Polysynaptic excitatory pathways induce heterosynaptic depression in the rat auditory cortex.
Short-term plasticity, the effect of a preceding synaptic response on the following response in a pair, in layers II/III of the rat auditory cortex slice after application of repetitive stimuli to layer IV, was investigated using a multichannel extracellular recording system. Paired-pulse depression, which is induced to a moderate degree in standard artificial cerebrospinal fluid, was markedly facilitated in the presence of bicuculline, a GABA(A) receptor antagonist, concurrent with the emergence of a polysynaptic component of the EPSP (polyEPSP) in the first response in a pair. This depression (bicuculline-facilitated synaptic depression, BFSD) was maximal at the minimum interval tested (50 ms), reduced as the interval was increased, and persisted beyond an interval of 2 s. The occurrence of BFSD was dependent on the presence of a polyEPSP regardless of the presence of the monosynaptic component of the EPSP, indicating that BFSD is induced by a heterosynaptic mechanism. D-AP5, an NMDA receptor antagonist, partially eliminated polyEPSPs and reversed BFSD. These results suggest that activation of polysynaptic excitatory pathways induces a heterosynaptic depression in the range of a few seconds and that NMDA receptor activity is involved in this heterosynaptic depression.