Localized ablation of olfactory receptor neurons induces both localized regeneration and widespread replacement of neurons in spiny lobsters.

نویسندگان

  • Paul J H Harrison
  • Holly S Cate
  • Charles D Derby
چکیده

The peripheral olfactory system of the spiny lobster Panulirus argus--located on paired antennules--undergoes continual postembryonic development. This process includes continuous addition of olfactory receptor neurons (ORNs) related to indeterminate growth, continuous replacement, and regeneration when necessitated by damage. We have shown previously that new olfactory tissue is continually added to the proximal margin of these populations, called the proximal proliferation zone (PPZ). Here, we show that focal damage to mature portions of the olfactory system causes localized degeneration of ORNs over 1-10 days after damage. Studies using the cell proliferation marker 5-bromo-2'-deoxyuridine show that localized degeneration was followed by rapid and localized regeneration of olfactory tissue. Rapidly dividing cells were recorded up to 40 days after damage, with regeneration of ORN clusters complete within 80 days. Focal damage appeared to stimulate widespread cell replacement (cell death and proliferation) within mature, undamaged ORN clusters. This response was observed in ORN clusters outside the damaged zone, including mature clusters in the contralateral antennule. The degree of widespread cell replacement was less than local repair after local damage, but it increased with more extensive damage. However, changes in on-going proliferation in the PPZ were not detected, at least not 20 days or longer after damage, suggesting damage-induced widespread proliferation may be specific to mature populations of ORNs. We speculate that localized regeneration involves activity of resident precursor cells not destroyed by the ablation and that unidentified regulatory signals released in response to localized damage induce widespread ORN replacement.

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عنوان ژورنال:
  • The Journal of comparative neurology

دوره 471 1  شماره 

صفحات  -

تاریخ انتشار 2004