The effects of potassium channel blocking agents on the responses of in vitro frog motoneurones to glutamate and other excitatory amino acids: an intracellular study.

Intracellular recordings were obtained from motoneurones of the slice preparation of the in vitro frog spinal cord to assess the participation of K+ channels in the generation of amino acid-induced excitation. The amino acids were applied by fast superfusion and at low temperature to reduce their uptake processes. Intracellular Cs+, bath-applied tetraethylammonium or 4-aminopyridine prolonged the spike and blocked its afterhyperpolarizations. Tetraethylammonium and 4-aminopyridine enhanced the synaptic activation of motoneurones which could be abolished by including Mn2+ in the superfusion fluid. Mn2+ reduced the duration of action potentials already prolonged by 4-aminopyridine but appeared to cause plateaus to develop on tetraethylammonium-prolonged spikes. The hypothesis that amino acids depolarize motoneurones by closing K+ channels was tested by observing the effects of K+ channel blocking agents on amino acid responses. Neither tetraethylammonium nor 4-aminopyridine reduced the excitatory depolarizations evoked by glutamate, N-methyl-D-aspartate, quisqualate or DL-homocysteate. Intracellular Cs+ blocked responses to amino acids irrespective of their receptor preference; an action which has been interpreted as non-specific.