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At least 37 records · Page 2Linked to original sources
PubMed2004

The presence of erythropoietin receptors in the human peripheral nervous system.

Erythropoietin (EPO) is a well-known hematopoietic factor and a major determinant of tissue oxygenation. EPO receptors have been identified on a wide variety of non-erythroid cell types including human central nervous system and peripheral nervous system of animal models. The presence or function of EPO receptors in human peripheral nervous system is unknown. By examining nerve segments from radicular and autonomic nerves using immunohistochemical methods, we demonstrated the presence of EPO receptors on myelin sheath of radicular nerves in the human peripheral nervous system.

Humans↗
PubMed2001

The impact of formal instruction in clinical examination skills on medical student performance -- the example of peripheral nervous system examination.

BACKGROUND: Peripheral nervous system examination is an essential part of the full medical clerking of a patient. We have investigated the effectiveness of formal instruction in peripheral nervous system examination compared to the traditional bedside ward teaching that our students usually receive. METHOD: We instructed an unselected group of 22 medical students in peripheral nervous system examination in a clinical skills centre and evaluated them with a 12 item marking schedule before and after instruction. The performance of this group was then compared to the rest of their year (220 students) in an end of year OSCE, which included a neurology station assessing sensory examination of the lower limbs. RESULTS: Students formally instructed in neurology significantly improved their scores after instruction and scored 15% higher marks (90% vs. 75%) than the rest of their year in the end of year neurology OSCE station 2 months later (P < 0.01, Mann Whitney U-test). They did not perform significantly better in the OSCE overall. CONCLUSIONS: Formal instruction in neurological examination resulted in a significant increase in the end of year neurology OSCE station score compared to traditional heterogeneous teaching methods.

Clinical Competence↗
PubMed1979

Immunocytochemical localization of rat peripheral nervous system myelin proteins: P2 protein is not a component of all peripheral nervous system myelin sheaths.

Specific antibodies have been developed against P1, P2, and P0 myelin proteins and were used to study the localization of these proteins in the rat peripheral nervous system. Both peripheral and central nervous system myelin sheaths contain P1 protein. P0 and P2 proteins are found exclusively in peripheral nervous system myelin sheaths. Antisera to P1 and P0 proteins stain all peripheral nervous system myelin sheaths uniformly. P2 protein is not a component of all peripheral nervous system myelin sheaths. In sheaths that do contain P2 protein, it is concentrated in the area of the Schmidt-Lanterman incisures.

Animals↗
PubMed2002

Postnatal histogenesis in the peripheral nervous system.

The issue of postnatal neurogenesis has gained great importance over the last few years and the recent amazing scientific advancements, changing our viewpoint on the long-lasting "no new neurons" dogma, have opened promising new perspectives on the treatment of the damaged nervous system. While most of the researchers have focused on the central nervous system, the peripheral nervous system has received little attention so far with respect to postnatal histogenesis. To attract scientific attention on this issue, the present article was written with the aim of reviewing the body of literature on postnatal histogenesis in the various districts of the peripheral nervous system, from the historical roots to the most recent reports.

Afferent Pathways↗
PubMed2006

Formation of the ascidian epidermal sensory neurons: insights into the origin of the chordate peripheral nervous system.

The vertebrate peripheral nervous system (PNS) originates from neural crest and placodes. While its developmental origin is the object of intense studies, little is known concerning its evolutionary history. To address this question, we analyzed the formation of the larval tail PNS in the ascidian Ciona intestinalis. The tail PNS of Ciona is made of sensory neurons located within the epidermis midlines and extending processes in the overlying tunic median fin. We show that each midline corresponds to a single longitudinal row of epidermal cells and neurons sharing common progenitors. This simple organization is observed throughout the tail epidermis, which is made of only eight single-cell rows, each expressing a specific genetic program. We next demonstrate that the epidermal neurons are specified in two consecutive steps. During cleavage and gastrula stages, the dorsal and ventral midlines are independently induced by FGF9/16/20 and the BMP ligand ADMP, respectively. Subsequently, Delta/Notch-mediated lateral inhibition controls the number of neurons formed within these neurogenic regions. These results provide a comprehensive overview of PNS formation in ascidian and uncover surprising similarities between the fate maps and embryological mechanisms underlying formation of ascidian neurogenic epidermis midlines and the vertebrate median fin.

Animals↗
PubMed1998

Cholinergic neurons and terminal fields revealed by immunohistochemistry for the vesicular acetylcholine transporter. II. The peripheral nervous system.

The peripheral sympathetic and parasympathetic cholinergic innervation was investigated with antibodies directed against the C-terminus of the rat vesicular acetylcholine transporter. Immunohistochemistry for the vesicular acetylcholine transporter resulted in considerably more detailed visualization of cholinergic terminal fields in the peripheral nervous system than reported previously and was well suited to also identify cholinergic perikarya. Vesicular acetylcholine transporter immunoreactivity completely delineated the preganglionic sympathetic terminals in pre- and paravertebral sympathetic ganglia, and in the adrenal medulla as well as postganglionic cholinergic neurons in the paravertebral chain. Cholinergic terminals of sudomotor and vasomotor nerves of skeletal muscle were optimally visualized. Mixed peripheral ganglia, including periprostatic and uterovaginal ganglia, exhibited extensive preganglionic cholinergic innervation of both noradrenergic and cholinergic postganglionic principal neurons which were intermingled in these ganglia. Varicose vesicular acetylcholine transporter-positive fibres and terminals, representing the cranial parasympathetic innervation of the cerebral vasculature, of salivary and lacrimal glands, of the eye, of the respiratory tract and of the upper digestive tract innervated various target structures including seromucous gland epithelium and myoepithelium, respiratory epithelium, and smooth muscle of the tracheobronchial tree. The only macrovascular elements receiving vesicular acetylcholine transporter-positive innervation were the cerebral arteries. The microvasculature throughout the viscera, with the exception of lymphoid tissues, the liver and kidney, received vesicular acetylcholine transporter-positive innervation while the microvasculature of limb and trunk skeletal muscle appeared to be the only relevant somatic target of vesicular acetylcholine transporter innervation. Vesicular acetylcholine transporter immunoreactivity was particularly useful for identification of parasympathetic intrinsic ganglia, and their terminal fields, in heart, uterus, and other peripheral organs receiving parasympathetic innervation. Extensive vesicular acetylcholine transporter-positive terminal fields were apparent in both atrial and ventricular tissues of the heart targeting cardiomyocytes as well as cardiac microvessels. Pericardiac brown adipose tissue was also supplied by vesicular acetylcholine transporter-positive varicose fibres. The enteric ganglia of the myenteric and submucous plexus, their synaptic junctions with circular and longitudinal smooth muscle, and terminal fields of the lamina propria of the stomach and intestine and of the local microvasculature were intensely vesicular acetylcholine transporter positive. Vesicular acetylcholine transporter-positive innervation was delivered to the exocrine and endocrine pancreas originating from vesicular acetylcholine transporter-positive intrapancreatic ganglia. Vesicular acetylcholine transporter immunoreactivity in urogenital organs revealed the patterns of terminal cholinergic fields arising from the sacral parasympathetic innervation of these structures. Components of the cholinergic nervous system in the periphery whose existence has been controversial have been confirmed, and the existence of new components of the cholinergic nervous system has been documented, with vesicular acetylcholine transporter immunohistochemistry. Visualization of vesicular acetylcholine transporter will allow documentation of changes in synaptic patency during development, in disease, and during changes in neurotransmission accompanying injury and dystrophy, in the peripheral nervous system.

Acetylcholine↗
PubMed1986

Cell line segregation during peripheral nervous system ontogeny.

The peripheral nervous system of vertebrates arises from the neural crest and the ectodermal placodes. Construction of quail-chick chimaeras has provided significant information on the migration and fate of the neural crest and placodal cells. Transplantation of neural crest tissue to various sites in these chimaeras has demonstrated that the differentiation of neural crest cells is controlled by environmental influences during their migration and, particularly, during gangliogenesis. Experiments with in vitro and monoclonal antibody techniques have shown that these environmental cues act on a heterogeneous population of neural crest cells whose developmental potencies are partly restricted to definite differentiation pathways.

Animals↗
PubMed1998

Nerve injury and inflammatory cytokines modulate gap junctions in the peripheral nervous system.

In the peripheral nervous system (PNS), myelinating Schwann cells express the gap junction protein connexin32 (Cx32) and lower levels of connexin43 (Cx43). Although the function of Cx43 in Schwann cells is not yet known, in adult mammals Cx32 is thought to form reflexive contacts within individual myelinating glial cells and provide direct pathways for intracellular ionic and metabolic exchange from the cell body to the innermost periaxonal cytoplasmic regions. In response to nerve injury, Schwann cells in the degenerating region down-regulate expression of Cx32 and there is increased expression of connexin46 (Cx46) mRNA and protein. The cascade of Schwann cell responses seen after the injury-induced decrease in Cx32, and the observation that dividing Schwann cells express Cx46, and possibly other connexins, and are coupled through gap junction channels, raise the intriguing possibility that there are coordinated changes in Schwann cell proliferation and connexin expression. Moreover, intercellular junctional coupling among cells in general may be important during injury responses. Consistent with this hypothesis, dividing Schwann cells are preferentially coupled through junctional channels as compared to non-dividing cells, which are generally uncoupled. Moreover, the strength of junctional coupling among cultured Schwann cells is modulated by a number of cytokines to which Schwann cells are exposed to in vivo after nerve injury, and Cx46 mRNA and protein levels correlate with the degree of coupling. Other injury-induced cellular changes in connexin expression that may be functionally important during injury responses include a transient increase in Cx43 in endoneurial fibroblasts. This paper reviews what is known about connexin expression and function in the adult mammalian PNS, and focuses on some of the changes that occur following nerve injury. Moreover, evidence that inflammatory cytokines released after injury modulate connexin expression and junctional coupling strength is presented.

Animals↗
PubMed1994

Amyloid and peripheral nervous system disease.

The peripheral nervous system can be involved in the following amyloid deposition diseases. (1) Amyloid deposition composed of beta 2-microglobulin in patients on long term hemodialysis causing a carpal tunnel syndrome; (2) deposition of light chain immunoglobulin derived amyloid leading to polyneuropathy, carpal tunnel syndrome and autonomic nervous system involvement in patients with primary amyloidosis, or amyloidosis secondary to or associated with multiple myeloma, Waldenström's macroglobulinemia, non-Hodgkin's lymphoma, and solid neoplasms like hypernephroma; and (3) several types of heredofamilial amyloid polyneuropathies, which are mainly caused by a point-mutation in the transthyretin gene on chromosome 18. The clinical and biochemical features of these three groups will be discussed, with special attention for recently developed therapy. In clinical practice, amyloid polyneuropathy should be considered in case of familial occurrence of a polyneuropathy and when a patient presents with a polyneuropathy and a monoclonal gammopathy.

Amyloid Neuropathies↗
PubMedDate not supplied

[Neurophysiology of the development and maturation of the peripheral nervous system].

INTRODUCTION: Peripheral nerve maturation accounts during fetal life and infancy and varies with age. Nerve conduction studies are an objective procedure to investigate the development of the motor and sensory nerves. METHOD: We present a review of peripheral nervous system maturation studies in infancy, including our normal control group of infants from 1 week to 6 years of age. Motor and sensory nerve conduction velocity at birth is about one-half that of the normal adults, increases very quickly during the first year of life and reaches adult values between 3 and 5 years of age. All these electrophysiologic changes parallel the increase in numbers of large myelinated fibres throughout infancy. CONCLUSIONS: Nerve conduction studies are an accurate and non-invasive method of evaluating the peripheral nerve maturation in paediatric population when motor and sensory functions are particularly difficult to assess clinically.

Electrophysiology↗
PubMed1989

[Electromagnetic stimulation of the nervous system. II. Normal values in the peripheral nervous system and comparison with electrical stimulation methods].

In 15 healthy subjects we stimulated the peripheral nervous system by a brief intense magnetic field and recorded evoked muscle potentials from peripheral muscles. Latencies were compared with those obtained by conventional electrical stimulation techniques. Amplitudes of muscle responses after magnetic stimulation were often smaller than those obtained after electrical stimulation; however, latencies were comparable at all stimulation sites.

Adult↗
PubMed1996

Expression pattern of collagen IX and potential role in the segmentation of the peripheral nervous system.

Segmentation of the peripheral nervous system of vertebrates requires guidance cues located in the adjacent somitic mesoderm. Recent experiments suggest that inhibitory molecules in the posterior somite may influence segmentation by restricting the outgrowth of axons and the migration of neural crest cells to the anterior somite. A potential candidate for an inhibitory molecule is collagen IX, a chondroitin sulfate proteoglycan made by sclerotome cells of the somite and by the notochord. Immunohistochemical localization of collagen IX demonstrated that its expression in the posterior sclerotome of the somite correlates with axon outgrowth and neural crest cell migration through the anterior sclerotome. In vitro, sensory neurites on fibronectin, and motor neurites on basal lamina extract, avoid regions which contain substrate-bound collagen IX. This effect can be abolished by chondroitinase treatment, suggesting that the glycosaminoglycan component of the molecule is responsible for this activity. Further, collagen IX elicits a similar avoidance behavior by neural crest cells in vitro. These data suggest that collagen IX contributes to the segmentation of the peripheral nervous system in vivo.

Animals↗
PubMed1993

Temporal central and peripheral nervous system changes induced by a paralytogenic mutant of Moloney murine leukemia virus TB.

BACKGROUND: The temporal localization of cellular targets for viral replication and the morphopathogenesis of neurodegeneration in the central nervous system (CNS) and peripheral nervous system induced by ts1, a neuropathogenic and lymphocytopathic mutant of Moloney murine leukemia virus-TB, were studied in the highly susceptible FVB/N mouse strain in order to better understand the mechanisms of this neurodegenerative disease. EXPERIMENTAL DESIGN: Newborn FVB/N mice were inoculated intraperitoneally with 0.1 ml of viral suspension containing 10(6) to 10(7) infectious units/ml. The mice were observed daily for clinical signs of disease and killed at specific time points. Their nervous system tissues were collected and processed for light and electron microscopy and for immunohistochemical viral-antigen detection. RESULTS: ts1-Infected FVB/N mice developed a rapidly progressive wasting disease that culminated in hindleg paralysis or paraplegia 30 to 35 days postinoculation (pi). CONCLUSIONS: Clear evidence of CNS lesions involving the cerebellar ventricular system, the grey and white matter of the brain stem and the spinal cord were seen as early as 5 to 10 days pi. These lesions, which began as mild perivascular and paraventricular neuropil spongiform changes and cytoplasmic vacuolation of neuronal and glial cell processes, progressed in severity with time and culminated in almost complete destruction of the white and gray matter in the brain stem and the cervical and lumbar spinal cord. Viruses were detected as early as 5 to 10 days pi in the fourth ventricle choroid plexus and ventricular lumen and budding from endothelial cells within the brain stem and cerebellum. Endothelial, ependymal, microglial, astroglial, and oligodendroglial cells were positive for gp70env. Astroglial and microglial cell proliferation with microglial syncytia formation was detected only within the areas showing spongiform degeneration. Viral replication was consistently high in the capillary endothelial cells of those areas showing spongiform degeneration, whereas in the glial cells, relatively few budding viruses were present. Neurodegeneration was accompanied by demyelinization within the CNS and peripheral nervous system and by hindleg muscle degeneration and necrosis. Multiple cellular targets for ts1 viral infection and replication were detected within the nervous system. The presence of budding virus and the immunodetection of viral antigen in the choroid plexus and ependymal cells of the fourth ventricle and the central canal of the spinal cord demonstrated that cerebrospinal fluid as well as blood can disseminate virus within the CNS. Pathologic and functional changes within the blood-brain barrier and glial system probably account for the neuronal necrosis and spongiform changes that result in paralysis induced by ts1 infection.

Animals↗