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The effects of N-methyl-D-aspartate (NMDA), glutamate, and glycine on the developmental axons of the neonatal rat spinal cord were investigated. Isolated dorsal column preparations from postnatal day (PN) 0 to 14 Long-Evans hooded rats (n = 119) were used in vitro. Compound action potentials (CAPs) were recorded from the cuneate and gracile fasciculi with a glass micropipette electrode. NMDA (100 microM) significantly increased CAP amplitude in PN 0-6 cords by 21.5 +/- 9.2% (mean +/- standard error of the mean, p &lt; 0.001, n = 8) and in PN 7-14 cords by 6.7 +/- 6.6% (p &lt; 0.001, n = 10). NMDA (10 microM) significantly increased the CAP amplitude by 6.3 +/- 2.9% in PN 0-6 cords (p &lt; 0.01, n = 10). The increase of CAP amplitude induced by NMDA (100 microM) in PN 0-6 cords was significantly greater than that in PN 7-14 cords (p &lt; 0.005). Glutamate (100 microM) significantly increased the CAP amplitude by 8.8 +/- 8.1% in PN 0-6 cords (p &lt; 0.001, n = 29) and 6.7 +/- 7.5% in PN 7-14 cords (p &lt; 0.01, n = 14), and glutamate (10 microM) significantly increased by 6.3 +/- 2.9% in PN 0-6 cords (p &lt; 0.01, n = 21). The amplitudes induced by glutamate (100 microM or 10 microM) did not significantly differ between PN 0-6 and PN 7-14 cords. Application of glycine (100 microM) did not significantly alter CAP amplitudes induced by NMDA (100 microM or 10 microM) and glutamate (100 microM or 10 microM). D(-)-2-amino-5-phosphonopentanoic acid (NMDA receptor antagonist) blocked the effects of NMDA and glutamate. These results suggest that NMDA receptor is present on afferent dorsal column axons and may modulate axonal excitability, especially during the 1st week after birth.

Effects of N-Methyl-D-Aspartate, Glutamate, and Glycine on the Dorsal Column Axons of Neonatal Rat Spinal Cord: In Vitro Study