Two kinds of recurrent inhibition of cat spinal alpha‐motoneurones as differentiated pharmacologically.

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Abstract
The effects of i.v. administration of the glycine-antagonist strychnine nitrate and the GABA-antagonists bicuculline hydrochloride and picrotoxin on the recurrent inhibition of lumbosacral .alpha.-motoneurons were studied in cats anesthetized with pentobarbitone sodium. As revealed from both monosynaptic reflex experiments and intracellular recordings, each of the drugs generally reduced, but rarely abolished, the recurrent inhibition. The amount of reduction was more or less identical for bicuculline and picrotoxin. By applying de- and hyperpolarizing currents intracellularly it was shown that both the strychnine-resistant and bicuculline/picrotoxin-resistant recurrent inhibitory potentials were genuinely post-synaptic in nature. The strychnine-resistant part of the recurrent inhibition had a later maximum and a longer duration than the part which was resistant to bicuculline/picrotoxin. The time course of the strychnine-resistant recurrent inhibition was more or less identical to that of the bicuculline/picrotoxin-sensitive recurrent inhibition. The bicuculline/picrotoxin-resistant recurrent inhibition was blocked by strychnine, and vice versa, the strychnine-resistant recurrent inhibition was blocked by bicuculline/picrotoxin. The combined administration of strychnine and bicuculline/picrotoxin always resulted in a virtual abolition of the recurrent inhibitory effects. The values for central delay suggested that both the strychnine-resistant and bicuculline/picrotoxin-resistant inhibitions were mediated via disynaptic pathways. Both glycine and GABA evidently act as transmitter substances of Renshaw cells in mediating recurrent inhibition to .alpha.-motoneurons. No organizational pattern of the 2 types of recurrent inhibition based on motor pool category or motor unit type could be detected.