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Autoreceptor regulation of glutamate and aspartate release from slices of the hippocampal CA1 area.

Publication ,  Journal Article
Martin, D; Bustos, GA; Bowe, MA; Bray, SD; Nadler, JV
Published in: J Neurochem
May 1991

Slices of hippocampal area CA1 were employed to test the hypothesis that the release of glutamate and aspartate is regulated by the activation of excitatory amino acid autoreceptors. In the absence of added Mg2+, N-methyl-D-aspartate (NMDA)-receptor antagonists depressed the release of glutamate, aspartate, and gamma-aminobutyrate evoked by 50 mM K+. Conversely, the agonist NMDA selectively enhanced the release of aspartate. The latter action was observed, however, only when the K+ stimulus was reduced to 30 mM. Actions of the competitive antagonists 3-[(+/- )-2-carboxypiperazin-4-yl]-propyl-l-phosphonic acid (CPP) and D-2-amino-5-phosphonovalerate (D-AP5) differed, in that the addition of either 1.2 mM Mg2+ or 0.1 microM tetrodotoxin to the superfusion medium abolished the depressant effect of CPP without diminishing the effect of D-AP5. These results suggest that the activation of NMDA receptors by endogenous glutamate and aspartate enhances the subsequent release of these amino acids. The cellular mechanism may involve Ca2+ influx through presynaptic NMDA receptor channels or liberation of a diffusible neuromodulator linked to the activation of postsynaptic NMDA receptors. (RS)-alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, a selective quisqualate receptor agonist, and kainate, an agonist active at both kainate and quisqualate receptors, selectively depressed the K(+)-evoked release of aspartate. Conversely, 6-cyano-7-nitro-quinoxaline-2,3-dione, an antagonist active at both quisqualate and kainate receptors, selectively enhanced aspartate release. These results suggest that glutamate can negatively modulate the release of aspartate by activating autoreceptors of the quisqualate, and possibly also of the kainate, type. Thus, the activation of excitatory amino acid receptors has both presynaptic and postsynaptic effects.

Duke Scholars

Published In

J Neurochem

DOI

ISSN

0022-3042

Publication Date

May 1991

Volume

56

Issue

5

Start / End Page

1647 / 1655

Location

England

Related Subject Headings

  • Tetrodotoxin
  • Receptors, Neurotransmitter
  • Receptors, N-Methyl-D-Aspartate
  • Receptors, Kainic Acid
  • Receptors, Cell Surface
  • Receptors, Amino Acid
  • Receptors, AMPA
  • Rats, Inbred Strains
  • Rats
  • Neurology & Neurosurgery
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Martin, D., Bustos, G. A., Bowe, M. A., Bray, S. D., & Nadler, J. V. (1991). Autoreceptor regulation of glutamate and aspartate release from slices of the hippocampal CA1 area. J Neurochem, 56(5), 1647–1655. https://doi.org/10.1111/j.1471-4159.1991.tb02063.x
Martin, D., G. A. Bustos, M. A. Bowe, S. D. Bray, and J. V. Nadler. “Autoreceptor regulation of glutamate and aspartate release from slices of the hippocampal CA1 area.J Neurochem 56, no. 5 (May 1991): 1647–55. https://doi.org/10.1111/j.1471-4159.1991.tb02063.x.
Martin D, Bustos GA, Bowe MA, Bray SD, Nadler JV. Autoreceptor regulation of glutamate and aspartate release from slices of the hippocampal CA1 area. J Neurochem. 1991 May;56(5):1647–55.
Martin, D., et al. “Autoreceptor regulation of glutamate and aspartate release from slices of the hippocampal CA1 area.J Neurochem, vol. 56, no. 5, May 1991, pp. 1647–55. Pubmed, doi:10.1111/j.1471-4159.1991.tb02063.x.
Martin D, Bustos GA, Bowe MA, Bray SD, Nadler JV. Autoreceptor regulation of glutamate and aspartate release from slices of the hippocampal CA1 area. J Neurochem. 1991 May;56(5):1647–1655.
Journal cover image

Published In

J Neurochem

DOI

ISSN

0022-3042

Publication Date

May 1991

Volume

56

Issue

5

Start / End Page

1647 / 1655

Location

England

Related Subject Headings

  • Tetrodotoxin
  • Receptors, Neurotransmitter
  • Receptors, N-Methyl-D-Aspartate
  • Receptors, Kainic Acid
  • Receptors, Cell Surface
  • Receptors, Amino Acid
  • Receptors, AMPA
  • Rats, Inbred Strains
  • Rats
  • Neurology & Neurosurgery