PubMed · 7233576
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A case for the panel.. https://doi.org/10.3109/01913128009141396
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Filamentous contacts are non-synaptic interneuronal junctions characteristic of thalamic relay nuclei. Symmetrical filamentous contacts occur between two dendrites, two somata or a dendrite and a soma; asymmetrical filamentous contacts occur between axon terminals and dendrites, or occasionally somata, chiefly between the large specific afferent axon terminals of the synaptic glomeruli and the shafts of relay cell dendrites. Both are arranged as extensive net-like (reticular) specializations. The strands of the network enclose fenestrae of variable shape and size and, in perpendicular thin sections, appear as stretches of slightly widened intercellular space containing an electron-dense material and bounded by plasma membranes, the cytoplasmic surfaces of which are coated by electron-dense material into which microfilaments appear to insert. The lamina of cytoplasmic material in dendrites and somata is thicker than that in axon terminals and contains distinct electron-dense sub-units. Regular synaptic junctions may be situated like islands within the territory of an asymmetrical filamentous contact, and small spot-like close membrane appositions resembling gap junctions are occasionally seen in the fenestrae adjacent to the strands of both varieties of contact. Bundles of neurofilaments running in different directions, but in a plane parallel to the plasma membrane, are prominent on either side of the symmetrical filamentous contact and on the dendritic side of the asymmetrical variety. The agranular reticulum also exhibits differences between the contact types. Because of their highly specialized ultrastructure and specific distribution, filamentous contacts probably do not serve a purely adhesive function. Their possible role in the establishment and maintenance of orderly connections between cells is discussed but not favoured. Filamentous contacts probably mediate some form of intercellular communication, possibly involving gap junctions.
Computationally efficient procedures are described for the deconvolution of disoriented fiber diffraction data to the resolution limit of measurable intensity in the patterns. The methods can be applied to diffraction data from imperfectly parallel arrays of one-dimensionally periodic rods or two-dimensionally periodic sheets, randomly rotated about their unique axes, to derive a representation of the intensity distribution corresponding to perfectly parallel orientation. With use of angular convolution and local angular regression, a set of uniform cylindrically averaged squared structure factors are iteratively adjusted, subject to a minimum-wavelength constraint, until they produce a disoriented pattern that fits the observed diffraction data. The results from this deconvolution provide a measure of the properly scaled cylindrically averaged squared structure factors, which can be used with other structural information to construct a physically plausible trial model suitable for further refinement. Sample deconvolutions of simulated X-ray patterns from partially oriented gap junction membranes are presented and the results from point-model deconvolutions are compared to those from constrained deconvolutions that began with the transform of a physically plausible trial model.
Previous studies have examined the influence of the gap-junction discontinuity on the steady-state response of a cardiac cable to electrical defibrillation. It is important to understand when steady-state conditions may be assumed. For this reason, the transient, subthreshold behavior of a discontinuous cardiac cable is examined in this study. The behavior of the cable reflects two characteristics: 1) the continuous nature of the entire cable and 2) the isolated behavior of individual cells imposed by the junction discontinuity. The results show two effective time constants of activation: a large time constant corresponding to the time constant of a continuous cable of equivalent length, and a small time constant reflecting the rapid activation of an isolated cell. The rapid activation establishes a voltage gradient across each cell of the cable with one end of the cell hyperpolarized and the opposite end depolarized. This pattern of hyperpolarization and depolarization reaches a maximum value in approximately 3 microseconds and may play an important role in the mechanism of defibrillation.