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N-methyl-D-aspartic acid (NMDA) and non-NMDA receptors regulating hippocampal norepinephrine release. I. Location on axon terminals and pharmacological characterization.
J Pharmacol Exp Ther. 1992 Jan; 260(1):232-7.JP

Abstract

The effects of endogenous and exogenous agonists at excitatory amino acid receptors mediating enhancement of [3H]norepinephrine [(3H]NE) release have been investigated using superfused rat hippocampal synaptosomes. In Mg(++)-free medium L-glutamic acid (L-Glu), L-aspartic acid (L-Asp), N-methyl-D-aspartic acid (NMDA), kainic acid, (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and quisqualic acid (QA) all increased the release of [3H]NE. L-Glu produced the largest effect. In the presence of Mg++ (1.2 mM), the effect of L-Glu decreased by about 40%; L-Asp and NMDA lost completely their activity while the effects of kainic acid, QA and AMPA did not change significantly. Similarly to NMDA, the effect of L-Asp was augmented by glycine and blocked by NMDA receptor antagonists, while it was insensitive to the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). The effect of L-Glu on [3H] NE release was partly decreased by the NMDA receptor channel blocker (+)-5-methyl-10,11-dihydro-5-H-dibenzo[a,d]cycloepten-5,10-imine (MK-801) and partly by CNQX; when present together, the two antagonists completely abolished the L-Glu effect. The QA enhancement of [3H]NE release was antagonized by CNQX but it was insensitive to other classical non-NMDA receptor antagonists.

IN CONCLUSION

1) release-enhancing NMDA and non-NMDA receptors exist on noradrenergic axon terminals of rat hippocampus; 2) L-Asp appears to be a potent selective NMDA receptor agonist while L-Glu can activate also non-NMDA receptors; 3) the NE-releasing receptor activated by QA may represent a QA/AMPA receptor subtype.

Authors+Show Affiliations

Istituto di Farmacologia e Farmacognosia, Università degli Studi di Genova, Italy.No affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

1370540

Citation

Pittaluga, A, and M Raiteri. "N-methyl-D-aspartic Acid (NMDA) and non-NMDA Receptors Regulating Hippocampal Norepinephrine Release. I. Location On Axon Terminals and Pharmacological Characterization." The Journal of Pharmacology and Experimental Therapeutics, vol. 260, no. 1, 1992, pp. 232-7.
Pittaluga A, Raiteri M. N-methyl-D-aspartic acid (NMDA) and non-NMDA receptors regulating hippocampal norepinephrine release. I. Location on axon terminals and pharmacological characterization. J Pharmacol Exp Ther. 1992;260(1):232-7.
Pittaluga, A., & Raiteri, M. (1992). N-methyl-D-aspartic acid (NMDA) and non-NMDA receptors regulating hippocampal norepinephrine release. I. Location on axon terminals and pharmacological characterization. The Journal of Pharmacology and Experimental Therapeutics, 260(1), 232-7.
Pittaluga A, Raiteri M. N-methyl-D-aspartic Acid (NMDA) and non-NMDA Receptors Regulating Hippocampal Norepinephrine Release. I. Location On Axon Terminals and Pharmacological Characterization. J Pharmacol Exp Ther. 1992;260(1):232-7. PubMed PMID: 1370540.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - N-methyl-D-aspartic acid (NMDA) and non-NMDA receptors regulating hippocampal norepinephrine release. I. Location on axon terminals and pharmacological characterization. AU - Pittaluga,A, AU - Raiteri,M, PY - 1992/1/1/pubmed PY - 1992/1/1/medline PY - 1992/1/1/entrez SP - 232 EP - 7 JF - The Journal of pharmacology and experimental therapeutics JO - J Pharmacol Exp Ther VL - 260 IS - 1 N2 - UNLABELLED: The effects of endogenous and exogenous agonists at excitatory amino acid receptors mediating enhancement of [3H]norepinephrine [(3H]NE) release have been investigated using superfused rat hippocampal synaptosomes. In Mg(++)-free medium L-glutamic acid (L-Glu), L-aspartic acid (L-Asp), N-methyl-D-aspartic acid (NMDA), kainic acid, (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and quisqualic acid (QA) all increased the release of [3H]NE. L-Glu produced the largest effect. In the presence of Mg++ (1.2 mM), the effect of L-Glu decreased by about 40%; L-Asp and NMDA lost completely their activity while the effects of kainic acid, QA and AMPA did not change significantly. Similarly to NMDA, the effect of L-Asp was augmented by glycine and blocked by NMDA receptor antagonists, while it was insensitive to the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). The effect of L-Glu on [3H] NE release was partly decreased by the NMDA receptor channel blocker (+)-5-methyl-10,11-dihydro-5-H-dibenzo[a,d]cycloepten-5,10-imine (MK-801) and partly by CNQX; when present together, the two antagonists completely abolished the L-Glu effect. The QA enhancement of [3H]NE release was antagonized by CNQX but it was insensitive to other classical non-NMDA receptor antagonists. IN CONCLUSION: 1) release-enhancing NMDA and non-NMDA receptors exist on noradrenergic axon terminals of rat hippocampus; 2) L-Asp appears to be a potent selective NMDA receptor agonist while L-Glu can activate also non-NMDA receptors; 3) the NE-releasing receptor activated by QA may represent a QA/AMPA receptor subtype. SN - 0022-3565 UR - https://www.unboundmedicine.com/medline/citation/1370540/N_methyl_D_aspartic_acid__NMDA__and_non_NMDA_receptors_regulating_hippocampal_norepinephrine_release__I__Location_on_axon_terminals_and_pharmacological_characterization_ L2 - https://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=1370540 DB - PRIME DP - Unbound Medicine ER -