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Query: UMLS:C0012739 (disseminated intravascular coagulation)
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Methods for the study of axons involve whole nerve preparations, teased preparations of axons that are excised from their proximal and distal connections, and tissue culture models. As a complement to these, it would be advantageous to study separated, isolated axons in vivo, still in continuity with the end organ distally and the spinal cord central nervous system neuron proximally. This would allow the study of axon function, normal or pathological, in a close relationship to its biological environment. To achieve this, we have passed the surgically isolated sciatic nerve of a rat through a chamber specially designed for enzymatic dissociation. This was based on principles derived from a prior in vitro method for dissociating nerve into axons. The chamber has controlled temperature and flow and is on an inverted microscope stage, allowing observation of the process. We perfused the chamber with a calcium-free solution followed by a series of enzymes: collagenase, trypsin, and hyaluronidase. This dissociates that part of the extracellular matrix external to the Schwann cells, leaving free, myelinated axons with their Schwann cells. In this acute preparation, the axons continue to conduct action potentials for at least 8 hours. Furthermore, an in vitro study of the axon after the in vivo dissociation demonstrated that axonal transport was maintained in over 90% of the axons, directly visualized on an AVEC-DIC type of microscope system. Properties of axonal transport or active spike propagation can thus be studied individually in an in vivo axon preparation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Model for the study of individual mammalian axons in vivo, with anatomical continuity and function maintained. 241 87

The development of AVEC-DIC microscopy and the application of this method to the study of fast axonal transport in isolated axoplasm extruded from the giant axon of the squid Loligo pealei provides a new paradigm for analyzing the intracellular transport of membranous organelles. The size of the axon, the number of transported particles, and the absence of permeability barriers like the plasma membrane in this preparation permit many experiments that are difficult or impossible to perform using other model systems. The use and features of this preparation are described in detail and a number of properties are evaluated for the first time. The process of extrusion is characterized. Particle movement is evaluated both in the interior of extruded axoplasm and along individual fibrils that extend from the periphery of perfused axoplasm. The role of divalent cations, particularly Ca2+, and the effects of elevated Ca2+ on axoplasmic organization and transport are analyzed. A series of pharmacological agents and polypeptides that alter cytoskeletal organization are used to examine the role of microfilaments and microtubules in fast transport. Finally, the effects of depleting ATP and of adding ATP analogues are discussed. The extruded axoplasm preparation is shown to be an invaluable model system for biochemical and pharmacological analyses of the molecular mechanisms of intracellular transport.
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PMID:Video microscopy of fast axonal transport in extruded axoplasm: a new model for study of molecular mechanisms. 258 Jun 32

We report a case of a mixed sensorimotor, predominantly axonal mononeuritis multiplex that developed after a severe meningococcal septicemia and disseminated intravascular coagulation (DIC) with associated distal limb necrosis. Ischemia resulting from the DIC-induced multiple vascular occlusions is suggested as the leading cause of this neuropathy.
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PMID:Peripheral neuropathy in meningococcal septicemia. 299 4

Native microtubules from extruded axoplasm of squid giant axons were used as a paradigm to characterize the motion of organelles along free microtubules and to study the dynamics of microtubule length changes. The motion of large round organelles was visualized by AVEC-DIC microscopy and analyzed at a temporal resolution of 10 frames per second. The movements were smooth and showed no major changes in velocity or direction. During translocation, the organelles paused very rarely. Superimposed on the rather constant mean velocity was a velocity fluctuation, which indicated that the organelles are subject to considerable thermal motion during translocation. Evidence for a regular low-frequency oscillation was not found. The thermal motion was anisotropic such that axial motion was less restricted than lateral motion. We conclude that the crossbridge connecting the moving organelle to the microtubule has a flexible region that behaves like a hinge, which permits preferential movement in the direction parallel to the microtubule. The dynamic changes in length of native microtubules were studied at a temporal resolution of 1 Hz. About 98% of the native microtubules maintained their length ("stable" microtubules), while 2% showed phases of growing and/or shrinking typical for dynamic instability ("dynamic" microtubules). Gliding and organelle motion were not influenced by dynamic length changes. Transitions between growing and shrinking phases were low-frequency events (1-10 minutes per cycle). However, a new type of microtubule length fluctuation, which occurred at a high frequency (a few seconds per cycle), was detected. The length changes were in the 1-3 micron range. The latter events were very prominent at the (+) ends. It appears that the native axonal microtubules are much more stable than the purified microtubules and the microtubules of cultured cells that have been studied thus far. Potential mechanisms accounting for the three states of microtubule stability are discussed. These studies show that the native microtubules from squid giant axons are a very useful paradigm for studying microtubule-related motility events and microtubule dynamics.
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PMID:Dynamic instability and motile events of native microtubules from squid axoplasm. 318 Feb 48

A previous study that used high-resolution video (VEC-DIC) microscopy to examine axonal growth cones of Aplysia giant neurons growing in culture had demonstrated that growth occurs by the extension of veils of membrane between filopodia and the subsequent morphological transformation of these veils, in place, into the swollen, organelle-filled central region of the growth cone and then into the cylindrical axon. The possible involvement of Ca2+ in this sequence of events was now examined using VEC-DIC microscopy. Reduction of [Ca2+]o from the normal level of 11 to 1.3 mM or below or the addition of 20 mM Co2+, which blocks Ca2+ channels, caused a large decrease in the area of immature veil (flat and with few organelles) in the growth cone within minutes. Ba2+, 20 mM, which flows well through Ca2+ channels, and 5 microM A23187, a Ca2+ ionophore, caused new immature veil to form in the presence of reduced [Ca2+]o. Maturation of veil into central region was not inhibited by reduced [Ca2+]o. In fact, the disappearance of immature veil was often the result partly, or entirely, of continued veil maturation in the absence of formation of new veil. The next step in maturation, conversion of the central region to cylindrical axon, was also probably not inhibited by reduced [Ca2+]o. Ca2+ was microapplied to large growth cones that had lost their veils by exposure to reduced [Ca2+]o. There was a strong tendency for the first, or only, incidence of veil formation to occur near the micropipette, the rest of the perimeter of the growth cone remaining quiescent. It is concluded that intracellular Ca2+ plays a role in veil formation and that the site of the Ca2+-dependent step is close to the site of veil formation. If this step is exocytosis, veil forms where there is net addition of membrane. Whether a change in [Ca2+]i, rather than some other factor, normally directly triggers veil formation remains uncertain, but, if it does, then the site of formation, which will strongly influence the direction of axon growth, is probably determined by focal changes in [Ca2+]i within the growth cone.
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PMID:Local role of Ca2+ in formation of veils in growth cones. 324 45

It was recently shown that, in addition to the well-established microtubule-dependent mechanism, fast transport of organelles in squid giant axons also occurs in the presence of actin filaments [Kuznetsov et al., 1992, Nature 356:722-725]. The objectives of this study were to obtain direct evidence of axoplasmic organelle movement on actin filaments and to demonstrate that these organelles are able to move on skeletal muscle actin filaments. Organelles and actin filaments were visualized by video-enhanced contrast differential interference contrast (AVEC-DIC) microscopy and by video intensified fluorescence microscopy. Actin filaments, prepared by polymerization of monomeric actin purified from rabbit skeletal muscle, were stabilized with rhodamine-phalloidin and adsorbed to cover slips. When axoplasm was extruded on these cover slips in the buffer containing cytochalasin B that prevents the formation of endogenous axonal actin filaments, organelles were observed to move at the fast transport rate. Also, axoplasmic organelles were observed to move on bundles of actin filaments that were of sufficient thickness to be detected directly by AVEC-DIC microscopy. The range of average velocities of movement on the muscle actin filaments was not statistically different from that on axonal filaments. The level of motile activity (number of organelles moving/min/field) on the exogenous filaments was less than on endogenous filaments probably due to the entanglement of filaments on the cover slip surface. We also found that calmodulin (CaM) increased the level of motile activity of organelles on actin filaments. In addition, CaM stimulated the movement of elongated membranous organelles that appeared to be tubular elements of smooth endoplasmic reticulum or extensions of prelysosomes. These studies provide the first direct evidence that organelles from higher animal cells such as neurons move on biochemically defined actin filaments.
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PMID:Movement of axoplasmic organelles on actin filaments from skeletal muscle. 795 51

We reported a case of motor neuropathy with pyramidal sign following prolonged administration of a high dose of muscle relaxant, pancuronium bromide (Myoblock). A 40-year-old male was admitted to our hospital with acute episode of pancreatitis. He was treated with artificial ventilation and Myoblock to manage delirious state, disseminated intravascular coagulation and multiple organ failure. Total dose of 823 mg (24 mg/day) of Myoblock was given intravenously over 36 days. After Myoblock was discontinued, he regained his consciousness and marked muscle weakness with atrophy was noted in both limbs, more severe in distal lower limbs, without any noticeable sensory and sphincter disturbances. Motor nerve conduction studies showed normal nerve conduction velocities with markedly decreased amplitude of compound muscle action potentials. Repetitive nerve stimulation studies revealed decrement response after tetanic stimulation, which disappeared later. Needle EMG showed active denervation potentials and marked polyphasic motor unit potentials. Muscle biopsy revealed neurogenic muscle atrophy with fragmented acetylcholine esterase-positive postsynaptic sites. Sural nerve biopsy showed slight to moderate degree of axonal degeneration of myelinated fibers. Clinical, electrophysiological, and pathological studies above indicated that the main affected sites were neuromuscular junctions including the terminal twigs of motor neurones and postsynaptic membrane, and pyramidal tracts, predominant in lower limbs. About one month after the recognition of the muscle weakness, his muscle strength improved gradually, however, spasticity with hyperreflexia and pathologic reflexes of both legs were found, and became more prominent thereafter. Intensive physiotherapy and rehabilitation led improvement to the point that he became able to ambulate with walking-aids about 7 months later, but marked spasticity persisted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of motor neuropathy with pyramidal sign due to prolonged administration of high dose of pancuronium bromide (Myoblock)]. 840 81

The popularity of infrared DIC videomicroscopy for a variety of anatomical and physiological studies in living brain slices has created a need for holding chambers to allow more than one slice to be examined during a single experiment. As is well known, the yield of experiments requiring living brain slices is severely limited by the conditions under which these slices are maintained prior to being examined. Previous electrophysiological and morphological studies have demonstrated that slices maintained submerged in solution deteriorate dramatically compared to those kept at the gas/fluid interface, even after only 1.5 hours and many recording chambers incorporate the interface principle in their design. However, to our knowledge, as obvious as it may seem, this principle has not been applied to the design of holding chambers, and those which are in current use are of the non-optimal, submerged type. We have designed a simple, but extremely effective holding chamber for incubation of brain slices floating at the gas-fluid interface. The slices held in this chamber have been maintained for at least 12 hours in excellent condition as shown here by rich labeling of their local axonal arbors. In addition, the chamber is designed to hold individual slices (up to 1 cm2 in size) in separate compartments for better preservation of brain slices from valuable species (e.g. animals subjected to experimental treatments, nonhuman primates and human biopsy tissue).
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PMID:An interface holding chamber for anatomical and physiological studies of living brain slices. 926 44

After severance, axons can restore structural barriers that are necessary for recovery of their electrical function. In earthworm myelinated axons, such a barrier to dye entry is mediated by many vesicles and myelin-derived membranous structures. From time-lapse confocal fluorescence and DIC images, we now report that Ca2+ entry and not axonal injury per se initiates the processes that form a dye barrier, as well as the subsequent structural changes in this barrier and associated membranous structures. The time required to restore a dye barrier after transection also depends only on the time of Ca2+ entry.
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PMID:Calcium entry initiates processes that restore a barrier to dye entry in severed earthworm giant axons. 1050 2

Hyperthermia above a critical threshold results in multisystemic changes that include neurological manifestations of heat stroke. It is unknown if the latter represents an intrinsic thermal sensitivity of the CNS or whether injury is secondary to physiological responses of non-CNS origin. To address this issue, the present work examined functional, structural, and biochemical changes in the CNS of dogs subjected to a thermal dosage immediately below that which induces disseminated intravascular coagulation with secondary multiple organ injury. The experimental approach is previously reported, inducing a 42.5 degrees C, 90 min, whole body hyperthermia while preventing other physiological responses to treatment, including respiratory alkalosis and significant reductions in mean arterial pressure. Functional analyses included neurologic examinations and brainstem auditory evoked potential recordings in the post-treatment interval in both hyperthermic and euthermic control populations. Biochemical and structural analyses examined the expression of 70-kDa heat shock proteins, cytokines, markers of astroglial and microglial injury/activation, evidence of vascular endothelial damage, and evidence of neuronal and axonal injury in brain between 0.5 h and 8 days from the end of the treatment. The only significant change associated with treatment was induction of the major inducible 70-kDa heat shock protein, this being most prominent in the cerebellum with maximal expression at 6 h and a return to baseline by 8 days.Collectively, from these results we suggest that the canine brain is intrinsically resistant to sublethal hyperthermia such that when CNS lesions occur, they do so in the presence of other physiological derangements.
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PMID:Intrinsic thermal resistance of the canine brain. 1212 84


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