Short‐term facilitation evoked during brief afferent tetani is not altered by long‐term potentiation in the guinea‐pig hippocampal CA1 region

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Abstract
The aim was to examine whether long-term potentiation (LTP) had effects on short-term synaptic plasticity outside those predicted from its effect on single volley-induced responses. Field recordings from the CA1 region of guinea-pig hippocampal slices were used, and short- term plasticity was evoked by five-impulse trains of 20 and 50 Hz. The five-impulse trains were evoked in the presence of D(-)-2-amino-5-phosphonopentanoic acid (D-AP5; 20-50 μm), picrotoxin (100 μm), and 2-OH-saclofen (200 μm), and care was taken to avoid initiation of postsynaptic spike activation. Field responses were thus considered to reflect non-NMDA receptor-mediated activity only, and demonstrated a net facilitation during the trains. The facilitation was found, on average, to be unaffected by LTP, evoked by strong afferent tetanization. This was true also when release probability had been altered either by the adenosine agonist N-cyclohexyladenosine (CHA; 100 nM) or the antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 200 nM). When examined for individual experiments, cases with increases, or decreases, of facilitation following LTP were observed. These deviations showed no relation to initial release probability or to LTP magnitude, and they were also observed in control inputs not subjected to LTP. Impairment of non-NMDA receptor desensitization by cyclothiazide (30 μm) increased facilitation observed during a 50 Hz, but not a 20 Hz, train. LTP had no effect on facilitation, in the presence of this drug, either during 20 or 50 Hz trains. The results suggest that the effect of LTP in the hippocampal CA1 region on non-NMDA receptor-mediated synaptic responses to a brief afferent tetanus does not differ from that on a low-frequency, single volley-induced response. They do not support the notion that LTP is based on changes in release probability of previously active synapses. If LTP is based on recruitment of previously, pre- or postsynaptically, silent synapses, these synapses must have, on average, release characteristics similar to the previously active ones.