Literature DB >> 2708575

Rapid changes in ultrastructure during deafferentation-induced dendritic atrophy.

J S Deitch1, E W Rubel.   

Abstract

This study describes qualitative and quantitative changes in dendritic ultrastructure during the rapid atrophy of nucleus laminaris (NL) dendrites following deafferentation. The dendrites of n. laminaris neurons in the chick auditory system are segregated into dorsal and ventral dendritic tufts, which receive spatially separated innervation from the ipsilateral and contralateral nucleus magnocellularis, respectively. We have previously shown that removing the input to the ventral side of NL results in the rapid atrophy of the ventral dendrites, whereas the nondeafferented dorsal dendrites of the same cells do not change in length. The ultrastructure of NL was examined in normal animals and after deafferentation. Changes in dendritic ultrastructure were not qualitatively apparent 4 hours after deafferentation. Between 12 and 48 hours the cytoplasm of the ventral dendrites became progressively more lucent, and a gap formed in the transition between the soma and ventral dendritic cytoplasm. Many of the dendrite tips, however, appeared normal even 2 days after deafferentation. Degeneration of dendrite plasma membrane was not visible until 2 days after deafferentation. On the other hand, quantitative measurements revealed a 30% decrease in microtubule density in the initial portion of the ventral dendrite by 4 hours, and a 50-60% decrease from 12 to 48 hours after deafferentation. Neurofilament density in the initial ventral dendrites decreased 50% by 12 hours, and 70% by 2 days after deafferentation. Many of the terminals of the severed afferents remained attached to the atrophying dendrite until 2 days after surgery, when they were in advanced stages of degeneration. Glia apparently were not involved in dendrite loss. The implications of these results on the role of cytoskeleton in the production and maintenance of dendritic shape are discussed.

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Year:  1989        PMID: 2708575     DOI: 10.1002/cne.902810207

Source DB:  PubMed          Journal:  J Comp Neurol        ISSN: 0021-9967            Impact factor:   3.215


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