Search PubMedSearch

PubMed · 438093

Changes in axonal numbers in developing human trochlear nerve.

Abstract

Complete axonal counts have been made in the intracranial parts of trochlear nerves from human fetuses of 9.2, 10 and 24 cm crown-rump length. A count was also made in the intraorbital part of the nerve from the 10 cm specimen. Schwann cell nuclei were also counted in typical cross sections, but do not necessarily reflect very accurately the schwann cell contents of the nerves. Axonal numbers conform to the propositions (1) that they do not all grow out at once, (2) do not all survive and (3) that degeneration may occur before or after myelination has begun. It seems inevitable that some loss of Schwann cells occurs in relation to the degeneration of myelinated axons, but there is no evidence for or against such a loss in relation to the degeneration of unmyelinated axons. Overall, however, Schwann cell numbers tend to increase as the number of myelinated axons increases.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

G Y Mustafa, H J Gamble. 1979. Changes in axonal numbers in developing human trochlear nerve.. https://pubmed.ncbi.nlm.nih.gov/438093/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

[Brain plasticity. New possibilities in the treatment of nerve damage?].

The article briefly reviews current views on the formation of neural pathways and appropriate connectivity between neurons during the development of the nervous system. The importance of axonal guidance and neurotrophic factors is pointed out. The relevance of these processes to clinical applications is illustrated by a few examples of recent attempts to develop new strategies for the treatment of certain neurological disorders. The prediction is that appreciable progress can be expected in the foreseeable future.

Axons

[A case of diffuse brain injury involving the medial part of the brain--its difference from diffuse axonal injury].

A 30-year-old male clinico-pathological case survived for 1 year and 9 months after being hit by a truck while riding on his motorbike on Aug. 21, 1988. On admission, his consciousness level was 5 according to the Glasgow Coma Scale, and a traumatic intraventricular hemorrhage and cerebral contusion were revealed by CT scanning. He underwent immediately an operation in order to drain blood from the ventricles at which time a right side dominant quadriplegia was noted. He made a gradual improvement and by January 1989 was able to tell us his name and address correctly. However, he remained incontinent and bedridden owing to the contracture of joints. He was put on rehabilitation exercises in March 1989 which trained him to operate a wheelchair. In April 1990 he regained urinary control, but was remarkably devoid of will power, perseverance and memory. He expired of pneumonia on May 11, 1990. At autopsy, his brain weighed 1180g. The cerebral convexity was discolored, especially the rectal gyri and bilateral olfactory bulbs were brownish-yellow. Old gross contusional scars were observed on the left rectal and orbital gyri, and the 3rd ventricle and inferior horns of the lateral ventricles were enlarged. Holzer's method revealed fibrillary gliosis in the corpus callosum, fornix, cingulate gyrus and a part of the caudate nucleus adjacent to the thalamus. Microscopically, axons were seen to be disrupted in the corpus callosum as well as in the anterior commissure, having the appearance of macrophages. (ABSTRACT TRUNCATED AT 250 WORDS)

Axons