Methylcobalamin (CH3-B12) enhanced postsynaptic field potential (PSP) elicited from hippocampal slices (around 180% at a maximum), lasting more than 1 h after washing out, while it had no effect on antidromic spike potential (AP). By contrast, cyanocobalamin containing CN- instead of CH3- showed no enhancement in the PSP amplitude, suggesting that CH3- plays an important role for the PSP enhancement by methylcobalamin. The treatment with N-methyl-D-aspartate (NMDA) receptor specific antagonist, DL-2-amino-5-phosphonovaleric acid (APV) inhibited methylcobalamin-induced PSP enhancement by 50%, suggesting that NMDA receptor is partially relevant to the formation of this enhancement. Glutamate release from electrically stimulated slices was not enhanced by the treatment with methylcobalamin, suggesting that methylcobalamin affects the postsynaptic sites in hippocampal neurons. In whole cell voltage clamp recordings using cultured hippocampal neurons, methylcobalamin increased the currents elicited by NMDA time-dependently. These results may indicate that CH3- is required to modulate the PSP amplitude at the postsynaptic site and at least, NMDA receptor is involved in the formation of long-lasting PSP potentiation induced by methylcobalamin.
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