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Intraocular kainic acid injection suppresses fast axonal transport in the developing rat optic nerve
Author(s) -
Riccio R. V.,
Calle R. P.,
Matthews M. A.
Publication year - 1985
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490140306
Subject(s) - kainic acid , optic nerve , axoplasmic transport , axon , retinal , retina , retinal ganglion cell , chemistry , ganglion , endocrinology , medicine , biology , anatomy , biochemistry , glutamate receptor , neuroscience , receptor
A single intraocular injection of 1 or 3 nmol kainic acid (KA) into the right eye of rats aged 5 days postnatal (5 dpn) significantly reduced the incorporation of 3 H‐proline into retinal proteins and suppressed the amount of 3 H‐proline‐labeled materials fast axonally transported in the optic nerve for at least 2 weeks thereafter. Intraocular KA injection within this dose range had no adverse effect on the optic axon population compared to normal nerves determined at 21 dpn; however, doses above 3 nmol (i.e., 6 nmol) caused significant axonal degeneration. Although partially recovered by 21 dpn this effect of KA on protein synthesis and axonal transport suggests that, as in the adult, retinal ganglion cells are also KA‐sensitive during postnatal development.