A microelectrophoretic and electrophysiological study on normal and Jimpy mutant mouse spinal neurones and reflexes

Summary This is the first detailed report of microiontophoretic experiments on normal and Jimpy mutant mouse spinal cords. From these experiments it is clear that spinal neurones in this species respond to mono- and dicarboxylic amino acids in essentially the same manner as do spinal neurones of other mammals. Furthermore, the sensitivity of glycine and GABA-induced responses in the normal mouse to strychnine and bicuculline are also qualitatively similar. However, it appears that the glycine receptor on mouse spinal neurones is somewhat more sensitive to bicuculline than similar receptors in the rat and cat. The results also suggest that the activity of uptake systems for l -glutamate and l -aspartate are essentially the same in the normal and Jimpy mutant mouse, and the rat. Thus it appears that oligodendroglia do not play a major role in the inactivation and removal of the amino acid neurotransmitter candidates, l -glutamate and l -aspartate. The effective removal of kainate from the neuronal environment is much more rapid in the Jimpy than the normal, suggesting that the lipophilic region of this compound attaches to the myelin in the normal mouse and impedes its removal. The evidence also suggests that there is no active uptake mechanism for kainate. The only overt electrophysiological abnormality which could be detected in the Jimpy in this study was a reduced conduction velocity.