Early loss of synaptic protein PSD-95 from rod terminals of rhodopsin P347L transgenic porcine retina

Scott M. Blackmon, You Wei Peng, Ying Hao, Suk Jin Moon, Leonardo B. Oliveira, Misako Tatebayashi, Robert M. Petters, Fulton Wong

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Retinitis pigmentosa (RP), a type of retinal degeneration involving first rod and then slow cone photoreceptor degeneration, can be caused by any of a number of mutations in different genes. In the cases of mutations affecting rod-specific genes such as rhodopsin, it is unclear how the mutations may cause degeneration of cones. We have used the porcine retina, which is rod-dominated and has an abundance of cones, to study the mutation-induced changes in both rod and cone photoreceptors. Like patients with the same mutation, rhodopsin P347L transgenic swine manifest rod-cone degeneration. In addition, the rod bipolar cells fail to form synaptic connections with rods; instead, they form ectopic synapses with cones. The mechanisms that prevent the formation of the rod-rod bipolar cell synaptic connection are not known. We used specific antibodies and immunocytochemistry to show that the synaptic protein, PSD-95, is present in both normal and transgenic porcine retinas. During neonatal development, however, PSD-95 is lost from rod terminals in the transgenic swine. This loss is virtually complete (90%) by postnatal day 5, at a time when greater than 80% of rod cell bodies still remain. Furthermore, the remaining rods retain their outer segments and their gross morphology appears relatively normal. In contrast, PSD-95 expression continues in cone terminals, even in 10-month-old transgenic swine, where the rods have all disappeared and the cones show signs of severe degeneration. These results suggest that loss of PSD-95 may not be a general consequence of the deteriorating cell. Rather, the very early and selective loss of PSD-95 from the rod terminals may be causally related to the absence of rod-rod bipolar cell synapses in the rhodopsin P347L transgenic retina. Copyright (C) 2000 Elsevier Science B.V.

Original languageEnglish (US)
Pages (from-to)53-61
Number of pages9
JournalBrain Research
Volume885
Issue number1
DOIs
StatePublished - Dec 1 2000

Fingerprint

Rhodopsin
Retina
Swine
Mutation
Retinal Cone Photoreceptor Cells
Proteins
Synapses
Retinal Rod Photoreceptor Cells
Retinal Degeneration
Vertebrate Photoreceptor Cells
Retinitis Pigmentosa
Genes
Immunohistochemistry
Antibodies

Keywords

  • PSD-95
  • Retinal degeneration
  • Retinitis pigmentosa

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

Cite this

Blackmon, S. M., Peng, Y. W., Hao, Y., Moon, S. J., Oliveira, L. B., Tatebayashi, M., ... Wong, F. (2000). Early loss of synaptic protein PSD-95 from rod terminals of rhodopsin P347L transgenic porcine retina. Brain Research, 885(1), 53-61. https://doi.org/10.1016/S0006-8993(00)02928-0

Early loss of synaptic protein PSD-95 from rod terminals of rhodopsin P347L transgenic porcine retina. / Blackmon, Scott M.; Peng, You Wei; Hao, Ying; Moon, Suk Jin; Oliveira, Leonardo B.; Tatebayashi, Misako; Petters, Robert M.; Wong, Fulton.

In: Brain Research, Vol. 885, No. 1, 01.12.2000, p. 53-61.

Research output: Contribution to journalArticle

Blackmon, SM, Peng, YW, Hao, Y, Moon, SJ, Oliveira, LB, Tatebayashi, M, Petters, RM & Wong, F 2000, 'Early loss of synaptic protein PSD-95 from rod terminals of rhodopsin P347L transgenic porcine retina', Brain Research, vol. 885, no. 1, pp. 53-61. https://doi.org/10.1016/S0006-8993(00)02928-0
Blackmon, Scott M. ; Peng, You Wei ; Hao, Ying ; Moon, Suk Jin ; Oliveira, Leonardo B. ; Tatebayashi, Misako ; Petters, Robert M. ; Wong, Fulton. / Early loss of synaptic protein PSD-95 from rod terminals of rhodopsin P347L transgenic porcine retina. In: Brain Research. 2000 ; Vol. 885, No. 1. pp. 53-61.
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