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Electrophysiological and morphological correlates of axotomy-induced deafferentation of the goldfish Mauthner cell

Academic Article
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Overview

authors

  • Wood, Malcolm R.
  • Faber, D. S.

publication date

  • February 1986

journal

  • Journal of Comparative Neurology  Journal

abstract

  • Axotomy-induced changes in afferent synapses to the goldfish Mauthner cell have been analyzed with intracellular recordings and with electron microscopy. The studies encompassed 7-208 days after cervical spinal cord transection. The physiological findings suggest a persistent and specific reduction in excitatory chemical inputs to the soma and proximal lateral dendrite, with no changes in somatic inhibition or in the electrotonic and chemical inputs to the more distal regions of the lateral dendrite. Corroborative morphological evidence includes swelling of the M-cell soma, as indicated by a 35% increase in the length of its minor diameter, an increased spacing and a quantitatively lower density of terminals on the soma, and the appearance of astrocytic processes partially or completely engulfing the terminals in that region. Similar changes were observed on the inferior dendrites projecting from the ventral surface of the soma, although these dendrites do not exhibit the chromatolytic changes observed at the soma. In contrast, there are no noticeable changes in either the synaptic investment of the lateral dendrite or its ultrastructure. Quantitative and qualitative data support the conclusion that there is a restricted and specific reduction in the proximal excitatory inputs to the M-cell. The evidence also suggests that electrotonic junctions between afferents and the M-cell remain intact, functionally and structurally.

subject areas

  • Afferent Pathways
  • Animals
  • Dendrites
  • Denervation
  • Endoplasmic Reticulum
  • Goldfish
  • Intercellular Junctions
  • Membrane Potentials
  • Microscopy, Electron
  • Nerve Endings
  • Neuroglia
  • Neurons
  • Synapses
  • Time Factors
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Identity

International Standard Serial Number (ISSN)

  • 0021-9967

Digital Object Identifier (DOI)

  • 10.1002/cne.902440402

PubMed ID

  • 3958235
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Additional Document Info

start page

  • 413

end page

  • 429

volume

  • 244

issue

  • 4

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