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At least 775 records · Page 43Linked to original sources
PubMed2006

Expression of protein 4.1G in Schwann cells of the peripheral nervous system.

The membrane-associated cytoskeletal proteins, including protein 4.1 family, play important roles in membrane integrity, protein targeting, and signal transduction. Although protein 4.1G (4.1G) is expressed ubiquitously in mammalian tissues, it can have very discrete distributions within cells. The present study investigated the expression and distributions of 4.1G in rodent sciatic nerve. Northern and Western blot analysis detected abundant 4.1G mRNA and protein in rat sciatic nerve extracts. Immunohistochemical staining with a 4.1G-specific antibody and double immunolabeling with E-cadherin, betaIV spectrin, and connexin 32 detected 4.1G in paranodal loops, Schmidt-Lanterman incisures, and periaxonal, mesaxonal, and abaxonal membranes of rodent sciatic nerve. Immunoelectron microscopy confirmed the immunodistribution of 4.1G in Schwann cells. In developing mouse sciatic nerves, 4.1G was diffusely distributed in immature Schwann cells and gradually localized at paranodes, incisures, and periaxonal and mesaxonal membranes during their maturation. These data support the concept that 4.1G plays an important role in the membrane expansion and specialization that occurs during formation and maintenance of myelin internodes in the peripheral nervous system.

Animals↗
PubMed1991

Differential localization and possible functions of aFGF and bFGF in the central and peripheral nervous systems.

We investigated the relative distribution of acidic and basic FGF (aFGF and bFGF) in the nervous system of the rat, using a combination of biological, biochemical, immunochemical, and immunohistochemical methods that can differentiate unambiguously between aFGF and bFGF. We found that different regions of the nervous system contained varying levels of aFGF and bFGF. In the central nervous system, bFGF was present nearly exclusively in astrocytes. Most neurons did not contain detectable amounts of bFGF immunoreactivity, with the notable exception of pyramidal cells in hippocampal area CA2. Interestingly, bFGF immunoreactivity was localized to the nucleus of both CA2 neurons and astrocytes. Astrocytes in vitro were also found to express bFGF, whereas cortical neurons in culture did not contain detectable amounts of bFGF. Transection of the optic nerve led to an approximately twofold increase of bFGF in the distal stump, which is consistent with the observation that bFGF is expressed by astrocytes. Transection of rat and chicken sciatic nerve resulted in a rapid and complete disappearance of aFGF from the distal nerve stump, suggesting that aFGF is present in axons projecting through the sciatic nerve. We observed, in agreement with this notion, that cultured sensory neurons contain reasonably high levels of FGF-like bioactivity. Similar levels of activity were found in developing sciatic nerve, suggesting that neuronal aFGF might be involved in regulating the development of the peripheral nervous system.

Animals↗
PubMed1991

Presence of the terminal complement complex (C5b-9) precedes myelin degradation in immune-mediated demyelination of the rat peripheral nervous system.

In this study, the terminal complement complex C5b-9 (TCC) was localized by immunocytochemistry at different clinical stages of experimental autoimmune neuritis. Deposits of TCC were found on the surface of Schwann cells and their myelin sheaths, and to some extent in the extracellular space at predilective sites of impending demyelination before onset of clinical signs and for a short period thereafter. Additionally, TCC was deposited on the surface of W3/13 positive leukocytes. No TCC immunoreactivity was seen in the distal stump of transected sciatic nerves 1 to 15 days after axotomy. The early and transient deposition of TCC on Schwann cells and myelin sheaths in experimental autoimmune neuritis before overt demyelination suggests that complement activation plays a pathogenic role in the initiation of immune-mediated myelin damage. The lack of TCC immunoreactivity after nerve transection excludes a nonspecific activation process. The signals involved in local TCC formation in demyelinating peripheral nervous system disorders have yet to be explored.

Animals↗
PubMed1996

Birthday of peripheral nervous system surgery: the contribution of Gabriele Ferrara (1543-1627).

SURGERY OF THE peripheral nerves has only recently achieved brilliant results thanks to technological advances in the development of neurosurgical instrumentation. In past centuries, few surgeons made relevant contributions to this topic and improvement was slow and difficult. Avicenna, Guglielmo da Saliceto, and Guido Lanfranchi reported some attempts to suture nerves directly, but Gabriele Ferrara was the first to give a lucid and succinct description of suturing of the stumps of a transected nerve. He described applying gentle traction on the retracted stumps, suturing using a special needle with an eye, after immersion in a decoction of red wine, rosemary, and roses (alcoholic disinfection?), and, finally, insulating the sutured segment with a mixture of oils. We are celebrating the 400th anniversary of the first edition of his fundamental work (1596-1996), and we truly esteem this surgeon, a pioneer of peripheral nerve surgery wo primarily contributed to its progress.

History, 16th Century↗
PubMed1983

Electron microscopic study of intramembranous changes in protein-extracted peripheral nervous system myelin.

Sciatic nerves from young mice were incubated for 2-8 hours in 0.5% Triton X-100 in 0.5 M ammonium acetate, a solution which solubilizes the large and small basic proteins of the myelin sheath. As previously noted (Peterson and Gruener, 1978), myelin sheaths from treated nerves extensively split and unravelled along major dense lines. Small focal areas of compact myelin remained. In freeze-fracture replicas, areas of myelin with lamellar splitting contained few intramembranous particles, while membrane areas with greater than normal densities of particles were associated with the patches of compact myelin membrane. Fixation for as short a time as 15 minutes stabilized the myelin membrane enough to prevent the Triton X-100 effects, even when incubations were extended to 20 hours. Controls, both untreated and 0.5 M ammonium acetate-treated nerves, had predominantly compact myelin sheaths; their leaflets were covered with numerous intramembranous particles. The data suggest that Triton X-100 alters the compact structure of peripheral nervous system myelin. In areas where lamellae are split and separated, there is a loss of intramembranous particles. It appears that the loss of intramembranous particles is related to the removal of the basic proteins which are located in major dense line regions of compact myelin sheaths.

Animals↗