PubMed · 1712078
By combining small colloidal gold probes with video-enhanced quantitative microscopy, the intracellular dynamics of specific proteins in living cells can now be studied.
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H Geerts, M de Brabander, R Nuydens. 1991-06-27. Nanovid microscopy.. https://doi.org/10.1038/351765a0
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OBJECTIVE: The double crush hypothesis (DC) proposes that a proximal lesion along an axon predisposes it to injury at a more distal site along its course through impaired axoplasmic flow. The frequency and severity of carpal tunnel syndrome (CTS) according to the level of cervical radiculopathy were investigated to evaluate the hypothesis of DC. METHODS: The frequency of CTS was investigated in 277 patients with C6, C7 or C8 radiculopathies and correlation between CTS and radiculopathy level was determined. We also investigated whether the degrees of abnormal sensory responses were more severe in C6, C7 radiculopathies and whether motor responses were more severe in C8 radiculopathy. RESULTS: Thirty-nine patients were diagnosed with CTS and concomitant cervical radiculopathy at the C6, 7, or C8 root levels. The frequency of coexisting CTS was not statistically different according to the level of radiculopathy. The electrophysiologic results revealed no significant correlation between median sensory parameters and C6, C7 cases, and no relationship was observed between median motor responses and C8 radiculopathy. CONCLUSIONS: The frequency and electrophysiologic data of CTS analyzed according to cervical radiculopathy level do not support a neurophysiological explanation. SIGNIFICANCE: Based on this study, the DC hypothesis could not be supported.
The mechanism of anterograde transport of alphaherpesviruses in axons remains controversial. This study examined the transport, assembly, and egress of herpes simplex virus type 1 (HSV-1) in mid- and distal axons of infected explanted human fetal dorsal root ganglia using confocal microscopy and transmission electron microscopy (TEM) at 19, 24, and 48 h postinfection (p.i.). Confocal-microscopy studies showed that although capsid (VP5) and tegument (UL37) proteins were not uniformly present in axons until 24 h p.i., they colocalized with envelope (gG) proteins in axonal varicosities and in growth cones at 24 and 48 h p.i. TEM of longitudinal sections of axons in situ showed enveloped and unenveloped capsids in the axonal varicosities and growth cones, whereas in the midregion of the axons, predominantly unenveloped capsids were observed. Partially enveloped capsids, apparently budding into vesicles, were observed in axonal varicosities and growth cones, but not during viral attachment and entry into axons. Tegument proteins (VP22) were found associated with vesicles in growth cones, either alone or together with envelope (gD) proteins, by transmission immunoelectron microscopy. Extracellular virions were observed adjacent to axonal varicosities and growth cones, with some virions observed in crescent-shaped invaginations of the axonal plasma membrane, suggesting exit at these sites. These findings suggest that varicosities and growth cones are probable sites of HSV-1 envelopment of at least a proportion of virions in the mid- to distal axon. Envelopment probably occurs by budding of capsids into vesicles with associated tegument and envelope proteins. Virions appear to exit from these sites by exocytosis.
Distal hereditary motor neuronopathies (dHMNs) are a clinically and genetically heterogeneous group of disorders in which motor neurons selectively undergo age-dependant degeneration. Mutations in the small heat-shock protein HSPB1 (HSP27) are responsible for one form of dHMN. In this study, we have analysed the effect of expressing a form of mutant HSPB1 in primary neuronal cells in culture. Mutant (P182L) but not wild-type HSPB1 led to the formation of insoluble intracellular aggregates and to the sequestration in the cytoplasm of selective cellular components, including neurofilament middle chain subunit (NF-M) and p150 dynactin. These findings suggest a possible pathogenic mechanism for HSPB1 whereby the mutation may lead to preferential motor neuron loss by disrupting selective components essential for axonal structure and transport.