The ionic mechanism of postsynaptic inhibition in motoneurones of the frog spinal cord.
The ionic mechanism of postsynaptic inhibition in frog spinal motoneurones was studied with conventional and with ion-sensitive microelectrodes. In these neurones the inhibitory postsynaptic potential was depolarizing, its reversal potential being 15 mV less negative than the resting membrane potential. During the inhibitory postsynaptic potential the input resistance of the motoneurones was reduced to 20% of the resting value, indicating a strong increase of membrane conductance. The Cl- equilibrium potential calculated from intra- and extracellular Cl- activity measurements coincided with the reversal potential of the inhibitory postsynaptic potential to within a few millivolts. During repetitive inhibitory postsynaptic activity the intracellular Cl- activity decreased markedly, while the extracellular Cl- activity increased slightly. These changes of intra- and extracellular Cl- activities were no longer found after suppression of the inhibitory postsynaptic potential by strychnine. Blockade of an active, inward-going Cl- transport system in motoneurones by NH+4 led to a shift of the Cl- equilibrium potential and the reversal potential of the inhibitory postsynaptic potential towards the resting membrane potential. After prolonged action of NH+4, the Cl- equilibrium potential approached the membrane potential to within 5 mV, while the reversal potential of the inhibitory postsynaptic potential and resting membrane potential coincided. The difference between Cl- equilibrium potential and membrane potential after blockade of the Cl- pump is traced back to interfering intracellular ions, such as HCO-3 or SO42-, leading to an overestimation of intracellular Cl- activity and to the calculation of an erroneous Cl- equilibrium potential. Inhibitory amino acids like gamma-aminobutyrate or beta-alanine evoked depolarizations with reversal potentials similar to that of the inhibitory postsynaptic potential. These depolarizations were associated with a marked decrease of neuronal input resistance during inhibition. During the actions of these compounds a decrease of intracellular and a small increase of extracellular Cl- activity were found. The activities of other ions (K+, Ca2+ and Na+) did not change significantly, with the exception of extracellular K+ activity, which was slightly increased. Evidence is presented that the inhibitory postsynaptic potential, as well as the depolarizing action of inhibitory amino acids in motoneurones, is the result of an increase in membrane Cl- permeability and an efflux of Cl- from these cells, while other ions do not seem to be involved.
Bührle
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D000596:Amino Acids / Q000494:pharmacology; D000818:Animals; D000870:Anterior Horn Cells / Q000502:physiology*; D002463:Cell Membrane Permeability / Q000187:drug effects; D002712:Chlorides / Q000502:physiology*; D004553:Electric Conductivity; D004594:Electrophysiology; D066298:In Vitro Techniques; D009046:Motor Neurons / Q000502:physiology*; D009433:Neural Inhibition / Q000187:drug effects; D011893:Rana esculenta; D013126:Spinal Nerve Roots / Q000502:physiology; D013569:Synapses / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects
D000596:Amino Acids; D002712:Chlorides