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

Accession number;05A0184617
Title;Effects of N-Methyl-D-Aspartate, Glutamate, and Glycine on the Dorsal Column Axons of Neonatal Rat Spinal Cord: In Vitro Study
Author; MATSUMOTO M (State Univ. New Jersey, New Jersey, Usa) SASAKI T (State Univ. New Jersey, New Jersey, Usa) NAGASHIMA H (State Univ. New Jersey, New Jersey, Usa) AHN E S (State Univ. New Jersey, New Jersey, Usa) YOUNG W (State Univ. New Jersey, New Jersey, Usa) KODAMA N (Fukushima Medical Univ., Fukushima)
Journal Title;Neurol Med Chir
Journal Code:Z0762A
ISSN:0470-8105
VOL.45;NO.2;PAGE.73-81(2005)
Figure&Table&Reference;FIG.3, TBL.1, REF.45
Pub. Country;Japan
Language;English
Abstract;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 .MU.M) significantly increased CAP amplitude in PN 0-6 cords by 21.5 .+-. 9.2% (mean .+-. standard error of the mean, p < 0.001, n = 8) and in PN 7-14 cords by 6.7 .+-. 6.6% (p < 0.001, n = 10). NMDA (10 .MU.M) significantly increased the CAP amplitude by 6.3 .+-. 2.9% in PN 0-6 cords (p < 0.01, n = 10). The increase of CAP amplitude induced by NMDA (100 .MU.M) in PN 0-6 cords was significantly greater than that in PN 7-14 cords (p < 0.005). Glutamate (100 .MU.M) significantly increased the CAP amplitude by 8.8 .+-. 8.1% in PN 0-6 cords (p < 0.001, n = 29) and 6.7 .+-. 7.5% in PN 7-14 cords (p < 0.01, n = 14), and glutamate (10 .MU.M) significantly increased by 6.3 .+-. 2.9% in PN 0-6 cords (p < 0.01, n = 21). The amplitudes induced by glutamate (100 .MU.M or 10 .MU.M) did not significantly differ between PN 0-6 and PN 7-14 cords. Application of glycine (100 .MU.M) did not significantly alter CAP amplitudes induced by NMDA (100 .MU.M or 10 .MU.M) and glutamate (100 .MU.M or 10 .MU.M). 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. (author abst.)
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