Summary
Spinal neurones from the 6th and 7th lumbar segments of cats were recorded intracellularly. Glutamic acid (GLUT) was applied extracellularly by means of the microelectrophoretic technique from another parallel electrode and caused, in almost all cells, a depolarization of the cell in association with conductance change. In some cases, initial depolarization occurred with no detectable conductance change.
Motoneurones could not be brought to continous firing except in two cases. High “doses” of GLUT (up to 2000 nA) caused maximal depolarization up to-30 mV (range -32 mV to -24 mV). The soma conductance was increased at this time by about 75% (range 60–90%).
The spikes and both EPSPs and IPSPs were attenuated by shunting. The peak latency of the EPSP was shortened. Spikes evoked by different EPSPs were found to exhibit different sensitivity to GLUT. Ocassionally, the IPSPs were initially increased following depolarization. The IPSP was sometimes reversed after the termination of GLUT application. The after-hyperpolarization following the antidromic spike of some motoneurones was converted into an after-depolarization for 1–2 min.
The present data show that the following criteria for an excitatory transmitter can be met by GLUT; (1) strong depolarizing action presumably associated with Na+ influx, (2) an associated conductance change and (3) an equilibrium potential. It could not be proven that the EPSP reversal point and the equilibrium potential for GLUT are the same.
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Zieglgänsberger, W., Puil, E.A. Actions of glutamic acid on spinal neurones. Exp Brain Res 17, 35–49 (1973). https://doi.org/10.1007/BF00234562
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DOI: https://doi.org/10.1007/BF00234562