Associative spike-timing dependent potentiation of the basal dendritic excitatory synapses in the hippocampus in vivo

Spike timing dependent plasticity in the hippocampus has rarely been studied in vivo. Using extracellular potential and current source density analysis in urethane-anesthetized adult rats, we studied synaptic plasticity at the basal-dendritic excitatory synapse in CA1 after excitation-spike (ES) pairing; E was a weak basal-dendritic excitation evoked by stratum oriens stimulation, and S was a population spike evoked by stratum radiatum apical-dendritic excitation. We hypothesize that positive ES pairing - generating synaptic excitation before a spike - results in long-term potentiation (LTP), while negative ES-pairing results in long-term depression (LTD). Pairing (50 pairs at 5 Hz) at ES intervals of -10 to 0 ms resulted in significant input-specific LTP of the basal-dendritic excitatory sink, lasting 60-120 min. Pairing at +10 to +20 ms ES intervals, or unpaired 5-Hz stimulation, did not induce significant basal-dendritic, or apical-dendritic LTP or LTD. No basal-dendritic LTD was found after stimulation of stratum oriens with 200 pairs of high-intensity pulses at 25 ms interval. Pairing-induced LTP was abolished by pre-treatment with an N-methyl-D-aspartate receptor antagonist 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP), which also reduced spike bursting during 5-Hz pairing. Pairing at 0.5 Hz did not induce spike bursts or basal dendritic LTP. In conclusion, ES pairing at 5 Hz resulted in input-specific basal-dendritic LTP at ES intervals of -10 ms to 0 ms, but no LTD at ES intervals of -20 to 20 ms. Associative LTP likely occurred because of theta-rhythmic coincidence of subthreshold excitation with a backpropagated spike burst, which are conditions that can occur naturally in the hippocampus.

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