Axonal Mitochondria Research Articles

Protection of the axonal cytoskeleton in anoxic optic nerve by decreased extracellular calcium

Since CNS white matter tracts contain axons, oligodendrocytes and astrocytes but not synapses, it is likely that anoxic injury of white matter is mediated by cellular mechanisms that do not involve synapses. In order to test the hypothesis, that anoxic injury of white matter is mediated by an influx of Ca 2+ into the intracellular compartment of axons, we compared the ultrastructure of axons in rat optic nerve exposed to 60 min of anoxia in artificial cerebrospinal fluid (aCSF) containing normal (2 mM) Ca 2+, and in aCSF containing zero-Ca 2+ together with 5 mM EGTA. Optic nerves fixed at the end of 60 min of anoxia in 2 mM Ca 2+ exhibit extensive ultrastructural alterations including disruption of microtubules and neurofilaments within the axonal cytoskeleton, development of membranous profiles and empty spaces between the axon and the ensheathing myelin, and swelling of mitochondria with loss of cristae. Bathing the nerves in zero-Ca 2+ aCSF during anoxia protected the axons from cytoskeletal changes; after 60 min of anoxia, optic nerve axons retained normal-appearing microtubules and neurofilaments. Membranous profiles were rare, and empty spaces between axons and myelin did not develop in anoxic optic nerves bathed in zero-Ca 2+ aCSF. Disorganization of cristae in axonal mitochondria was observed in anoxic optic nerves even when Ca 2+ was omitted from the medium. Because Ca 2+-mediated injury is known to disrupt the axonal cytoskeleton, these results support the hypothesis that anoxia triggers an abnormal influx of Ca 2+ into myelinated axons in CNS white matter.

Microtubules have special physical associations with smooth endoplasmic reticula and mitochondria in axons

Ultrastructural morphometry was used to document the non-random spatial distributions of organelles within the compact myelinated region of avian oculomotor axons. These regions contain large numbers of loosely packed neurofilaments (NFs) (241/μm 2) and only a relatively small number of microtubules (MTs) (4/μm 2), mitochondria (0.6/μm 2), and smooth endoplasmic reticulum (SER) (1.6/μm 2). Random co-occurrences between the relatively sparsely distributed MTs, mitochondria, and SER are probably infrequent in these axons. The actual co-occurrences of MTs, mitochondria, and SER with MTs were counted and compared to the co-occurrences expected in a random Poisson distribution. At long distances (200 nm), the co-occurrences were random. At shorter distances (40 nm and less), MTs were still randomly associated with other MTs. However, at these shorter distances, the spatial associations of mitochondria with MTs and of SER with MTs were not random; such preferential stable associations may be produced by specific MT associated cross-bridging proteins. In axons, MTs tend to be clustered together, giving the appearance of MT bundles. We propose that the MT-MT bundling is an indirect result of MT concentration along the continuous intra-axonal SER network, to which the MTs are apparently tied directly by dynamic molecular cross-bridges.

Elevation of intracellular calcium content in area CA1 of hippocampus is not directly correlated with the development of long-term potentiation

Electron microscopic localization of calcium-containing mitochondria in stratum radiatum of CA1 of hippocampal slices was performed after (I) low-frequency stimulation, (2) high-frequency stimulation, and (3) blocking N- methyl- d-aspartate (NMDA) receptors during high-frequency stimulation. Dendritic mitochondria containing Ca deposits were found in a narrow band of stratum radiatum 280–350 μm distant from stratum pyramidale. Axonal mitochondria containing Ca deposits were evently distributed in stratum radiatum. The total number of calcium containing-mitochondria was highest in long-term potentiated slices, and less in slices treated with APV; the lowest values were obtained with low-frequency stimulation.

Distribution of elements in rat peripheral axons and nerve cell bodies determined by x-ray microprobe analysis.

X-ray microprobe analysis was used to determine concentrations (millimoles of element per kilogram dry weight) of Na, P, Cl, K, and Ca in cellular compartments of frozen, unfixed sections of rat sciatic and tibial nerves and dorsal root ganglion (DRG). Five compartments were examined in peripheral nerve (axoplasm, mitochondria, myelin, extraaxonal space, and Schwann cell cytoplasm), and four were analyzed in DRG nerve cell bodies (cytoplasm, mitochondria, nucleus, and nucleolus). Each morphological compartment exhibited characteristic concentrations of elements. The extraaxonal space contained high concentrations of Na, Cl, and Ca, whereas intraaxonal compartments exhibited lower concentrations of these elements but relatively high K contents. Nerve axoplasm and axonal mitochondria had similar elemental profiles, and both compartments displayed proximodistal gradients of decreasing levels of K, Cl, and, to some extent, Na. Myelin had a selectively high P concentration with low levels of other elements. The elemental concentrations of Schwann cell cytoplasm and DRG were similar, but both were different from that of axoplasm, in that K and Cl were markedly lower whereas P was higher. DRG cell nuclei contained substantially higher K levels than cytoplasm. The subcellular distribution of elements was clearly shown by color-coded images generated by computer-directed digital x-ray imaging. The results of this study demonstrate characteristic elemental distributions for each anatomical compartment, which doubtless reflect nerve cell structure and function.

Lectin binding sites in axon-myelin-Schwann cell complex.

The distribution of α-D-N-acetylgalactosamine residues on the membranes of axon-myelin-Schwann cell complexes of rabbit and rat sciatic nerves was visualized by means of a one-step method with HRP labelled soybean agglutinin. The compact myelin was found to be very rich in lectin binding sites whereas mesaxons and split myelin lamellae, as well as the Schwann cell plasma membrane were almost negative. The labelling of the axolemma was most pronounced in the nodal and paranodal regions. The smooth endoplasmic reticulum and mitochondria in axons and glial cells were also labelled.

Axoplasmic incorporation of amino acids in myelinated fibers of the cat

Incorporation of amino acids into the axoplasm of nerve fibers of the cat was studied with radioautography. The dorsal funiculus of the spinal cord, or the sciatic nerve, was exposed to tritiated leucine, lysine, and proline; the tissue was processed 1 h later or the following day. In all instances, a radioautographic response of widely varying intensity was observed over the axoplasm; this response could not be adscribed to emissions originating from axonal mitochondria or myelin. The axoplasmic response ranged to as much as 56% compared with that over nearby glial cytoplasm and was often conspicuously greater than that over the surrounding myelin. We interpret our findings as axoplasmic synthesis of proteins. This finding has implications in the maintenance of the neuron.

Sural nerve biopsies from workers with a history of chronic exposure to organic solvents and from normal control cases. Morphometric and ultrastructural studies.

An ultrastructural and morphometric study was performed on sural nerve biopsies of four industrial spray painters (35-59 years) and 11 controls (6-64 years). No difference could be shown in spray painters and age-matched controls as to the number of myelinated nerve fibres per area, their size distribution, variation of internodal length along single nerve fibres or the ratio between the number of myelin lamellae and the axon circumference. There was marked scattering of the two latter parameters in older exposed and and control individuals. The distribution of NADH2-tetrazolium reductase activity was similar in exposed and control cases. The general ultrastructural appearance of nodal-paranodal regions in controls conformed with that noted in experimental animals. The overall ultrastructural organization and age-related changes of nerves of exposed cases were similar to those of control cases except for a presence of paranodal axonal mitochondria which contained glycogen-like particles in exposed cases. In one exposed case abundant dispersed or clustered glycogen-like particles were seen in the paranodal axoplasm. These findings are suggested to be an effect of chronic exposure to organic solvent vapours. Ageing seems, however, to have a much greater impact on the morphology of the sural nerve fibre than occupational exposure to organic solvent.

Slow axonal transport of the molecular forms of butyrylcholinesterase in a peripheral nerve

Butyrylcholinesterase was found in chick sciatic nerve in four main molecular forms—G 1, G 2, G 4 and A 12—distinguishable by their sedimentation coefficients in sucrose gradients (4.2S, 6.4S, 11.3S and 19S, respectively). Axonal transport of butyrylcholinesterase was studied by measuring the accumulation of its molecular forms on each side of a transected sciatic nerve. Twenty-four hours after transection, butyrylcholinesterase activity had risen by about 32% at the extremity of the proximal stump, and by 20% at the extremity of the distal stump. Proximal accumulation was due to a two-fold rise in G 4 activity and to a six-fold rise in A 12 activity, whereas distal accumulation was exclusively due to a 50% increase in G 4 activity, accompanied by the complete loss of A 12. The activities of G 1 and G 2 remained stable in both directions. Under our experimental conditions, the accumulation of butyrylcholinesterase activity cannot be attributable to local protein synthesis, cross-contamination with accumulated acetylcholinesterase or the presence of plasma butyrylcholinesterase. Hence we conclude that all A 12 butyrylcholinesterase molecules were carried in the anterograde direction, moving at11.6 ± 4.2 mm/day, and that probably some of the G 4 molecules were slowly transported in both directions. These findings suggest that some of the butyrylcholinesterase is located in the axonal mitochondria and/or axolemma.

Relationships between mitochondrial outer membranes and agranular reticulum in nervous tissue: ultrastructural observations and a new interpretation.

This study is concerned with extensions of the outer membranes of mitochondria in cells of nervous tissue, and with possible relationships between the extensions and the agranular reticulum. A variety of preparative techniques was applied to a large number of different central nervous tissues (CNS) and peripheral nervous tissues (PNS), using conventional thin sections, thicker sections (100 nm or more) and 3-dimensional reconstructions of serial thin sections. Extensions were commonly observed, particularly from the ends of longitudinally oriented mitochondria in axons and dendrites. Often these had the appearance of, and could be traced into apparent continuity with, adjacent elements of the agranular membrane. In addition to these apical tubular extensions, we also observed and reconstructed short lateral tubular or sac-like extensions and vesicular protrusions of the outer mitochondrial membrane. We discuss and discount the possibility that the extensions are artefacts, consider the structural and biochemical similarities between the outer mitochondrial membrane and agranular reticulum and propose that the outer mitochondrial is part of the agranular reticulum (or a specialized portion of the agranular reticulum). We suggest that the translocation of mitochondria in nerve cells, and probably in other cells as well, involves movement of the inner mitochondrial membrane and the enclosed matrix (mitoplast) within channels of agranular reticulum in continuity, or in transient continuity, with the outer mitochondrial membrane.

Cytochemical localization of phosphodiesterase: Axonal mitochondria and microtubules

Phosphodiesterase activity has been found associated with axonal microtubules in the sensory nerves of the blowfly, Phormia regina, taste receptors. A specific reaction product for this enzyme was also observed within axonal mitochondria, but not within the mitochondria of the surrounding glial cells. A possible explanation for these data is discussed.

Degeneration of sensory and motor axons in transplanted segments of a crustacean peripheral nerve.

Segments of sensory and motor axons 0.3-0.5 mm in length were taken from crayfish peripheral limb nerves and transplanted into the abdominal cavity of the same animal. Transplanted sensory axons showed relatively few ultra-structural changes after one week, many had undergone complete lysis within two weeks, and almost all degenerated within three weeks. Transplanted motor axons appeared normal after one week, except for some hypertrophy of their surrounding glial sheaths. After two weeks, glial sheaths were grossly hypertrophied around motor axons; axonal mitochondria had increased in number and many had migrated from the periphery to the centre of the axon. The axonal membranes of all motor axons were still intact after three weeks, although most were no longer continuous after four weeks. By five weeks, all axonal material had completely disintegrated. These data suggest that axonal synthetic processes in crayfish sensory (and presumably motor) axons can maintain the axons relatively intact for 7-14 days and that transfer of substances form hypertrophied glial cells to motor axons may account for the longer survival times of transplanted motor axons.

Axon retraction following guanethidine treatment: studies of sympathetic neurons in tissue culture.

The ultrastructural appearance of cultured sympathetic nerve cell bodies and axons during guanethidine-induced retraction of axons has been described and correlated with phase contrast microscopic observations. In retracting axons, morphological alterations (notably aggregation of smooth membranous tubules and formation of myeloid whorls) occurred in swellings, which appeared to correspond to varicosities. Intervaricose regions of axons showed no significant changes; the organization of neurotubules and neurofilaments appeared to be normal. Axonal mitochondria were apparently undamaged, except in regions close to their cell bodies. In the cell bodies of sympathetic neurons, the early phase of degeneration was characterized by specific mitochondrial damage accompanied by some loss of free ribosomes and rough endoplasmic reticulum. This was followed by a second phase in the cell bodies in which there was substantial accumulation of myeloid whorls and organelles, including neurotubules and neurofilaments. It is suggested that this accumulation has resulted from transfer of some of the contents of the axons to the cell body as a consequence of axon retraction. The morphological features of these two proposed phases bear striking resemblance to ultrastructural alterations characteristic of the first two phases of degeneration of adrenergic neuronsin vivo after guanethidine treatment. Various possibilities are discussed concerning the mechanism underlying guanethidine-induced axon retraction.

Effects of thallium salts on neuronal mitochondria in organotypic cord-ganglia-muscle combination cultures.

A functionally coupled organotypic complex of cultured dorsal root ganglia, spinal cord peripheral nerve, and muscle has been employed in an experimental approach to the investigation of the neurotoxic effects of thallium. Selected cultures, grown for up to 12 wk in vitro, were exposed to thallous salts for periods ranging up to 4 days. Cytopathic effects were first detected after 2 h of exposure with the appearance of considerably enlarged mitochondria in axons of peripheral nerve fibers. With time, the matrix space of these mitochondria became progressively swollen, transforming the organelle into an axonal vacuole bounded by the original outer mitochondrial membrane. Coalescence of adjacent axonal vacuoles produced massive internal axon compartments, the membranes of which were shown by electron microprobe mass spectrometry to have an affinity for thallium. Other axoplasmic components were displaced within a distended but intact axolemma. The resultant fiber swelling caused myelin retraction from nodes of Ranvier but no degeneration. Impulses could still propagate along the nerve fibers throughout the time course of the experiment. Comparable, but less severe changes were seen in dorsal root ganglion neurons and in central nerve fibers. Other cell types showed no mitochondrial change. It is uncertain how these findings relate to the neurotoxic effects of thallium in vivo, but a sensitivity of the nerve cell and especially its axon to thallous salts is indicated.

Der Einfluss von Colchizin und Ethidium-Bromid auf den Gehalt radioaktiv markierter Uridin-Verbindungen in optischen Axonen von Teleosteern

After application of colchicine to one eye, and subsequent injections of3H-histidine or3H-uridine into both eyes, a blockage of the transport in the optic system of teleosts could be demonstrated only for the fast protein-components. However, colchicine is able to depress the effectivity of ethidium-bromide, a blocker of mitochondrial RNA-synthesis. This finding is discussed in connection with the possibility that axonal mitochondria are associated with the neurotubules.

Electron microscopic study on aspartate carbamoyltransferase in mitochondria of axons and dendrites in the temporal cerebrum of the rat.

Aspartate carbamoyltransferase (carbamoyl phosphate:L aspartate Carbamoyltransferase, EC 2.1.3.2), the enzyme catalyzing the first step in pyrimidine biosynthesis, has been localized in nerve cell processes of glutaraldehyde-fixed rat temporal cerebrum. Carbamoyl phosphate is made to react with aspartate. On subsequent hydrolysis orthophosphate is released and precipitated with lead ions. Aspartate Carbamoyltransferase is found in mitochondria of axons and dendrites between the outer and inner membranes and in the cristae. When aspartic acid is either omitted from the reaction mixture or substituted by ornithine, no lead phosphate deposits are found in mitochondria.

The fine structure of puromycin-induced changes in mouse entorhinal cortex.

Bitemporal intracerebral injections of puromycin in mice suppress indefinitely expression of memory of avoidance-discrimination learning. Ultrastructural studies of the entorhinal cortex of puromycin-treated mice revealed the following: (a) Abnormalities were not observed in presynaptic terminals and synaptic clefts; many postsynaptic dendrites or somas contained swollen mitochondria. (b) Dispersion of polyribosomes into single units or condensation of ribosomes into irregular aggregates with loss of "distinctiveness" was noted in a few neurons 7-27 hr after puromycin treatment. (c) Cytoplasmic aggregates of granular or amorphous material were frequently noted within otherwise normal neuronal perikarya. (d) Mitochondria in many neuronal perikarya and dendrites were swollen. Mitochondria in axons, presynaptic terminals, and glial cells were unaltered. The relationships between these lesions and the effect of puromycin on protein synthesis and memory are examined. It is suggested that the disaggregation of polysomes is too limited to explain the effect of puromycin on memory. Special emphasis is given to the swelling of mitochondria. The possible mechanisms and the significance of this lesion are discussed.

Electron microscopic studies on the effect of anisotonic solutions on the structure of unmyelinated splenic nerve fibers of the cat

In the first series of experiments unmyelinated splenic nerve fibers were fixed in highly hypotonic and hypertonic osmium tetroxide solutions. Fixation in a solution made up of distilled water produces only small changes in the fibers, observable as a slight swelling of the axons and of some of the axon mitochondria. Fixation in a solution made up of Tyrode's fluid containing 10 times its original content of sodium chloride brings about a shrinkage of axons and Schwann cells, along with compact axon mitochondria. In a second series of experiments nerve fibers were soaked in media with different ionic strengths before fixation with osmium tetroxide. Exposure to distilled water results in a swelling of the Schwann cells and a shrinkage of the axons. In Tyrode's fluid with reduced sodium chloride content, the Schwann cells swell and the axons either swell or shrink. In Tyrode's fluid with increased sodium chloride content, the Schwann cells, as well as many axons, shrink. The axon mitochondria swell in highly hypotonic media and appear compact after exposure to hypertonic media. The pattern of the filamentous material of the axoplasm is sensitive to treatment with anisotonic media. In contrast to the results reported by Robertson (15), the relationship and spacing of the axon and Schwann cell plasma membranes remains unchanged in all these experiments, with the exception of a possible widening of the cell boundaries in highly hypertonic media.

ULTRASTRUCTURAL CHANGES IN THE SENSORY NERVE FIBRES IN THE SKIN OF THE FROG (RANA TEMPORARIA) AFTER CIRCUMSCRIPT IRRADIATION WITH Po210α‐PARTICLES (5,3 MeV)

The effect of ionizing radiation on the morphology and electrical activity of nerve fibers was studied with isolated fibers irradiated with 750- 34,500 rep from a cylindrical Po/sup 210/ source. Even the lowest dose of radiation caused intense swelling and vacuolation of Schwarn cell cytoplasm, and at higher doses (10,000 rep) cytoplasmic structures are completely obliterated. In the axoplasm, neurofilaments retained their integrity up to 5000-rep doses and were destroyed at 20,000-rep doses. The most sensitive elements of axoplasm were the ergastoplasmic channels which were fragmented into vesicles at the lowest dose (750 rep). These elements could no longer be identified at higher doses. Axonal mitochondria were swollen and partially fragmented also by low doses. Myelin sheaths were destroyed by moderate doses (5000-20,000 rep), and after irradiation appeared as coiled or spiraled structures. Ac tion potentials of the nerve fibers were not affected by doses up to 2000 rep despite the morphologic changes which occurred, but after 5000 rep the potentials were almost completely depressed within 30 min after irradiation. It is suggested that the impairment of electrical activity of irradiated fibers is most closely related to the injury of ergastoplasmic channels and neurofilaments. (H.H.D.)

The Fine Structure of Degenerating Nerve Fibers, their Sheaths, and their Terminations in the Central Nerve Cord of the Cockroach (Periplaneta americana)

The connectives above and below the second thoracic ganglion and nerves to and from the mesothoracic leg were severed in Periplaneta americana. Isolated ganglia and severed nerve cord were examined in the electron microscope. In the connectives, sheaths of degenerating fibers remain continuous but become thicker and more dense. There is increase in number and more haphazard disposition of the neuroglial processes which ensheath the axons. The cytoplasm contains vacuoles. Dense droplets normally intercalated between the layers of neuroglial processes ensheathing the axons are strikingly increased in number. The axoplasm with its organelles forms dense clumps. Mitochondria in axons are enlarged, the intramitochondrial matrix is more dense, and the internal folds are disorganized. In ganglia, mitochondrial changes in terminal parts of the axons appear similar to those described in the parent axons in the connective. The synaptic portions of nerve fibers appear very dense. Alterations of the sheath are minimal. Synaptic particles in the degenerating axoplasmic coagulum undergo only slight morphological changes and are still present up to 6 days after severance of their nerve fibers. It is difficult to assess whether there are any alterations in the total number of synaptic particles during degeneration.

PRESSURE BLOCK IN NERVES PROVIDED WITH ARTERIAL SLEEVES

ArticlesPRESSURE BLOCK IN NERVES PROVIDED WITH ARTERIAL SLEEVESPaul Weiss, and Hallowell DavisPaul Weiss, and Hallowell DavisPublished Online:01 Jul 1943https://doi.org/10.1152/jn.1943.6.4.269MoreSectionsPDF (3 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited BySynthesis and biomedical applications of aerogels: Possibilities and challengesAdvances in Colloid and Interface Science, Vol. 236Investigation of crosslinked silica aerogels for implant applicationsAn in vivo evaluation of a biodegradable genipin-cross-linked gelatin peripheral nerve guide conduit materialBiomaterials, Vol. 26, No. 18Effect of low-power pulsed laser on peripheral nerve regeneration in ratsMicrosurgery, Vol. 25, No. 1Multilayered peptide incorporated collagen tubules for peripheral nerve repairBiomaterials, Vol. 25, No. 13Nerve Guide Material Made from Fibronectin: Assessment of in Vitro PropertiesTissue Engineering, Vol. 9, No. 2Locally Administered Nerve Growth Factor Suppresses Ginsenoside Rb1 -enhanced Peripheral Nerve Regeneration5 April 2012 | The American Journal of Chinese Medicine, Vol. 31, No. 05Effects of percutaneous electrical stimulation on peripheral nerve regeneration using silicone rubber chambers1 January 2001 | Journal of Biomedical Materials Research, Vol. 57, No. 4Peripheral nerve regeneration using silicone rubber chambers filled with collagen, laminin and fibronectinBiomaterials, Vol. 21, No. 15Pathophysiology of Nerve Compression SyndromesThe Journal of Bone & Joint Surgery, Vol. 81, No. 11Biodegradable Controlled Release Glass in the Repair of Peripheral Nerve Injuries29 August 2016 | Journal of Hand Surgery, Vol. 23, No. 5Peripheral nerve repair with collagen conduitsClinical Materials, Vol. 9, No. 3-4A collagen-based nerve guide conduit for peripheral nerve repair: An electrophysiological study of nerve regeneration in rodents and nonhuman primatesThe Journal of Comparative Neurology, Vol. 306, No. 4Clinical Symptoms, Electrophysiological and Morphological Findings in Traumatic Lesions of the Ischiadic Nerve in Domestic FowlNerve regeneration through artificial tubular implantsProgress in Neurobiology, Vol. 33, No. 2Effects of pressure on fast axoplasmic flow. An in vitro study in the vagus nerve of rabbitsActa Physiologica Scandinavica, Vol. 104, No. 3REFERENCESThe nerve lesion in the carpal tunnel syndrome.Journal of Neurology, Neurosurgery & Psychiatry, Vol. 39, No. 7DYNAMICS AND MECHANICS OF NEUROPLASMIC FLOWCritical Evaluation and Implications of Denervation and Reinnervation Studies of Cross-Striated MuscleEffects of vinblastine and colchicine on neural regulation of the fast and slow skeletal muscles of the ratExperimental Neurology, Vol. 37, No. 3Control of myelin formation by axon caliber. (With a model of the control mechanism)The Journal of Comparative Neurology, Vol. 144, No. 2Sensory conduction from digit to palm and from palm to wrist in the carpal tunnel syndromeJournal of Neurology, Neurosurgery & Psychiatry, Vol. 34, No. 3NEURONAL DYNAMICS AND NEUROPLASMIC (“AXONAL”) FLOWBIDIRECTIONAL SHIFT OF MITOCHONDRIA IN AXONS AFTER INJURYSyntheseort und Ferntransport von Proteinen im FischhirnZeitschrift f�r Zellforschung und Mikroskopische Anatomie, Vol. 86, No. 2Mast Cells in the Nervous SystemStudies on vascular permeability in peripheral nervesActa Neuropathologica, Vol. 7, No. 1A banded structure in the connective tissue of nerveJournal of Ultrastructure Research, Vol. 11, No. 5-6The Use of a Resorbable Wrapper for Peripheral-Nerve RepairJournal of Neurosurgery, Vol. 21, No. 9Quantitativ-morphologische Befunde zur Hypothese des Mitochondrientransportes im NeuronZeitschrift f�r Zellforschung und Mikroskopische Anatomie, Vol. 62, No. 4Protein Metabolism of The Nervous SystemAn experimental method for compressing the sciatic nerveExperientia, Vol. 18, No. 11Elektronenmikroskopische Befunde zur Feinstruktur von Axonver�nderungen in regenerierenden Nervenfasern des Nervus ischiadicus der wei�en RatteActa Neuropathologica, Vol. 1, No. 5Experimental observations on the prevention of neuroma formationJournal of Surgical Research, Vol. 1, No. 3Further evidence of perpetual growth of nerve fibers: Recovery of fiber diameter after the release of prolonged constrictionsJournal of Experimental Zoology, Vol. 142, No. 1Studies on the phrenic nerves and the diaphragm of the dogThe American Journal of Surgery, Vol. 97, No. 6Cell migrations from the rhombic lip to the inferior olive, the nucleus raphe and the pons. A morphological and experimental investigation on chick embryosThe Journal of Comparative Neurology, Vol. 100, No. 1Experiments on the mechanism of nerve growthJournal of Experimental Zoology, Vol. 107, No. 3Nerve Regeneration: A Comparative Experimental Study Following Suture by Clot and ThreadJournal of Neurosurgery, Vol. 5, No. 1The Technology of Nerve Regeneration: a Review. Sutureless Tubulation and Related Methods of Nerve RepairJournal of Neurosurgery, Vol. 1, No. 6Further experimental evidence against “neurotropism” in nerve regenerationJournal of Experimental Zoology, Vol. 95, No. 2 More from this issue > Volume 6Issue 4July 1943Pages 269-286 https://doi.org/10.1152/jn.1943.6.4.269History Published online 1 July 1943 Published in print 1 July 1943 Metrics