PubMed · 13880597
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
K J COLLINS, J S WEINER. 1961. Axon reflex sweating.. https://pubmed.ncbi.nlm.nih.gov/13880597/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Computer models of neurons are used to simulate neural behavior, and are important tools for designing neural prostheses. Computation time remains an issue when simulating large numbers of neurons or applying models to real time applications. Warman et al. developed a method to predict excitation thresholds for axons using linear models and a predetermined critical voltage. We calculated threshold prediction error as a function of the location of an extracellular electrode using two different axon models to examine further threshold prediction using linear models. Threshold prediction error was low (<3% error) under the conditions examined by Warman et al., but under more general conditions, threshold prediction error was as high as 23.6%. Linear models were limited as effective tools for single fiber threshold prediction because accuracy was dependent on the nonlinear and linear models used, and any parameter that affected the extracellular potential distribution. Threshold prediction could be improved by appropriately choosing the membrane conductance of the linear model, but determination of an optimal conductance was computationally expensive. Finally, although single fiber threshold prediction error was partially masked when considering the input-output (I/O) properties of populations of axons, relatively large errors still occurred in population I/O curves generated with linear models.
Trauma in the adult mammalian central nervous system (CNS) has devastating clinical consequences due to the failure of injured axons to spontaneously regenerate. Over 20 years ago, pioneering work demonstrated that the non-permissive nature of CNS myelin for axon outgrowth contributes to this regenerative failure. Over the past few years, tremendous progress has been made in our understanding of the inhibitory components of CNS myelin, the axonal receptors that respond to these cues, and the intracellular signaling cascades mediating axon outgrowth inhibition. Several approaches designed to antagonize molecular mediators of axon inhibition have been tested in an effort to promote regenerative growth after CNS injury. These studies have validated the role of many candidate proteins in axon outgrowth inhibition; however, other approaches such as the generation of knockout mice for myelin-associated inhibitors have created new questions in the field.
A group of 13 patients with early onset diaphragmatic palsy in association with a progressive neuropathy is presented. All eight of those tested were found to have mutations in the same gene encoding the immunoglobulin mu-binding protein 2 (IGHMBP2) in patients with spinal muscular atrophy (SMA) with respiratory distress type 1. Six out of these eight patients had either homozygous or compound heterozygous mutations, and two had only a single heterozygous mutation. Detailed analysis of the clinical picture and the neurophysiological and histopathological findings indicated that these patients shared similar characteristics, which were further developed as a set of diagnostic criteria. Some of the most striking of these were early onset of respiratory compromise, a markedly low birth weight, very slow motor nerve conduction velocities and a general decrease in the size of myelinated fibres on sural nerve biopsy. Extensive histological examination of the spinal cord in one patient failed to find any evidence of an SMA. Four out of the five not tested genetically were positive for all diagnostic criteria. None of the cases of early onset neuropathies or spinal muscular atrophies with early respiratory failure reviewed in the literature shares the exact characteristics, but many do have very close similarities. Their classification varies, but the discovery of mutations in IGHMBP2 in cases that are variously classified as SMA plus or severe infantile neuropathy with respiratory distress points to a need for the search for this genetic defect to be widened to include both groups. The fact that we identified other, similar cases of neuropathy and early respiratory failure with and without IGHMBP2 mutations suggests genetic as well as clinical heterogeneity in these infants. It is possible that infants that do not have mutations in the IGHMBP2 gene will be found to have mutations in a similar functioning gene.