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Effects of denervation upon receptor cell survival and basal cell proliferation in tuberous electroreceptor organs of a weakly electric fish
Author(s) -
Weisleder Pedro,
Lu Ying,
Zakon Harold H.
Publication year - 1994
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.903470406
Subject(s) - biology , electric fish , basal (medicine) , denervation , fish <actinopterygii> , cell , microbiology and biotechnology , anatomy , neuroscience , endocrinology , genetics , fishery , insulin
Weakly electric fish generate electric fields for the purposes of electrolocation and communication. These fields are detected by specialized receptor organs: the tuberous organs. In the present study we investigated the effects of denervation upon receptor cell survival and progenitor (basal) cell proliferation rate. The left, infraorbital, anterior lateral line nerve of brown ghosts ( Apteronotus leptorhynchus ) was sectioned, and the proximal stump was dipped in ricin to prevent regrowth. In groups of four, the animals were given two daily injections of the cell proliferation marker bromodeoxyuridine (BrdU) for 2 days at 1, 2, 3, or 4 weeks following denervation. At the completion of the BrdU injection schedule, a piece of cheek skin, rostroventral to the eye, was removed from the left (denervated) and the right (intact) sides and processed for light microscopy or immunocytochemistry. Our results show: (1) there is progressive receptor cell death and tuberous organ degeneration following denervation; (2) basal cell proliferation increases steadily with time after denervation and tuberous organ degeneration; and (3) despite denervation, some proliferating basal cells differentiate into receptor cells, but these new receptor cells eventually die. These results suggest that innervation is essential for tuberous electroreceptor cell survival and that the rate at which basal cells proliferate is regulated by receptor cell health, locally released factors, or both. © 1994 Wiley‐Liss, Inc.