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The possible role of glutamate, aspartate, sulfur-containing excitatory amino acids and gamma-glutamyl peptides as major transmitters in the rat optic nerve was evaluated. Four days following optic nerve lesion the K(+)-evoked Ca(2+)-dependent glutamate release was reduced to 31 +/- 16% (+/- S.D., n = 9) comparing release from slices of the denervated (contralateral to the lesion) and non-denervated (ipsilateral) superior colliculus, indicative of a major transmitter function for glutamate. However, significant decreases in glutamate release could not be detected seven days following the lesion (n = 5). Other studies have shown that optic nerve denervation induce formation of synapses of non-retinal origin and cause other cellular changes which may reduce the effect of deafferentation on glutamate release after 7 days. No significant change was observed in aspartate release following the lesion. The concentrations of cysteine sulfinate, cysteate, homocysteine sulfinate, homocysteate and O-sulfo-serine in the optic layers of the superior colliculus were below 1 nmol/g tissue (n = 6). Theoretical considerations indicate that this level is too low for a function of any of these as a major optic nerve transmitter. All postsynaptic components in the rat superior colliculus response, evoked by electrical optic nerve stimulation, were reduced by kynurenate (1-10 mM), a broad spectrum glutamate-receptor antagonist. The study gives further support for the view that glutamate is a major transmitter in the rat optic nerve.
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