Effects of N-methyl-D-aspartate, glutamate, and glycine on the dorsal column axons of neonatal rat spinal cord: In vitro study

Masato Matsumoto, Tatsuya Sasaki, Hiroyasu Nagashima, Edward S. Ahn, Wise Young, Namio Kodama

Research output: Contribution to journalArticle

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 μM) 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 μM) 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 μM) in PN 0-6 cords was significantly greater than that in PN 7-14 cords (p <0.005). Glutamate (100 μM) 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 μM) significantly increased by 6.3 ± 2.9% in PN 0-6 cords (p <0.01, n = 21). The amplitudes induced by glutamate (100 μM or 10 μM) did not significantly differ between PN 0-6 and PN 7-14 cords. Application of glycine (100 μM) did not significantly alter CAP amplitudes induced by NMDA (100 μM or 10 μM) and glutamate (100 μM or 10 μM). 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.

Original languageEnglish (US)
Pages (from-to)73-80
Number of pages8
JournalNeurologia Medico-Chirurgica
Volume45
Issue number2
DOIs
StatePublished - Feb 2005
Externally publishedYes

Fingerprint

N-Methylaspartate
Glycine
Action Potentials
Axons
Spinal Cord
Glutamic Acid
N-Methyl-D-Aspartate Receptors
2-Amino-5-phosphonovalerate
Long Evans Rats
Glass
N-methylglutamate
In Vitro Techniques
Electrodes
Parturition

Keywords

  • Axon
  • Development
  • Glutamate receptor
  • N-methyl-D-aspartate receptor
  • Rat
  • Spinal cord

ASJC Scopus subject areas

  • Clinical Neurology
  • Surgery

Cite this

Effects of N-methyl-D-aspartate, glutamate, and glycine on the dorsal column axons of neonatal rat spinal cord : In vitro study. / Matsumoto, Masato; Sasaki, Tatsuya; Nagashima, Hiroyasu; Ahn, Edward S.; Young, Wise; Kodama, Namio.

In: Neurologia Medico-Chirurgica, Vol. 45, No. 2, 02.2005, p. 73-80.

Research output: Contribution to journalArticle

Matsumoto, Masato ; Sasaki, Tatsuya ; Nagashima, Hiroyasu ; Ahn, Edward S. ; Young, Wise ; Kodama, Namio. / Effects of N-methyl-D-aspartate, glutamate, and glycine on the dorsal column axons of neonatal rat spinal cord : In vitro study. In: Neurologia Medico-Chirurgica. 2005 ; Vol. 45, No. 2. pp. 73-80.
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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 μM) 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 μM) 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 μM) in PN 0-6 cords was significantly greater than that in PN 7-14 cords (p <0.005). Glutamate (100 μM) 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 μM) significantly increased by 6.3 ± 2.9{\%} in PN 0-6 cords (p <0.01, n = 21). The amplitudes induced by glutamate (100 μM or 10 μM) did not significantly differ between PN 0-6 and PN 7-14 cords. Application of glycine (100 μM) did not significantly alter CAP amplitudes induced by NMDA (100 μM or 10 μM) and glutamate (100 μM or 10 μM). 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.",
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AU - Young, Wise

AU - Kodama, Namio

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N2 - 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 μM) 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 μM) 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 μM) in PN 0-6 cords was significantly greater than that in PN 7-14 cords (p <0.005). Glutamate (100 μM) 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 μM) significantly increased by 6.3 ± 2.9% in PN 0-6 cords (p <0.01, n = 21). The amplitudes induced by glutamate (100 μM or 10 μM) did not significantly differ between PN 0-6 and PN 7-14 cords. Application of glycine (100 μM) did not significantly alter CAP amplitudes induced by NMDA (100 μM or 10 μM) and glutamate (100 μM or 10 μM). 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.

AB - 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 μM) 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 μM) 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 μM) in PN 0-6 cords was significantly greater than that in PN 7-14 cords (p <0.005). Glutamate (100 μM) 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 μM) significantly increased by 6.3 ± 2.9% in PN 0-6 cords (p <0.01, n = 21). The amplitudes induced by glutamate (100 μM or 10 μM) did not significantly differ between PN 0-6 and PN 7-14 cords. Application of glycine (100 μM) did not significantly alter CAP amplitudes induced by NMDA (100 μM or 10 μM) and glutamate (100 μM or 10 μM). 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.

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