STUDIES ON THE IDENTITY OF THE RAT OPTIC-NERVE TRANSMITTER

The possible role of glutamate, aspartate, sulfur-containing excitator y 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 Ca2+-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 dete cted seven days following the lesion (n = 5). Other studies have shown that optic nerve denervation induce formation of synapses of non-reti nal origin and cause other cellular changes which may reduce the effec t of deafferentation on glutamate release after 7 days. No significant change was observed in aspartate release following the lesion. The co ncentrations of cysteine sulfinate, cysteate, homocysteine sulfinate, homocysteate and O-sulfo-serine in the optic layers of the superior co lliculus were below 1 nmol/g tissue (n = 6). Theoretical consideration s indicate that this level is too low for a function of any of these a s a major optic nerve transmitter. All postsynaptic components in the rat superior colliculus response, evoked by electrical optic nerve sti mulation, were reduced by kynurenate (1-10 mM), a broad spectrum gluta mate-receptor antagonist. The study gives further support for the view that glutamate is a major transmitter in the rat optic nerve.