ABSTRACT
In hippocampus, numerous studies have shown that N-methyl-D-aspartate (NMDA) receptors are essential for the initiation of long-term potentiation (LTP), whereas the expression of LTP is primarily mediated by the phosphorylation of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors and the increased insertion of postsynaptic AMPA receptors. However, in recent years there is also evidence that NMDA receptor channels contribute to the expression of LTP under physiological conditions. It was examined whether NMDA receptor channels contributed to the expression of LTP of C-fiber evoked field potentials in rat spinal dorsal horn by intravenous or spinal application of NMDA receptor antagonists after the establishment of LTP. It was found that MK 801 (a non-competitive NMDA receptor antagonist) at dose of 0.1 mg/kg (iv) had no effect on the spinal LTP and at the dose of 0.5 mg/kg depressed the LTP significantly. However, the inhibitory effect of MK 801 at higher dose (1.0 mg/kg)was not different from that produced by the dose of 0.5 mg/kg. The similar inhibitory effect on spinal LTP was also observed, when MK 801 was applied locally at the recording segments of spinal cord. To confirm the above results, a competitive NMDA receptor antagonist AP V was tested. Spinal application of AP V at a concentration of 100 μmol/L produced a stronger depression than at 50 μmol/L. When the concentration of AP V increased to 200 μmol/L, no further depression was observed. These results indicate that NMDA receptor channels are involved in the expression of LTP of C-fiber evoked field potentials in the rat spinal dorsal horn.