Jeanne M. Smith

The sizes of nerve fibers supplying cerebral cortex

Abstract The nerve fiber supply to various cortical areas of several vertebrate animals has been examined by means of the electron microscope, the fibers measured in cross sections of white matter as it approaches cortex, and plots made of numbers of fibers vs diameters. Most of the fibers are myelinated in mammals, and the relatively few unmyelinated structures are not clearly distinguishable from glial elements. In mammals, each distribution curve shows a maximum at approximately 1 μ, some fibers as small as 0.2 μ, a rapid decrease in numbers up to 4 μ, and a plateau finally declining to zero at diameters of 5 to 14 μ in different cortical areas of different species. In some small areas sampled there may be few or no fibers over 3 μ. In the motor area of the macaque monkey, a second maximum, at 8 to 9 μ presumably represents the Betz cell axons. Otherwise no secondary maxima such as the alpha to delta peaks of peripheral nerves are obvious, but reasons are presented for fividing the total size spectrum range into three ranges, corresponding to the large myelinated afferents passing into the dorsal cord column, medium-sized fibers whose postsynaptics cross the cord to ascend in the ventrolateral column, and the unmyelinated fibers taking a similar course through the cord. There are reasons for considering these three size groupings in spinal nerves to be phylogenetically successive, and to have been extended by relays successively to higher centers. The smaller fiber group is then the most primitive, and evidence here presented indicates that similar-size components have been successively acquired during the phylogenetic development of the mammalian cortex. Similar examination of the white matter of reptilian cortex shows few myelinated fibers, and few of these are as large as 4 μ. They are inferred to be the precursors of the 0.2 to 3 μ range of mammals, to which successively higher mammals have added increasing numbers of fibers of increasing diameter. The fiber size distributions of the pyramidal tract, optic tract and olfactory nerve have been analyzed for contrast with the trigeminal nerve distribution. The results are consistent with the phylogenetic interpretation suggested. Examination of the cortex of an insectivore, the mole, a relatively primitive mammal, shows the typical mammalian pattern of fiber size distribution, but with small areas of white matter containing no fibers over 3 μ, others with none over 5 μ, but an overall of 9 μ. It is proposed that these morphological components, whose axons are recognizable physiologically in terms of thresholds and conduction rates, may contribute phylogenetically successive functional patterns to cortical activity. Tracing the origins of paths activating cortex, and destination of paths originating in cortex, may lead to identification of types of response correlated with fiber sizes.

Motor organization of the spinal accessory nerve in the monkey

The segmental and topographical organization of motoneurons of the spinal accessory nerve was studied in monkeys with horseradish peroxidase (HRP). The sternomastoid muscle is innervated primarily from the C1-C2 level of the cord and the motor column is medial in the ventral horn. The trapezius muscle, however, is innervated primarily from the C2-C3-C4 levels of the cord and the motor column lies in the ventrolateral region of the ventral horn. The data are discussed with regard to treatment of torticollis.

Fine structure of the rubrospinal terminals in the cervical cord of the cat

Rubrospinal fibers in cat do not terminate on anterior motor horn cells in the spinal cord but on the interneurons, mostly in the lateral portion of Rexeds lamina of V-VII, the so-called Lateral Basal Region. The ultrastructure of rubrospinal terminals at the cervical cord level (C8) was investigated in 8 adult cats with partial or complete stereotaxic lesions of the red nuclei. Animals were sacrificed from 1 to 7 days after the lesions were made and the earliest forms of degeneration found were infrequent dense preterminal axon changes and clumping and coalescing of synaptic vesicles in the terminals. Multiple dense or polymembranous inclusions were seen in some terminals and these contained vesicular profiles; dense terminal shrinking was seen in others after 24 hours. Neurofilamentous proliferation appeared in some degenerating terminals after 48--72 hours. Degenerating terminals were related to different sized dendrites to determine regional axodendritic specificity for rubrospinal endings on LBR neurons.

Familial ataxia of the rabbit Sawin-Anders type

SummaryThis hereditary animal ataxia is selective in its sites of involvement within the nervous system, which include principally the central cerebellar, vestibular and cochlear nuclei. Ultrastructural detail has been described for central cerebellar and vestibular nuclei. Herein the cochlear complex of 18 rabbits with this ataxic condition (ax/ax from the strain AX of the Jackson Laboratory) have been examined. The gene is a lethal one, but the animals were used before they became moribund and between 7 and 57 days after the onset of symptoms.By light microscopy nine cell types (Osen, 1969a, b; 1970) have been identified in the cochlear nuclei of the cat. That distribution can also be identified in electron micrographs of rabbit cochlear nuclei, providing there is a singular opportunity to compare cellular vulnerabilities within the ataxic condition, and establish the principal features of associated neuropil alterations. The cochlear nuclei, cerebellar cortex and central nuclei, and the vestibular nuclei, arise from the ependyma of the rhombic lip of the fourth ventricle, making them close allies in their genetic origins.Pathological alterations were evident in scattered neurons from all nuclear sources by 7–15 days following symptom onset. At 15 days the number of altered neurons evident in electronmicrographs had increased markedly, cells becoming involved at a more rapid pace than those already affected could be removed. Much glycogen is evident from 7 days onwards in both neuropil and neurons. It occurs in considerable amounts in astrocytic processes and less abundantly in endbulbs and somata. By 20 to 25 days spongioform changes in neuropil are prominent, and thereafter the extracellular spaces coalesce to produce a lacunar appearance showing little glycogen. It would appear, therefore, that all neuron types, the endbulbs, and the astrocytic processes are markedly involved simultaneously in the spongioform transformation which features this type of ataxia. Involvement of cochlear nuclei only differs in pathological detail from that found at the other involved sites, and the differences seen relate principally to the architectonics of the nuclei, including size and density of the packing of contained elements.