Abstract
Two forms of short-term synaptic plasticity, paired-pulse depression (PPD) and frequency depression, were prominent in the adult rat geniculo-cortical visual pathway in vivo. Iontophoresis of GABAa receptor antagonist (bicuculline methiodide) or GABAb receptor antagonist (2-hydroxy-saclofen) in the primary visual cortex significantly reduced the short-term synaptic depression. When NMDA or AMPA/kainate receptors were blocked, no obvious change of synaptic depression was observed. Application of high [Ca 2+] enhanced the short-term synaptic depression. Our results suggest that the presynaptic Ca 2+-dependent neurotransmitter depletion and postsynaptic GABAergic inhibition may be crucial for short-term synaptic depression in the geniculo-cortical pathway.
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