On the postsynaptic action of glutamate in frog spinal motoneurons.

In the isolated frog spinal cord depolarization of motoneurons (MNs) induced by glutamate (GLUT) was not accompanied by measurable changes of neuronal input resistance when chemical synaptic transmission was blocked by Mn2+ or Mg2+. The GLUT depolarization was, however, paralleled by a considerable increase in K+ in the extracellular space. To clarify, whether the GLUT depolarization was exclusively due to a reduction of the transmembrane K+ gradient or whether ion conductances not detectable by measurements of neuronal input resistance were involved, membrane potential (MP) was plotted semilogarithmically versus extracellular K+ activity (aKe+). During experimental elevation of aKe+ the function delta MP/dec. delta aKe+ was found to agree fairly with the Nernst equation. The slope of this function was much steeper during GLUT superfusion, indicating an influx of positive ions. The elevation of aKe+ during the GLUT action can mimic postsynaptic effects by release of transmitter from presynaptic terminals synapsing with the recorded cell. In vivo preparations do not allow blockade of chemical synaptic transmission. Therefore, it is impossible to decide, whether the recorded cell is depolarized either postsynaptically by GLUT or by K+ release from surrounding GLUT sensitive cells. As an experimental proof of the postsynaptic GLUT action is not feasible in such preparations, the ubiquitous action of GLUT in the CNS may have been overestimated.