The excitation and depression of spinal neurones by ibotenic acid.

1. The firing of spinal interneurones and Renshaw cells by microelectrophoretic (+/‐)‐ibotenate, which was approximately eight times more active as an excitant than L‐glutamate, was followed by prolonged depression of the sensitivity of the neurones to excitant amino acids and acetylcholine. 2. The depression, which lasted for 15‐‐30 min when ibotenate was ejected for 3‐‐6 min, was blocked by the GABA‐antagonist bicuculline methochloride, and was independent of prior firing since it occurred with subthreshold concentrations of ibotenate and when ibotenate firing had been blocked by DL‐alpha‐aminoadipate. 3. When administered electrophoretically for 5 min, muscimol, a potent GABA agonist, reduced neuronal excitability for prolonged periods and this effect was also prevented by bicuculline methochloride. 4. The depression of neuronal excitability produced by GABA, taurine, isoguvacine or 3‐aminopropane sulphonate, ejected for periods of 5‐‐6 min, recovered rapidly. 5. It is suggested that ibotenate is converted in vivo to muscimol or a related compound which has a prolonged, bicuculline‐sensitive depressant action on the excitability of neurones.