抄録
We previously reported that arachidonic acid (AA) diet preserved the degree of LTP thus the synaptic plasticity was maintained in the aged rats at the hippocampal synapse as same as young control. One of the plausible mechanism to preserve LTP is switching the contribution of calcium entry from N-methyl-D-aspartate (NMDA) receptor channel to voltage dependent calcium channel (VDCC). We examine whether the primary calcium entry channel altered during aging and AA diet complemented the degraded calcium entry channel. Rats of 24 months old administered AA ester (old arachidonic group: OA) or control diet (old control group: OC) for at least 3.5 months or of 2 months old supplemented with control diet (young control group: YC) were used to record LTP from hippocampal slice of 300 μm with 6 x 6 multi-electrode-array. LTP was induced by θ-burst stimulation. Ca2+ channel was discriminated by perfusion of ACSF containing APV in 50 μM and nifedipin of 10 μM. VDCC dependent LTP (VDCC-LTP) tended to be greater than NMDA dependent LTP (NMDA-LTP) in OC compared with YC, whereas NMDA-LTP seemed to be more prominent than VDCC-LTP in OA as YC. The primary source of calcium entry from outside of a cell was predominant through NMDA receptor channel rather than VDCC in OA. This raised the possibility that oxygenated unsaturated fatty acid in the membrane of hippocampal neuron was complemented with AA diet in aged animal. [Jpn J Physiol 54 Suppl:S226 (2004)]
