Acta Neuropathologica

, Volume 52, Issue 2, pp 111–118 | Cite as

Morphometric evaluation of primary sensory neurons in experimental p-bromophenylacetylurea intoxication

  • Akio Ohnishi
  • Masato Ikeda
Original Works


To evaluate the three-dimensional pathology of lumbar primary sensory neurons in p-bromophenylacetylurea intoxication, the number and size distribution of neurons and of myelinated fibers were evaluated at the L-6 spinal ganglion level and at proximal and distal levels of sural nerve and thoracic (proximal) and cervical (distal) levels of Goll's tract, respectively, 2 and 6 weeks after the intoxication in rats. The number and size distribution of ganglion neuron cell bodies were not significantly different between intoxicated and control rats. The distal level of sural nerve had, significantly fewer large myelinated fibers than did control, and a significantly higher frequency of fibers undergoing degeneration. Proximal levels of sural nerve showed similar, but less severe changes. Similarly, the myelinated fibers of Goll's tract were significantly more affected at cervical than at thoracic level. Therefore, by morphometric criteria both centrally and peripherally directed myelinated fibers are most affected distally and less affected proximally while neuron cell bodies are not affected at all. These three-imensional morphological changes must be taken into consideration in formulating possible mechanisms for the development of this neuropathy.

Key words

Primary sensory neuron Neuropathy Morphometry Para-bromophenylacetylurea Neurotoxins 


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Blakemore WF, Cavanagh JB (1969) “Neuroaxonal dystrophy” occurring in an experimental “dying-back” process in the rat. Brain 92:789–804Google Scholar
  2. 2.
    Bouldin TW, Cavanagh JB (1979) Organophosphorus neuropathy. I. A teased-fiber study of the spatiotemporal spread of axonal degeneration. Am J Pathol 94:241–252Google Scholar
  3. 3.
    Bouldin TW, Cavanagh JB (1979) Organophosphorus neuropathy. II. A fine-structural study of the early stages of axonal degeneration. Am J Pathol 94:253–270Google Scholar
  4. 4.
    Cavanagh JB (1964) The significance of the “dying-back” process in experimental and human neurological disease. Int Rev Exp Pathol 3:219–267Google Scholar
  5. 5.
    Cavanagh JB (1964) Peripheral nerve changes in orthocresyl phosphate poisoning in the cat. J Pathol Bacteriol 87:356–383Google Scholar
  6. 6.
    Cavanagh JB, Chen FCK, Kyu MH, Ridley A (1968) The experimental neuropathy in rats caused by p-bromophenylacetylurea. J Neurol Neurosurg Psychiat 31:471–478Google Scholar
  7. 7.
    Chen HC, Lin CS, Lien IN (1967) Vascular permeability in experimental kernicterus: An electron microscopic study of the blood brain barrier. Am J Pathol 51:69–100Google Scholar
  8. 8.
    Cho ES (1977) Toxic effects of adriamycin on the ganglia of the peripheral nervous system: A neuropathological study. J Neuropathol Exp Neurol 36:907–915Google Scholar
  9. 9.
    Diezel PB, Quadbeck G (1960) Nervenschädigung durch p-Bromophenylacetyl-Harnstoff. Naunyn-Schmiedeberg's Arch Exp Path Pharmak 238:534–541Google Scholar
  10. 10.
    Dyck PJ, Kawamura Y, Low PA, Shimono M, Solovy JS (1978) The number and sizes of reconstructed peripheral autonomic, sensory and motor neurons in a case of dysautonomia. J Neuropathol Exp Neurol 37:741–755Google Scholar
  11. 11.
    Dyck PJ, Stevens JC, Mulder DW, Espinosa RE (1975) Frequency of nerve fiber degeneration of peripheral motor and sensory neurons in amyotrophic lateral sclerosis. Morphometry of deep and superficial peroneal nerves. Neurology (Minneap) 25:781–785Google Scholar
  12. 12.
    Gonatas NK, Baird HW, Evangelista I (1968) The fine structure of neocortical synapses in infantile amaurotic idiocy. J Neuropathol Exp Neurol 27:39–49Google Scholar
  13. 13.
    Gonates NK, Evangelista I, Walsh GO (1967) Axonic and synaptic changes in a case of psychomotor retardation in an electron microscopic study. J Neuropathol Exp Neurol 26:179–199Google Scholar
  14. 14.
    Gonatas NK, Goldensohn ES (1965) Unusual neocortical presynaptic terminals in a patient with convulsions, mental retardation, and cortical blindness: an electron microscopic study. J Neuropathol Exp Neurol 24:539–562Google Scholar
  15. 15.
    Greenfield JG (1954) The spino-cerebellar degenerations. Blackwell, OxfordGoogle Scholar
  16. 16.
    Hedley-Whyte ET, Gilles FH, Uzman BG (1968) Infantile neuroaxonal dystrophy: A disease characterized by altered terminal axons and synaptic endings. Neurology (Minneap) 18:891–906Google Scholar
  17. 17.
    Herman MM, Huttenlocher PR, Bensch KG (1969) Electronmicroscopic observations in infantile neuroaxonal dystrophy. Arch Neurol (Chic) 20:19–34Google Scholar
  18. 18.
    Jacobs JM, Carmichael N, Cavanagh JB (1975) Ultrastructural changes in the dorsal root and trigeminal ganglion of rats poisoned with methylmercury. Neuropathol Appl Neurobiol 1:1–19Google Scholar
  19. 19.
    Jacobs JM, Carmichael N, Cavanagh JB (1972) Ultrastructural changes in the nervous system of rabbits poisoned with methylmercury. Toxicol Appl Pharmacol 39:249–261Google Scholar
  20. 20.
    Jones AL, Fawcett DW (1966) Hypertrophy of the agranular endoplasmic reticulum in hamster liver induced by phenobarbital (With a review of the functions of this organelle in liver). J Histochem Cytochem 14:215–232Google Scholar
  21. 21.
    Lampert PW, Blumberg JM, Pentschew A (1964) An electronmicroscopic study of dystrophic axons in the gracile and cuneate nuclei of vitamin-E-deficient rats. J Neuropathol Exp Neurol 23:60–77Google Scholar
  22. 22.
    Lampert P, Cressman M (1964) Axonal degeneration in the dorsal columns of the spinal cord of adult rats. An electron microscopic study. Lab Invest 13:825–839Google Scholar
  23. 23.
    Lentz TL (1967) Fine structure of nerves in the regenerating limb of the Newt Triturus. Am J Anat 121:647–670Google Scholar
  24. 24.
    Offord K, Ohta M, Oenning RF, Dyck PJ (1974) Method of morphometric evaluation of spinal and autonomic ganglia. J Neurol Sci 22:65–71Google Scholar
  25. 25.
    Ohnishi A, Schilling K, Brimijoin WS, Lambert EH, Fairbanks VF (1977) Lead neuropathy. (1) Morphometry, nerve conduction and choline acetyltransferase transport: New findings of endoneurial edema associated with segmental demyelination. J Neuropathol Exp Neurol 36:499–518Google Scholar
  26. 26.
    Prineas J (1969) The pathogenesis of dying-back polyneuropathies. Part I. An ultrastructural study of experimental triorthocresyl phosphate intoxication in the cat. J Neuropathol Exp Neurol 28:571–597Google Scholar
  27. 27.
    Prineas J (1969) The pathogenesis of dying-back polyneuropathies. Part II. An ultrastructural study of experimental acrylamide intoxication in the cat. J Neuropathol Exp Neurol 28:598–621Google Scholar
  28. 28.
    Schaumburg HH, Wiśniewski H, Spencer PS (1974) Ultrastructural studies of the dyring-back process. I. Peripheral nerve terminal and axon degeneration in systemic acrylamide intoxication. J Neuropathol Exp Neurol 33:260–284Google Scholar
  29. 29.
    Schoental R, Cavanagh JB (1977) Mechanisms involved in the “dying-back” process — an hypothesis implicating coenzymes. Neuropathol Appl Neurobiol 3:145–157Google Scholar
  30. 30.
    Shimono M, Otha M, Asada M, Kuroiwa Y (1976) Infantile jeuroaxonal dystrophy: Ultrastructural study of peripheral nerve. Acta Neuropathol (Berl) 36:71–79Google Scholar
  31. 31.
    Spencer PS, Schaumburg HH (1973) An ultrastructural study of the normal feline pacinian corpuscle. J Neurocytol 2:217–235Google Scholar
  32. 32.
    Spencer PS, Schaumburg HH (1977) Central-peripheral distal axonopathy — The pathology of dying-back polyneuropathies. Prog Neuropathol 3:253–295Google Scholar
  33. 33.
    Spencer PS, Schaumburg HH (1977) Ultrastructural studies of the dying-back process. III. The evolution of experimental peripheral giant axonal degeneration. J Neuropathol Exp Neurol 36:276–299Google Scholar
  34. 34.
    Spencer PS, Schaumburg HH (1977) Ultrastructural studies of the dying-back process. IV. Differential vulnerability of PNS and CNS fibers in experimental central-peripheral distal axonopathies. J Neuropathol Exp Neurol 36:300–320Google Scholar
  35. 35.
    Spencer PS, Sabri MI, Schaumburg HH, Moore CL (1979) Does a defect of energy metabolism in the nerve fiber underlie axonal degeneration in polyneuropathies? Ann Neurol 5:501–507Google Scholar
  36. 36.
    Tsukita S, Ishikawa H (1976) Three-dimensional distribution of smooth endoplasmic reticulum in myelinated axons. J Electron Microsc 25:141–149Google Scholar

Copyright information

© Springer-Verlag 1980

Authors and Affiliations

  • Akio Ohnishi
    • 1
  • Masato Ikeda
    • 2
  1. 1.Department of Neuropathology, Neurological InstituteKyushu UniversityFukuokaJapan
  2. 2.Department of Public Health, Faculty of MedicineKyushu UniversityFukuokaJapan

Personalised recommendations