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OPA1 expression in the normal rat retina and optic nerve
Author(s) -
Ju WonKyu,
Misaka Takumi,
Kushnareva Yulia,
Nakagomi Saya,
Agarwal Neeraj,
Kubo Yoshihiro,
Lipton Stuart A.,
BossyWetzel Ella
Publication year - 2005
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.20586
Subject(s) - retina , biology , optic nerve , inner plexiform layer , ganglion , ganglion cell layer , inner nuclear layer , microbiology and biotechnology , retinal ganglion cell , giant retinal ganglion cells , outer plexiform layer , neuroscience , retinal , anatomy , biochemistry
Autosomal dominant optic atrophy (DOA) is the most common form of hereditary optic neuropathy. DOA presents in the first decade of life and manifests as progressive vision loss. In DOA retinal ganglion cells and the optic nerve degenerate by an unknown mechanism. The gene mutated in DOA, Optic Atrophy Type 1 (OPA1), encodes a dynamin‐related GTPase implicated in mitochondrial fusion and maintenance of the mitochondrial network and genome. Here, we determine which cell types in the normal retina and the optic nerve express OPA1. In the normal rat retina, OPA1 is expressed in the ganglion cell layer as well as in the outer plexiform layer, the inner nuclear layer, and the inner plexiform layer. In the ganglion cell layer, OPA1 is expressed predominantly in retinal ganglion cells. By contrast, OPA1 protein is low or undetectable in astrocytes and oligodendrocytes of the optic nerve. Additionally, OPA1 protein is present in axonal mitochondria. Last, OPA1 expression is present in mitochondria of processes and cell bodies of purified retinal ganglion cells and of the RGC‐5 cell line. Thus, OPA1 is predominantly expressed in retinal ganglion cells of the normal rat retina and axons of the optic nerve. These findings may explain the selective vulnerability of retinal ganglion cells to OPA1 loss of function. J. Comp. Neurol. 488:1–10, 2005. © 2005 Wiley‐Liss, Inc.