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Characterization of the glutamate receptors mediating release of somatostatin from cultured hippocampal neurons.
J Neurochem. 1996 Jan; 66(1):161-8.JN

Abstract

L-Glutamate, NMDA, DL-alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA), and kainate (KA) increased the release of somatostatin-like immunoreactivity (SRIF-LI) from primary cultures of rat hippocampal neurons. In Mg(2+)-containing medium, the maximal effects (reached at approximately 100 microM) amounted to 737% (KA), 722% (glutamate), 488% (NMDA), and 374% (AMPA); the apparent affinities were 22 microM (AMPA), 39 microM (glutamate), 41 microM (KA), and 70 microM (NMDA). The metabotropic receptor agonist trans-1-aminocyclopentane-1,3-dicarboxylate did not affect SRIF-LI release. The release evoked by glutamate (100 microM) was abolished by 10 microM dizocilpine (MK-801) plus 30 microM 1-aminophenyl-4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine (GYKI 52466). Moreover, the maximal effect of glutamate was mimicked by a mixture of NMDA+AMPA. The release elicited by NMDA was sensitive to MK-801 but insensitive to GYKI 52466. The AMPA- and KA-evoked releases were blocked by 6,7-dinitroquinoxaline-2,3-dione (DNQX) or by GYKI 52466 but were insensitive to MK-801. The release of SRIF-LI elicited by all four agonists was Ca(2+) dependent, whereas only the NMDA-evoked release was prevented by tetrodotoxin. Removal of Mg2+ caused increase of basal SRIF-LI release, an effect abolished by MK-801. Thus, glutamate can stimulate somatostatin release through ionotropic NMDA and AMPA/KA receptors. Receptors of the KA type (AMPA insensitive) or metabotropic receptors appear not to be involved.

Authors+Show Affiliations

Istituto di Farmacologia e Farmacognosia, Genova, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

8522949

Citation

Fontana, G, et al. "Characterization of the Glutamate Receptors Mediating Release of Somatostatin From Cultured Hippocampal Neurons." Journal of Neurochemistry, vol. 66, no. 1, 1996, pp. 161-8.
Fontana G, De Bernardi R, Ferro F, et al. Characterization of the glutamate receptors mediating release of somatostatin from cultured hippocampal neurons. J Neurochem. 1996;66(1):161-8.
Fontana, G., De Bernardi, R., Ferro, F., Gemignani, A., & Raiteri, M. (1996). Characterization of the glutamate receptors mediating release of somatostatin from cultured hippocampal neurons. Journal of Neurochemistry, 66(1), 161-8.
Fontana G, et al. Characterization of the Glutamate Receptors Mediating Release of Somatostatin From Cultured Hippocampal Neurons. J Neurochem. 1996;66(1):161-8. PubMed PMID: 8522949.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Characterization of the glutamate receptors mediating release of somatostatin from cultured hippocampal neurons. AU - Fontana,G, AU - De Bernardi,R, AU - Ferro,F, AU - Gemignani,A, AU - Raiteri,M, PY - 1996/1/1/pubmed PY - 1996/1/1/medline PY - 1996/1/1/entrez SP - 161 EP - 8 JF - Journal of neurochemistry JO - J Neurochem VL - 66 IS - 1 N2 - L-Glutamate, NMDA, DL-alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA), and kainate (KA) increased the release of somatostatin-like immunoreactivity (SRIF-LI) from primary cultures of rat hippocampal neurons. In Mg(2+)-containing medium, the maximal effects (reached at approximately 100 microM) amounted to 737% (KA), 722% (glutamate), 488% (NMDA), and 374% (AMPA); the apparent affinities were 22 microM (AMPA), 39 microM (glutamate), 41 microM (KA), and 70 microM (NMDA). The metabotropic receptor agonist trans-1-aminocyclopentane-1,3-dicarboxylate did not affect SRIF-LI release. The release evoked by glutamate (100 microM) was abolished by 10 microM dizocilpine (MK-801) plus 30 microM 1-aminophenyl-4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine (GYKI 52466). Moreover, the maximal effect of glutamate was mimicked by a mixture of NMDA+AMPA. The release elicited by NMDA was sensitive to MK-801 but insensitive to GYKI 52466. The AMPA- and KA-evoked releases were blocked by 6,7-dinitroquinoxaline-2,3-dione (DNQX) or by GYKI 52466 but were insensitive to MK-801. The release of SRIF-LI elicited by all four agonists was Ca(2+) dependent, whereas only the NMDA-evoked release was prevented by tetrodotoxin. Removal of Mg2+ caused increase of basal SRIF-LI release, an effect abolished by MK-801. Thus, glutamate can stimulate somatostatin release through ionotropic NMDA and AMPA/KA receptors. Receptors of the KA type (AMPA insensitive) or metabotropic receptors appear not to be involved. SN - 0022-3042 UR - https://www.unboundmedicine.com/medline/citation/8522949/Characterization_of_the_glutamate_receptors_mediating_release_of_somatostatin_from_cultured_hippocampal_neurons_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0022-3042&date=1996&volume=66&issue=1&spage=161 DB - PRIME DP - Unbound Medicine ER -