Torii N, Tsumoto T, Uno L, Astrelin A V, Voronin L L
Department of Neurophysiology, Biomedical Research Centre, Osaka University Medical School, Japan.
Neuroscience. 1997 Jul;79(2):317-21. doi: 10.1016/s0306-4522(97)00129-2.
Long-term depression together with long-term potentiation represent popular experimental models to study synaptic plasticity. However, analyses of the mechanisms underlying the expression of cortical long-term depression are in their infancy and have been confined to the hippocampus. Short- and long-term depression in neocortex is not well understood. Here we recorded small excitatory postsynaptic potentials intracellularly from rat visual cortex slices. The responses fluctuated between several amplitude levels suggesting a quantal nature of the synaptic transmission. Consistent changes in the quantal steps accompanied neither paired-pulse depression (50 ms interval within the pair) nor long-term depression (induced by 1 Hz, 5 min stimulation). The amplitude distributions shifted to smaller values suggesting decreases in the number of quanta released without essential changes in the postsynaptic quantal efficiency. Both the coefficient of variation of response amplitudes and the number of response failures increased; cases were encountered suggesting a very low release probability after depression. Changes in quantal content estimated from the deconvolution analysis were correlated with the magnitude of depression. The findings suggest predominantly presynaptic loci for expression of short- and long-term neocortical depressions. The likely underlying mechanism is a decrease in transmitter release probability. Long-term depression decreased the probability so strongly that some inputs became virtually silent.
