The excitation and depression of spinal neurones by ibotenic acid.

Abstract

The firing of spinal interneurons and Renshaw cells by microelectrophoretic (.+-.)-ibotenate, which was approximately 8 times more active as an excitant than L-glutamate, was followed by prolonged depression of the sensitivity of the neurons to excitant amino acids and acetylcholine. 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. When administered electrophoretically for 6 min, muscimol, a potent GABA agonist, reduced neuronal excitability for prolonged periods; this effect was also prevented by bicuculline methochloride. The depression of neuronal excitability produced by GABA, taurine, isoguvacine or 3-aminopropane sulfonate, ejected for periods of 5-6 min, recovered rapidly. Ibotenate is perhaps converted in vivo to muscimol or a related compound which has a prolonged, bicuculline-sensitive depressant action on the excitability of neurons.