Effects of retinal lesions upon the distribution of nicotinic acetylcholine receptor subunits in the chick visual system

Academic Article


  • Immunohistochemistry was used in this study to evaluate the effects of retinal lesions upon the distribution of neuronal nicotinic acetylocholine receptor subunits in the chick visual system. Following unilateral retinal lesions, the neuropil staining with an antibody against the β2 receptor subunit, a major component of α‐bungarotoxin‐insensitive nicotinic receptors, was dramatically reduced or completely eliminated in all of the contralateral retinorecipient structures. On the other hand, neuropil staining with antibodies against two α‐bungarotoxinsensitive receptor subunits, α7 and α8, was only slightly affected after retinal lesions. Decreased neuropil staining for α7‐like immunoreactivity was only observed in the nucleus of the basal optic root and layers 2–4 and 7 of the optic tectum. For α8‐like immunoreactivity, slight reduction of neuropil staining could be observed in the ventral geniculate complex, griseum tecti, nucleus lateralis anterior, nucleus lentiformis mesencephali, layers 4 and 7 of the tectum, and nucleus suprachiasmaticus. Taken together with previous data on the localization of nicotinic receptors in the retina, the present results indicate that the β2 subunit is transported from retinal ganglion cells to their central targets, whereas the α7 and α8 subunit immunoreactivity appears to have a central origin. The source of these immunoreactivities could be, at least in part, the stained perikarya that were observed to contain α7 and α8 subunits in all retinoreceipient areas. In agreement with this hypothesis, the β2 subunit of the nicotinic acetylcholine receptors was not frequently found in perikarya of the same areas. © 1994 Wiley‐Liss, Inc. Copyright © 1994 Wiley‐Liss, Inc.
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    Author List

  • Britto LRG; Torrao AS; Hamassaki‐Britto DE; Mpodozis J; Keyser KT; Lindstrom JM; Karten HJ
  • Start Page

  • 473
  • End Page

  • 484
  • Volume

  • 350
  • Issue

  • 3