evidence for the widely accepted idea that the sympathetic innervation of the viscera is diffuse. Unfortunately, the previous reports did not assess the non-preganglionic fibers in the nerves examined, and the limitations of light microscopy precluded accurate unmyelinated fiber counts. Thus, a recalculation of these ratios is necessary. The present study recalculates these ratios for the cervical sympathetic system of the rat. All fiber counts are done with the electron microscope which has the resolution necessary for accurately determining axon numbers. Selective surgical procedures establish that 84% of the axons in the cervical sympathetic trunk are preganglionic, 11% are postganglionic, and 5% are sensory. Thus, the numbers of preganglionic fibers can now be accurately assessed and compared to the number of postganglionic neurons in the superior cervical ganglion. When this is done, a preganglionic/postganglionic ratio of approximately 1:4 is obtained. This ratio differs considerably from those previously published.

Animals↗

PubMed1982

A study of the extrinsic innervation of the guinea pig pylorus with the horseradish peroxidase tracing technique.

The extrinsic innervation of the guinea pig pylorus was studied by the use of the horseradish peroxidase (HRP) tracing technique. Forty-eight hours after injection of HRP into the pyloric sphincter labeled neurons of varying sizes were found throughout the rostrocaudal extent of the dorsal motor nuclei of the vagus. No HRP positive cells were seen in the medial solitary nuclei or the ambiguous nuclei. Many HRP-positive cells were observed in the celiac-superior mesenteric ganglion complex. Occasional cells in the superior cervical and stellate ganglia were also labeled. When the vagal ganglia were analyzed many enzyme-containing cells were found in the nodose ganglia and some cells in the jugular ganglia. Furthermore, about 15-20% of the labeled afferent neurons were located in dorsal root ganglia on both sides, with the majority of cells at the T5--T10 levels. The results are discussed in relation to recent transmitter histochemical findings as well as possible functional roles of the neurons.

Animals↗

PubMed1988

Origin of sympathetic and sensory innervation of the elbow joint in the rat: a retrograde axonal tracing study with wheat germ agglutinin conjugated horseradish peroxidase.

After injection of wheat germ agglutinin conjugated horseradish peroxidase (WGA-HRP) into the elbow joint of adult rats, labeled neurons were found in the stellate and the T2-T4 ganglia of the ipsilateral sympathetic trunk, and also in dorsal root ganglia at the C4-T4 levels. Most labeled sympathetic cells, 90% or more, were located in the stellate ganglion. The sensory innervation to the joint originated mainly from the dorsal root ganglia at the levels of C7-T1.

Afferent Pathways↗

PubMed1989

GABA-immunoreactive neurons and terminals in the lateral cervical nucleus of the cynomolgus monkey.

An antiserum against the inhibitory transmitter substance gamma-aminobutyric acid (GABA) was used to investigate the distribution of GABAergic nerve terminals and cell bodies in the lateral cervical nucleus (LCN) of the cynomolgus monkey. Light microscopic immunohistochemistry demonstrated GABA-immunoreactive puncta, suggestive of nerve terminals, scattered throughout the LCN. The terminal-like profiles are often present along the somata of unlabeled neurons, but most are located in the neuropil. GABA-immunoreactive neurons are present in the LCN, but constitute a very small number of the LCN neurons. Electron microscopy showed that the GABA-positive neurons are small with a relatively large nucleus. They are contacted by few somatic boutons. Numerous GABA-immunoreactive terminals containing densely packed round to oval synaptic vesicles were also found. Most GABA-positive terminals make synaptic contact with dendrites, but synapses with cell bodies are also present. Synaptic contacts between labeled and unlabeled terminals were not observed. Some GABA-positive terminals make contact with GABA-positive neurons. The present findings suggest that GABA is a major inhibitory transmitter substance in the LCN of the monkey. However, in comparison with other somatosensory relay nuclei, there are few GABA-immunoreactive neurons in the LCN. This may imply that the GABA-positive neurons branch extensively in the LCN or that an extrinsic source of GABAergic input exists.

Animals↗

PubMed2003

Developmental changes in neurite outgrowth responses of dorsal root and sympathetic ganglia to GDNF, neurturin, and artemin.

The ability of glial cell line-derived neurotrophic factor (GDNF), neurturin, and artemin to induce neurite outgrowth from dorsal root, superior cervical, and lumbar sympathetic ganglia from mice at a variety of development stages between embryonic day (E) 11.5 and postnatal day (P) 7 was examined by explanting ganglia onto collagen gels and growing them in the presence of agarose beads impregnated with the different GDNF family ligands. Artemin, GDNF, and neurturin were all capable of influencing neurite outgrowth from dorsal root and sympathetic ganglia, but the responses of each neuron type to the different ligands varied during development. Neurites from dorsal root ganglia responded to artemin at P0 and P7, to GDNF at E15.5 and P0, and to neurturin at E15.5, P0, and P6/7; thus, artemin, GDNF, and neurturin are all capable of influencing neurite outgrowth from dorsal root ganglion neurons. Neurites from superior cervical sympathetic ganglia responded significantly to artemin at E15.5, to GDNF at E15.5 and P0, and to neurturin at E15.5. Neurites from lumbar sympathetic ganglia responded to artemin at all stages from E11.5 to P7, to GDNF at P0 and P7 and to neurturin at E11.5 to P6/7. Combined with the data from previous studies that have examined the expression of GDNF family members, our data suggest that artemin plays a role in inducing neurite outgrowth from young sympathetic neurons in the early stages of sympathetic axon pathfinding, whereas GDNF and neurturin are likely to be important at later stages of sympathetic neuron development in inducing axons to enter particular target tissues once they are in the vicinity or to induce branching within target tissues. Superior cervical and lumbar sympathetic ganglia showed temporal differences in their responsiveness to artemin, GDNF, and neurturin, which probably partly reflects the rostrocaudal development of sympathetic ganglia and the tissues they innervate.

Animals↗

PubMed2003

Identification and regulation of tissue-specific cis-acting elements associated with the human AP-2alpha gene.

Mice lacking transcription factor AP-2alpha exhibit defects in the formation of the head, body wall, heart, neural tube, eye, and limbs, reflecting important sites of AP-2alpha expression in the developing embryo. AP-2alpha is also expressed in the postnatal mammary gland and has been linked to tumor progression and defects in growth regulation in the breast. We have used a transgenic mouse approach to identify tissue-specific cis-acting sequences associated with expression of the human AP-2alpha gene. Our analysis indicates that multiple elements located throughout the gene contribute to expression in the trigeminal ganglia, spinal cord, mammary gland, and epidermis. A discrete cis-element located within the fifth intron is required for expression in the face and limbs, and we have derived a permanent line of AP-2alpha::lacZ transgenic mice to assess expression of this latter enhancer throughout morphogenesis. We also introduced this transgene into an AP-2alpha-null mouse background and detected subtle alterations of its expression within the progress zone and apical ectodermal ridge of the forelimbs. Similar changes in lacZ expression were observed within the zeugopod, and these correlated with defects in radius condensation in AP-2alpha-knockout mice. Taken together, these findings indicate that cell:cell communication within the forelimb is altered in the absence of AP-2alpha and reveal novel regulatory potential for AP-2alpha in limb development.

Animals↗

PubMed2003

Expression of murine ELL-associated factor 2 (Eaf2) is developmentally regulated.

Eaf2, ELL-associated factor 2, encodes a protein that is homologous to the human EAF1, which was shown to interact with the transcriptional elongation factor MEN/ELL. During mouse embryogenesis, Eaf2 is preferentially expressed in the central nervous system and in sensory and neuroendocrine organs, including the brain, spinal cord, cranial and spinal ganglia, developing otocyst, the retina, and the pituitary. Eaf2 transcripts were also found in sites where active epithelium-mesenchymal interactions are occurring. These included the invaginating tooth buds, mammary gland anlage, submandibular glands, the lung, the pancreas, and the kidney. Other sites of expression included bladder and intestine. In the developing lens, Eaf2 transcripts were absent in the proliferating anterior lens epithelial cells but were present in the terminally differentiated primary lens fiber cells and also in nonproliferating lens fiber cells in the equatorial zone where lens epithelial cells withdraw from cell cycle and terminally differentiate into secondary lens fiber cells. This spatially restricted pattern of Eaf2 expression in the developing lens suggests that Eaf2 may play an important role in regulating lens maturation.

Amino Acid Sequence↗

PubMed2005

Localization of Apaf1 gene expression in the early development of the mouse by means of in situ reverse transcriptase-polymerase chain reaction.

Apoptosis is an essential ubiquitous process that controls the duration of the life span of cells, thus playing a crucial role in morphogenetic, histogenetic, and phylogenetic developmental processes. Apaf1 (apoptosis protease activating factor 1) is one of the central mediators of the intrinsic apoptotic pathway and a part of the apoptosome, which activates procaspase-3 and promotes cell death. Gene knockout of Apaf1 in mice leads to late embryonic lethality with malformations such as the persistence of interdigital webs and hyperplasia of brain and retina. Therefore, Apaf1 is generally believed to play a crucial role in developmental apoptosis and have a widespread expression. However, its pattern of expression in early development remains unknown. To specify whether Apaf1 indeed plays this key role, we investigated the pattern of gene expression for Apaf1 in mouse embryos on day 7, 9, and 12 of development. Our results show, that gene expression for Apaf1 first occurs within the embryo between day 7 and 9 of development, becoming more widespread toward day 12 and then includes structures, such as yolk sac, mesenchyme, cartilage, heart anlage, otic vesicle, peridermis, and anlagen of the spinal ganglia and vertebral bodies. Our results also show that gene expression for Apaf1 is not ubiquitous in early mouse development. This finding indicates that cell death processes are independent of or less dependent on Apaf1 during this time. Of interest, an active gene expression for Apaf1 is also present in organ anlagen such as heart or intestine, in which no obvious phenotype is seen after Apaf1 deletion. This finding suggests a possible role for Apaf1 in such anlagen as a putative alternative compensatory pathway, which could be switched on in the case of defects in the mediators that are normally involved in such organs.

Animals↗

PubMed2006

Regulation of the neurofibromatosis 2 gene promoter expression during embryonic development.

Mutations in the Neurofibromatosis 2 (NF2) gene are associated with predisposition to vestibular schwannomas, spinal schwannomas, meningiomas, and ependymomas. Presently, how NF2 is expressed during embryonic development and in the tissues affected by neurofibromatosis type 2 (NF2) has not been well defined. To examine NF2 expression in vivo, we generated transgenic mice carrying a 2.4-kb NF2 promoter driving beta-galactosidase (beta-gal) with a nuclear localization signal. Whole-mount embryo staining revealed that the NF2 promoter directed beta-gal expression as early as embryonic day E5.5. Strong expression was detected at E6.5 in the embryonic ectoderm containing many mitotic cells. beta-gal staining was also found in parts of embryonic endoderm and mesoderm. The beta-gal staining pattern in the embryonic tissues was corroborated by in situ hybridization analysis of endogenous Nf2 RNA expression. Importantly, we observed strong NF2 promoter activity in the developing brain and in sites containing migrating cells including the neural tube closure, branchial arches, dorsal aorta, and paraaortic splanchnopleura. Furthermore, we noted a transient change of NF2 promoter activity during neural crest cell migration. While little beta-gal activity was detected in premigratory neural crest cells at the dorsal ridge region of the neural fold, significant activity was seen in the neural crest cells already migrating away from the dorsal neural tube. In addition, we detected considerable NF2 promoter activity in various NF2-affected tissues such as acoustic ganglion, trigeminal ganglion, spinal ganglia, optic chiasma, the ependymal cell-containing tela choroidea, and the pigmented epithelium of the retina. The NF2 promoter expression pattern during embryogenesis suggests a specific regulation of the NF2 gene during neural crest cell migration and further supports the role of merlin in cell adhesion, motility, and proliferation during development.

Animals↗

PubMed1991

Pax-3, a novel murine DNA binding protein expressed during early neurogenesis.

We describe the isolation and characterization of Pax-3, a novel murine paired box gene expressed exclusively during embryogenesis. Pax-3 encodes a 479 amino acid protein with an Mr of 56 kd containing both a paired domain and a paired-type homeodomain. The Pax-3 protein is a DNA binding protein that specifically recognizes the e5 sequence present upstream of the Drosophila even-skipped gene. Pax-3 transcripts are first detected in 8.5 day mouse embryos where they are restricted to the dorsal part of the neuroepithelium and to the adjacent segmented dermomyotome. During early neurogenesis, Pax-3 expression is limited to mitotic cells in the ventricular zone of the developing spinal cord and to distinct regions in the hindbrain, midbrain and diencephalon. In 10-12 day embryos, expression of Pax-3 is also seen in neural crest cells of the developing spinal ganglia, the craniofacial mesectoderm and in limb mesenchyme of 10 and 11 day embryos.

Amino Acid Sequence↗

PubMed1985

How do the migratory and adhesive properties of the neural crest govern ganglia formation in the avian peripheral nervous system?

The peripheral nervous system derives mainly from the neural crest both in the head and trunk. Using markers such as fibronectin (FN), neural cell-adhesion molecule (NCAM), the nucleolar marker for quail cells in chimaeric embryos, and NC-1, a monoclonal antibody specific to crest cells and their neural derivatives, we have attempted to reconstruct the processes that lead to the formation of peripheral ganglia. Our observations allow us to propose a model of the formation of ganglia based on morphogenetic movements and on variations of crest cell adhesiveness. In most cases, crest cells migrate in morphologically defined and transient pathways that lead them to their final site of arrest; these pathways are always associated with FN, which appears necessary for crest cell attachment and movement in vitro. The directionality of crest cell migration is probably dictated by the cells' motile properties and population pressure in restricted areas suitable for cell movement. The disappearance of the pathways and of the substrate necessary for migration while the population is rapidly dividing may be responsible for the aggregation of crest cells in the case of the sensory ganglia. To the contrary, the aggregation of crest cells into autonomic ganglia (sympathetic, enteric, and ciliary ganglia) does not seem to obey the same rules, no disappearance of the substratum or of the pathways being obvious; rather, their formation seems correlated with the de novo synthesis of adhesive molecules such as NCAM.

Animals↗

PubMed1989

Glucocorticoid-induced PNMT-immunoreactive sympathetic cells in the superior cervical ganglion of the rat.

Light and electron microscopic immunocytochemical techniques were used to study the effect of glucocorticoids on the development of phenylethanolamine-N-methyltransferase (PNMT)-immunoreactive cells in the superior cervical ganglion (SCG) of early postnatal rats. Rats were injected daily with hydrocortisone acetate on postnatal days 2-6. The first PNMT-immunoreactive cells were detected 6 hours after the first glucocorticoid injection and their number increased after subsequent injections. No PNMT-immunoreactive cells were detected in uninjected controls. PNMT-immunoreactive fibres were seen in the ganglion 6 hours after the first glucocorticoid injection. The PNMT-immunoreactive cells consistently showed processes 2 days after beginning the glucocorticoid treatment, and long processes and fibre networks were seen in ganglia of 7-day-old rats. However, no PNMT-immunoreactive fibres were seen in the iris, which is innervated by the SCG. Ultrastructurally, most of the PNMT-immunoreactive cells had the look of small granule-containing (SGC) cells, including heterochromatin clumps along the nuclear envelope and in the center of the nucleoplasm as well as dense core vesicles. SGC cells, nonimmunoreactive to PNMT antiserum, also were seen. However, some PNMT-immunoreactive cells showed ultrastructural characteristics of nerve cells. In contrast to the SGC cells, these cells were characterized by a voluminous cytoplasm, dispersed nuclear heterochromatin, and a lack of granular vesicles. These results demonstrate that glucocorticoids induce PNMT immunoreactivity both in SGC cells and also in cells with characteristics of principal neurons.

Animals↗

PubMed1989

Small, intensely fluorescent cells and the paraneuron concept.

Sympathetic ganglia contain large principal nerve cells and, in addition, many smaller cells that resemble the endocrine cells of the adrenal medulla in morphology and chromaffinity. The advent of the formaldehyde-induced fluorescence technique proved to be an invaluable tool for studying this unique cell type, and it was this method that accounted for their descriptive name of small, intensely fluorescent cells, now universally abbreviated to SIF cells. Electron microscopy also proved of great importance in detailing the structure of SIF cells and their relationship with neighbouring neurones. Fine structural observations revealed that the cells contained numerous dense-cored granules, and this led to their electron microscopic name of small, granule-containing cells. SIF cells are most abundant, and very well studied, in the rat superior cervical ganglion, where they both receive and give synapses. Early researchers suggested that SIF cells were interneurones appropriately situated between pre- and postganglionic elements and thus capable of influencing ganglion signals. SIF cells also are known to exist in the form of richly vascularized, compact clusters of varying size. Clustered chromaffin cells do not necessarily give rise to processes that would contact the principal neurones. The existence of singly occurring as well as clustered SIF cells has given rise to a proposed designation of type I and type II cells, with I representing the interneuronal-like form and II possibly performing as an endocrine-like component. Despite a wealth of knowledge concerning SIF cells, their exact role(s) in the overall functioning of the autonomic nervous system is still not completely understood.

Animals↗

PubMed2004

AFM/CLSM data visualization and comparison using an open-source toolkit.

There is a vast difference in the traditional presentation of AFM data and confocal data. AFM data are presented as surface contours while confocal data are usually visualized using either surface- or volume-rendering techniques. Finding a common meaningful visualization platform is not an easy task. AFM and CLSM technologies are complementary and are more frequently being used to image common biological systems. In order to provide a presentation method that would assist us in evaluating cellular morphology, we propose a simple visualization strategy that is comparative, intuitive, and operates within an open-source environment of ImageJ, SurfaceJ, and VolumeJ applications. In order to find some common ground for AFM-CLSM image comparison, we have developed a plug-in for ImageJ, which allows us to import proprietary image data sets into this application. We propose to represent both AFM and CLSM image data sets as shaded elevation maps with color-coded height. This simple technique utilizes the open source VolumeJ and SurfaceJ plug-ins. To provide an example of this visualization technique, we evaluated the three-dimensional architecture of living chick dorsal root ganglia and sympathetic ganglia measured independently with AFM and CLSM.

Animals↗

PubMed1994

Detection of varicella-zoster virus-specific DNA sequences in cerebrospinal fluid from patients with acute aseptic meningitis and no cutaneous lesions.

Acute aseptic meningitis (AAM) is considered as an uncommon manifestation of varicella-zoster virus (VZV) recrudescence and is usually regarded as a complication of the cutaneous infection in patients with impaired cellular immunity. Indirect evidence suggests, however, that VZV-associated AAM may also respond to direct spread of the virus to the leptomeninges from the cells supporting the latency. The polymerase chain reaction (PCR) was used to amplify VZV-specific DNA sequences in serial cerebrospinal fluid (CSF) samples from 21 patients with AAM, who presented laboratory evidence of intrathecal production of VZV-specific antibody on follow-up. Eleven of these patients never showed cutaneous zosteriform lesions. VZV-DNA sequences were detected in the CSF from all patients with cutaneous zoster, as well as from six patients (55%) lacking skin lesions. Viral DNA sequences were present in six cases before the rise in specific antibody was seen in CSF, disappearing during follow-up in the seven positive cases. These results support the proposed involvement of VZV in the etiology of AAM seen among normal young adults and strongly suggest that the virus can reach directly and infect the CNS from the latently infected spinal ganglia.

Acute Disease↗