Abstract
The spinal cord represents a fold of the ectoderm, and its elements merely represent transformed epithelial cells. The primordial phases of this transformation are known today from the fundamental observations of His (1879, 1883, 1886, 1887, 1889) made preferentially in the human embryo.
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
Footnotes
It is in the embryology section of this study that Kupffer states the fundamental thesis on the origin of nerve fibers.
Some authors, however, attribute a proliferative capacity to nerve cells of small size. Thus, Levi (1898), who has studied the healing of cerebral wounds in the guinea pig, reports to have seen mitoses in small pyramidal cells, but not in the large ones or in motor cells of the spinal cord, i.e. in neurons with centralized chromatin; which, on passing, confirms our opinion that the centralization of the chromatin implies the incapacity to divide.
We formulated this doctrine already in our second work on the cerebellum (Cajal, 1890b; see also Cajal, 1893c).
Golgi recognized well the general pattern of the epithelium which he described as formed by radial fibers extending from the ependyma to the pia where they would end either by a conical enlargement or by fine threads inserted on capillaries. Secondary branchlets would emerge in the course of radial fibers, terminating in part on vessels. This scholar did not study, however, the morphology of the epithelium in different spinal radii, nor its histogenetic relationships with the neuroglia. Also Falzacappa (1889) apparently impregnated, at least partially, the primitive epithelium of birds embryos, according to a brief mention in his report.
[We believe that the intercellular anastomoses recently described by Held in the trigeminal ganglion of the duck embryo at the 56th incubation hour, are just products of the coupling of irregular appendages of certain neuroblasts. In our neurofibrillar preparations made from chick embryos of the same incubation period, the immense majority of neurons show indeed a frankly bipolar pattern.]
[However, radial interstices between ependymal cells could also play a role in determining this orientation.]
Annotations
Fig. 233.— a, cell with beginning of a central process; b, c, same as A, i.e. neurons in apolar stage.
Fig. 234.— d, ganglion cell in bipolar phase.
Fig. 236.— a, unidentified; b, intranuclear rod; c, axoplasmic substance.
Fig. 238.— E, bipolar cell with very incipient central process.
Fig. 239.— C, dorsal horn bundle; c, same as b, i.e. cone bound for the dorsal horn bundle.
Fig. 242.— A, normal neuroblast extending the peripheral process toward the dorsal horn bundle; C, same as D, E, i.e. neuroblast re-entering the ependyma; F, faulty pathway leading the growth cone to the columnar and nuclear layers; H, unidentified; c, probably commissural neuroblasts.
Fig. 243.— F, fibers of the medial longitudinal fasciculus; a, other looping trochlear nerve fibers.
Fig. 246.— d, motor nerve; f, muscle.
Histologie reads in error Fig. 269E instead of Fig. 246E, which is the equivalent of Fig. 242E of the present version.
Fig. 247.— a, spherule ending; b, two new branches ending in conical swellings.
Fig. 249.— a, zone of entry and bifurcation of dorsal root fibers; e, mitotic cell.
*Fig. 250.— E, white matter of the dorsal funiculus; c, unidentified.
mThe risk taken by extrapolating adult morphology from that of early developmental stages is clear in the behavior of a certain kind of striatal neurons, which having spines on their dendrites in the early postnatal period (and such was the material used by Cajal in his descriptions of the corpus striatum in Volume III), loose the spines in later periods [Di Figlia, Pasik, Pasik (1980) J Comp Neurol 190: 303-332].
nFig. 251.— c, collaterals of the lateral funiculus.
oTextura reads in error Fig. 192a instead of Fig. 81a, which is the equivalent of Fig. 109a of the present version.
pSee annotations a and b in Chapter IX for discussion on myelin formation.
qFig. 254.— B, ventral horn; C, inner zone or epithelial wall.
rFig. 255.— a, soma and nucleus of epithelial cell.
sFig. 256.— E, surface of central cavity with cilia of ependymal cells.
tFig. 257.— C, early stage with the soma still attached to the ependymnal wall; E, same as D, i.e. astroblast.
uFig. 258.— D, more mature neuroglia of the gray matter; G, neuroglia of the white matter with remnants of ependymal processes, and peripheral process attached to the pia.
vFig. 262.— a, nucleus of satellite cell; b, mitotic cell; c, dense neurofibrillar bundle in a process of a cell at the bipolar state.
wAfter much debate, Cajal’s view of the origin of the single stem of unipolar ganglion cells from an elongated portion of the soma, and not from the fusion of the original two processes, has received ample confirmation by both transmission and scanning electron microscopy [Takahashi and Ninomiya (1987) Progr Neurobiol 29: 393-410].
xFig. 266.— C, simple growth cone; D, F, G, bifurcating growth cones.
yFig. 267.—e, mesodermic cell.
zThe ectodermic origin of Schwann cells was eventually demonstrated [Plenk (1934) Ztschr mikr-anat Forsch 36: 191-214].
Fig. 270.— e, unidentified; f, g, nuclei of mesodermic cells.
The discovery of the oligodendrocyte [Rio Hortega (1921) Bol Real Soc Espan Hist Nat 21: 63-92], and its role in myelin formation of central nervous system fibers is a much later event. See annotation b in Chapter IX.
Figs. 256 and 257 are from human embryo and newborn mouse, repectively. ddHistologie reads in error neuroblasts instead of neurodesms.
Rights and permissions
Copyright information
© 1999 Springer-Verlag Wien
About this chapter
Cite this chapter
y Cajal, S.R. (1999). Histogenesis Of The Spinal Cord And Spinal Ganglia. In: Texture of the Nervous System of Man and the Vertebrates. Springer, Vienna. https://doi.org/10.1007/978-3-7091-6435-8_21
Download citation
DOI: https://doi.org/10.1007/978-3-7091-6435-8_21
Publisher Name: Springer, Vienna
Print ISBN: 978-3-7091-7323-7
Online ISBN: 978-3-7091-6435-8
eBook Packages: Springer Book Archive