Effects of intracellular potassium and sodium injections on the inhibitory postsynaptic potential

Abstract

Two barrels of double microelectrodes have been filled with different salts so that the electrophoretic injection of Na$^{+}$ and K$^{+}$ ions could be investigated in alternating sequence on the same motoneuron in the cat spinal cord. The effects of these injections on the mechanism generating the IPSP were evaluated by determining the equilibrium potential for the IPSP (the E$_{IPSP}$), i.e. the membrane potential at which the IPSP is zero. Such determinations have been made every 5 to 10 s after ion injections and have provided the most direct evidence of the ionic mechanism generating the IPSP. Comparison of the Na$^{+}$ and K$^{+}$ ion injections shows that the former injection always displaced the E$_{IPSP}$ much farther in the depolarizing direction and that recovery was much slower, with a half-time of 70 to 120 s, in contrast to about 20 s after the K$^{+}$ injection. In the discussion and evaluation of these results it was postulated that almost all of the displacement of the E$_{IPSP}$ in the depolarizing direction was due to the increased intracellular Cl$^{-}$ concentration, the (Cl$^{-}$)$_{i}$. Under normal conditions a high (Cl$^{-}$)$_{i}$ declines by diffusional exchange across the cell membrane with a half-time of about 20 s, but this decline is much slower when the internal potassium is depleted. An explanation of this difference will be given in the following paper.