海馬ＣＡ１・ＣＡ３・歯状回におけるＴＥＡ誘導性シナプス可塑性に対するＧＡＢＡ受容体阻害の効果

抄録

Tetraethylammonium (TEA), a K⁺ channel blocker, reportedly induces long-term potentiation (LTP) of hippocampal CA1 synaptic responses in an NMDA receptor-independent manner. However, the characteristics of TEA-induced plasticity and modulation by inhibitory interneurons at CA3 and the dentate gyrus (DG) remain unclear. This study recorded field EPSPs from CA1, CA3 and DG to examine the involvement of GABAergic modulation in TEA-induced synaptic plasticity at each region. In Schaffer collateral-CA1 synapses, bath application of 25 mM TEA for 12 min induced LTP in the presence and absence of 100 μM picrotoxin (PTX), a GABA_A receptor blocker, suggesting little modulation by interneurons in the CA1 region. In CA3, associational fiber (AF)-CA3 synapses showed TEA-induced LTP regardless of PTX, but mossy fiber (MF)-CA3 synaptic plasticity were influenced by PTX application; TEA-induced LTP was detected only in the absence of PTX. In DG, synaptic plasticity was modulated by GABAergic inputs, but characteristics differed between lateral perforant path (LPP) and medial perforant path (MPP). LPP-DG synapses showed TEA-induced LTP in the presence of PTX, but no changes in the absence of PTX. At MPP-DG synapses, TEA-induced long-term depression (LTD) was observed in the absence of PTX, but no changes were seen in the presence of PTX. This series of results demonstrated that TEA-induced plasticity at perforant path-DG synapses and MF-CA3 synapses are modulated by GABAergic inputs, and that the effects of GABAergic modulation on plasticity are inhibitory (LPP- and MPP-DG) or excitatory (MF-CA3). [J Physiol Sci. 2006;56 Suppl:S85]