Ipsilateral corticotectal pathway inhibits the formation of long-term potentiation (LTP) in the rat superior colliculus through GABAergic mechanism

The purpose of the present experiments was to clarify the possible mechanism for the depression of long term potentiation (LTP) induction in the superficial gray layer of the rat superior colliculus after optic nerve stimulation. A postsynaptic field potential was recorded in vitro in the superficial gray layer of superior colliculus slices after stimulation of the optic layer. Tetanic optic layer stimulation (50 Hz, 20 s) induced LTP of the postsynaptic field potential elicited in the superficial gray layer. The postsynaptic field potential, with unitary discharges, produced in the superficial gray layer by optic nerve stimulation in vivo was depressed by a conditioning stimulus to the visual cortex. Identical inhibition of the cortical response of the superficial gray layer was produced by optic nerve stimulation. The application of picrotoxin (2.5 mg/kg, i.p.), a GABAA antagonist or methoxypyridoxine (100 mg/kg, i.v.), an anti-glutamate decarboxylase agent which reduces GABA levels, blocked the inhibitory interaction between the optic nerve-superficial gray layer and visual cortex-superficial gray layer. Tetanic optic nerve stimulation (50 Hz, 20 s) failed to induce LTP in the superficial gray layer of the intact rat. LTP was only elicited by tetanic optic nerve stimulation when picrotoxin or methoxypyridoxine was administered prior to the tetanic stimulation and when the ipsilateral visual cortex was removed. These results indicate that GABAergic interneurons in the superficial gray layer activated by corticotectal input, may stop the formation of LTP in the superficial gray layer.