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Fine structure of the olfactory epithelium in the goldfish, Carassius auratus. A study of retrograde degeneration.

The fine structure of the goldfish olfactory epithelium was studied by transmission and scanning electron microscopy. Six different cell types were distinguished. Identification of the olfactory receptor cell was accomplished by use of retrograde degeneration studies. Two morphologically distinct types of olfactory receptor cells were identified: one type bears radially oriented cilia (Type I cell); the other type bears microvilli (Type II cell). The other four cell types were not identifiable as olfactory receptor cells: they are ciliated cells (Type III), rod-shaped cells (Type IV), supporting cells (Type V), and basal cells (Type VI).

Animals

[Characteristics of residual neurons during retrograde degeneration in the lateral geniculate bodies of cats].

The daynamics of functional-structural characteristics of residual neurons was studied in the degenerated lateral geniculate body (LGB) in various periods of time (4-12 months) after neuronal isolation of the neocortex under which all geniculo-cortical connections were cut. Background and evoked spike activity in the degenerated geniculate body were studied as well as the number of persisting cells and their diameters. Neuronal receptive fields were found to undergo destruction along with the prolongation of postoperative period. A gradual diminution in the quantity of light sensitive cells was revealed. Background spike activity was predominantly of a simple type. Progressing decrease in cell number and cell diameters was observed under the morphological examination. Special features inherent in geniculate interneuronal relations are discussed.

Animals

Retrograde degeneration of autonomic neurons and other cell groups of the spinal cord following extirpation the thoracic sympathetic ganglia.

Examination of vegetative, as well as sensitive and motor spinal neurons after surgery performed on the peripheral part of the vegetative nervous system in the thoracic cavity of 34 dogs reveals reactive and degenerative changes in the nerve cells. Alterations in the neuronal structure are already observed on the 7th day after the operation and they reach thir maximum on the 60th day. During the time mentioned, most of the nervous cells undergo a complete pyknosis; among them, however, there are neurons restoring their normal structure. Therefore, it is possible to believe that after operations on the thoracic cavity, certain morphological disturbances occur in the corresponding vegetative centers, which are followed by disorders in the nervous regulation of the internal organs after the operation.

Animals

Thalamic projections to parietal cortex.

Thalamic projections to parietal regions of cerebral cortex were investigated in the cat by retrograde degeneration and retrograde transport techniques. Studies of retrograde cellular changes indicate cortically projecting cells in the lateroporterior nucleus (LP), rostral pulvinar (Pul), and the ventral part of the laterodorsal nucleus (LD). When lesions were placed in the cortex of young kittens, clear chromatolytic changes and cell loss were also consistently observed in middle and caudal parts of the ventroanterior nucleus (VA). Investigations of retrograde transport following intracortical injections of horseradish peroxidase have confirmed the results of retrograde degeneration studies by demonstrating cortically projecting cells in VA, LP, LD, and Pul. Retrograde transport studies also indicate cortically projecting cells in the central lateral nucleus. Material from both experimental techniques demonstrates a loose topographic organization of the projections from the lateral thalamus. Anterior parts of LP project to the anterior lateral gyrus and anterior middle suprasylvian gyrus. Middle LP and rostral Pul project to the middle suprasylvian gyrus.

Animals

Long term post-traumatic retrograde corticospinal degeneration in man.

The spinal cord and brain of a man who died 18 years after a crush injury of lumbar segments contained some unusual lesions. There was a reduced number of myelinated axons in the corticospinal tracts as high as the fifth cervical segment. Such retrograde degeneration has been described in human pyramidal tracts only a few times. The results of reported studies of experimental retrograde degeneration have been inconsistent. The course of the fasciculus gracilis, as delineated by gliosis, was atypical, and an unusual glial nodule, possibly neoplastic, was present in the dorsal columns at C8.

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Thalamic projections of the dorsomedial prefrontal cortex in the rhesus monkey (Macaca mulatta).

Cortical aspirations were made of the dorsomedial prefrontal sector in the rhesus monkey and the resultant anterograde and retrograde degeneration plotted. Retrograde changes were mapped using both cresyl violet and modified Fink-Heimer techniques. Following large dorsomedial lesions, small numbers of degenerating fibers were traced through the medial part of the magnocellular ventral anterior nucleus (VAmc) and the ventral part of the internal medullary lamina surrounding the anterior nuclei. Degenerating fibers were also traced medially through the inferior thalamic peduncle and rostrodorsally through the basal thalamic region into the mediodorsal nucleus. All pathways converged on areas in the dorsal part of the parvocellular mediodorsal nucleus (MDpc) containing fine-grain dust and argyrophilic neurons, reactions usually associated with retrograde degenerative changes. Sparse fiber degeneration was also noted in the ventral part of the magnocellular mediodorsal nucleus (MDmc). After a longer survival period, slight to moderate cell loss and gliosis were seen in MDpc along with an increase in the number of degenerating fibers passing through the medial part of VAmc. Rostral dorsomedial lesions resulted in small numbers of degenerating fibers in the medial part of VAmc; no degenerating fibers appeared in the basal thalamic region. Fine-grain dust was noted in the dorsal part of MDpc along with sparse preterminal degeneration in the dorsal and ventral parts of MDpc and MDmc respectively. Following caudal dorsomedial lesions, fiber degeneration was traced through the medial part of VAmc and through the inferior thalamic peduncle and basal thalamic regions to areas of degenerating preterminals in the dorsal part of MDpc. Sparse fiber degeneration was also noted in MDmc. No evidence of cell loss and gliosis or increased numbers of degenerated fibers was noted following longer survival periods. Dorsolateral and orbital lesions resulted in large areas of fine-grain dust, argyrophilic neurons, and severe cell loss in MDpc and MDmc respectively. A large combined dorsolateral and orbital lesion made 32 days prior to sacrifice of the animal resulted in coarse fiber degeneration in the medial part of VAmc and in the anterior nuclear capsule. Severe cell loss and fiber degeneration were evident in the entire MD. These results suggest that the rostral dorsomedial prefrontal sector receives projections from MDpc while the caudal sector does not. This projection courses dorsally and rostrally through the ventral part of the capsule surrounding the anterior nuclei and into the medial part of VAmc. The entire dorsomedial sector projects sparsely to both MDpc and MDmc. The projection from the rostral medial surface passes through the medial part of VAmc while that from the caudal surface reaches MD both by the dorsal approach through VAmc and through a ventral approach via the inferior thalamic peduncle and the basal thalamic region.

Animals

Retrograde changes in motor and sensory conduction velocity after nerve injury.

Nerve section is followed by a reduction of motor and sensory conduction velocity in the proximal segment of the injured nerve. This reduction of velocity is associated with retrograde changes in fiber size. If reinnervation does not occur within the next 1 1/2--2 years, retrograde degeneration of nerve fibers results, and the amplitude of the evoked nerve potential in the proximal segment of the injured nerve decreases. This retrograde degeneration is probably significant in view of the poor results frequently obtained after nerve transplantation which is carried out too late.

Humans

Abnormal retino-geniculate and geniculo-cortical pathways in several genetically distinct color phases of the mink (Mustela vison).

Several genetically distinct color phases of mink, which all show an abnormal reduction of pigment in the retinal pigment epithelium and which also show abnormalities of the retinofugal pathways, have been studied. Autoradiographic methods have been used to demonstrate the retino-geniculate pathways, and retrograde degeneration or the retrograde transport of horseradish peroxidase has been used for the geniculo-cortical pathways. The retino-geniculate abnormality is mild in some of the color phases and extremely severe in others, but within any one color phase the variability is relatively low. Although the severity of the abnormality varies between color phases, a rather specific pattern of abnormal geniculate innervation is recognizable for mink in general and this is distinct from that found in Siamese cats. In the abnormal mink the size of geniculate lamina A1 is reduced and there is an abnormal crossed input going to the intermediate sectors of this reduced layer. Layer C1 also receives an abnormal crossed input, but this is more variable than that going to A1 and there appears to be little correspondence, retinotopically, between the normal inputs to layers A1 and C1. In some of the abnormal mink there are interruptions within the cytoarchitectionically definable layer A1, and opposite these gaps reduplications of layer A are commonly seen, as though there is an intrinsic geniculate mechanism for generating the characteristic multilaminar geniculate structure. However, there are also numerous examples of fusions between layers receiving afferents from the same eye, and these demonstrate that the development of geniculate lamination must also be under the influence of the retinal inputs. The geniculo-cortical pathway shows a normal topography in most of the mink. Abnormal geniculo-cortical projections, comparable to the "Boston" pattern of Siamese cats are extremely rare, and their occurrence could not be correlated with the severity of the retino-geniculate abnormality or with the laminar pattern in the lateral geniculate nucleus. We suggest that the development of one or the other pattern of geniculo-cortical projection may depend upon the relative timing of the two mechanisms that produce the geniculate lamination.

Animals

Extent of recovery from neonatal damage to the cortical visual system in cats.

Cats that received either marginal or marginal plus extramarginal lesions as 3-day-old kittens were assessed on a series of tests of visually guided behavior. These cats were not conspicuously different from normal controls in avoiding obstacles or in activity level. Yet these same operated cats were severely impaired in performance on the visual cliff and in visual discrimination learning, even when the lesions were limited to the geniculocortical portion of the visual system. However, maximum losses in pattern and form discrimination learning were observed only in cats with severe retrograde degeneration in both the lateral geniculate nucleus and the complex of the pulvinar and nucleus lateralis posterior. Photically evoked potentials were recorded in the lateral regions of the neocortex more reliably from operated cats that had made fewer errors in discrimination learning than from more severely debilitated cases; this relation was present even among cases with nearly equivalent amounts of retrograde degeneration in the visual thalamus. These findings suggest that in the cat (a) recovery of vision is incomplete after neonatal lesions of the visual cortex and (b) a cortical system lateral to the geniculocortical projections may be involved in pattern vision.

Animals

Neuronal degeneration and regeneration in the olfactory epithelium of pigeon following transection of the first cranial nerve.

The pigeon olfactory nerve has been sectioned to explore the course of retrograde degeneration of the sensory neurons' perikarya, which are located in the olfactory neuroepithelium. Both light- and electron-microscopic observations have shown that from 3 to 8 days after axotomy the sensory neurons undergo retrograde, irreversible degeneration. Following disappearance of the mature neurons, the basal cells of the neuroepithelium actively divide and differentiate into mature olfactory sensory neurons. Consequently, the basal cells represent true stem cells of the olfactory sensory neurons. The olfactory mucosa regains a structural organization close to normal in a period of 30-50 days after axotomy. These observations indicate that, when the primary olfactory neurons degenerate as a consequence of the experimental section of their axons, restitutio ad integrum of the sensory olfactory connections can be reestablished by new elements which differentiate from basal cells of the olfactory neuroepithelium.20

Animals

Ultrastructural changes of the nerve elements following disruption of the organ of Corti. I. Nerve elements in the organ of Corti.

3-137 days after disruption of the guinea pig organ of Corti by perilymphatic perfusion with 20% streptomycin (SM), ultrastructural changes of the nerve fibers in the organ were observed. Most of nerve fibers began to degenerate after a latent period of 4 days. On the other hand, a number of fibers survived reactively enlarged and later developed into myelinated and unmyelinated fibers by becoming enclosed in Schwann cells which entered the organ of Corti through the habenula perforata. Regeneration and sprouting of the surviving nerve fibers also occurred. The fibers became mature, but atrophied after 60 days and then gradually disappeared. The regenerating fibers were mainly of the myelinated and unmyelinated efferent type. Retrograde degeneration occurred in both afferent and efferent fibers. In the less damaged organ of Corti perfused with 2% SM or Ringer's solution, Schwann cell invasion was not found.

Animals

Origin of brain macrophages and the nature of the so-called microglia.

Two aspects of the so-called microglia were studied by silver impregnation and 3H-TdR ARG in light and electron microscopy. (1) So-called microglioblasts are glioblasts differentiated from matrix cells. They are progenitors of the so-called resting microglia as well as of astrocytes and oligodendroglia. (2) Brain macrophages in stab wounds, experimental Japanese encephalitis and retrograde degeneration of the facial nucleus are all found to be of hematogenous origin. Infiltrating hematogenous cells cannot stay permanently in the brain parenchyma unless pathological alterations persist indefinitely.

Animals

Sparing of function in rats with early prefrontal cortex lesions.

Previous work has shown that medial frontal lesions in adult rats produce deficits on spatial reversals, delayed responses, and active avoidance, whereas more ventrolateral (orbital) lesions have little effect on these tasks. These findings were confirmed. However, when lesions were made at 2, 5 or 9 days of age, rats tested as adults showed dramatic sparing of function on all these tasks, whereas similar lesions inflicted at 35 or 40 days of age produced deficits on delayed responses and spatial reversals. Orbital frontal lesions failed to significantly alter behavior on any task at any age. The effects of the neonatal lesions are in striking contrast to the effects of juvenile or adult lesions, even though the infant lesions were considerably larger. Histological analysis revealed no retrograde degeneration in the dorsomedial thalamic nucleus of the rats operated in infancy unless the lesions were so large that the adjacent caudate-putamen was also damaged. The contrast between these results, and results obtained after similar lesions in adults may indicate the growth of sustaining collaterals after the infant lesions which might be involved in the observed behavioral sparing.

Age Factors

Neurogenesis and neuron regeneration in the olfactory system of mammals. II. Degeneration and reconstitution of the olfactory sensory neurons after axotomy.

This report describes the retrograde degeneration affecting olfactory sensory neurons of rats after severance of their axons and illustrates the reconstitution of new neurons originating from stem cells located at the base of the olfactory neuroepithelium. Degeneration of the mature, axotomized neurons, signalled by an increased electron density of their cytoplasmic matrix and by the appearance of lipofuscin-like granules, can be detected in the neuroepithelium as early as 24 h after surgery and becomes conspicuous between the second and the third day. Degenerating neurons can be observed in decreasing number up to the tenth post-operative day. They are removed by macrophages which invade the epithelium. The reconstitution of new neurons begins to occur after eight days, when the stem cells undergo vigorous mitotic activity and differentiate into neurons. The morphology of the reconstituted neurons has been described in detail at different stages of their maturation. After 30 days, the olfactory epithelium appears similar to controls. On the basis of both morphological (in rats) and autoradiographic ( in mice) observations, the basal cells have been recognized as stem cells of the olfactory neurons.

Animals