Comments on "Cortical activity and the explanatory gap".
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Biomedical subjects
Publications and source records attributed to T S Schilhab.
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The time course of the formation of synaptic long-term depression was analysed in neurons of Helix pomatia. Polysynaptic excitatory postsynaptic potentials were evoked in identified neurons by stimulation of the right pallial nerve. First, synaptic depression was observed during four consecutive series of excitatory postsynaptic potentials spaced by either 2, 10 or 60 min in the presence and absence of compounds inhibiting protein synthesis. Inhibition of RNA translation (but not of transcription) reduced the increasing depression of series spaced by 10 and 60 min but not by 2 min. This demonstration of translation-dependent depression present only 10 min after a previous excitatory postsynaptic potential series was analysed further by observations of the time course of excitatory postsynaptic potential recovery from short-term depression in experiments with intact versus inhibited protein synthesis. When synthesis was inhibited, recovery occurred along a double-exponential trajectory. However, when synthesis was intact, the exponential recovery was interrupted discontinuously 6-10 min after a series of excitatory postsynaptic potentials by the onset of a spontaneous and increasing depression lasting for at least 12 h. Puromycin, anisomycin and actinomycin D were used as inhibitors not affecting the short-term properties of excitatory postsynaptic potentials. Experiments with camptothecin, on the other hand, revealed that this inhibitor enhanced excitatory postsynaptic potential amplitudes and reduced their short-term depression. It is concluded that long-term depression, depending upon de novo protein synthesis, was initiated only 10 min after a series of excitatory postsynaptic potentials. Evidence was obtained indicating that this early initiated protein synthesis circumvented the transcription processes within the cell nuclei.
Kinetic properties of synaptic depression were analysed for excitatory postsynaptic potentials in neuron number 3 in the right pallial ganglion of Helix pomatia. It was observed that long-term depression did not only suppress the amplitudes of excitatory postsynaptic potentials but also changed the kinetics of short-term depression. Early during each experiment (before the induction of long-term depression), the degree of short-term depression was inversely related to the frequency of excitatory postsynaptic potentials (contrary to most earlier reports). Later in the experiments, after the formation of long-term depression induced by four spaced excitatory postsynaptic potential series, the inverse frequency dependency had changed into a direct proportionality between short-term depression and frequency. This change was associated with, and could be at least partially explained by, an alternation of recovery from short-term depression induced by long-term depression: early in experiments, recovery showed a transient phase of large recovery between excitatory postsynaptic potentials separated by 3 to 45 s. After the induction of long-term depression, this large and transient recovery was absent. The relationship between the amount of long-term depression formed and the number of preceding excitatory postsynaptic potentials inducing the depression was analysed, and it was observed that a significant long-term depression was present 10 min after only six excitatory postsynaptic potentials. The results point towards the implication that many previous investigations of the kinetics of short-term depression observed in experiments involving a high number of excitatory postsynaptic potentials have been performed under the influence of variable degrees of long-term depression. Since long-term depression (at least in Helix) induced substantial alterations of the kinetic properties of short-term depression, such changes may have significantly influenced the conclusions of earlier reports.