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Actions of Excitatory Amino Acids on Somatostatin Release from Cortical Neurons in Primary Cultures
Author(s) -
TapiaArancibia Lucia,
Astier Helene
Publication year - 1989
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1989.tb07406.x
Subject(s) - kainate receptor , nmda receptor , somatostatin , glutamate receptor , chemistry , glycine , inhibitory postsynaptic potential , excitatory postsynaptic potential , medicine , veratridine , nbqx , strychnine , kainic acid , endocrinology , biology , biochemistry , ampa receptor , receptor , amino acid , sodium , sodium channel , organic chemistry
L‐Glutamate, N ‐methyl‐D‐aspartic acid (NMDA), quisqualate, and kainate were found to increase endogenous somatostatin release from primary cultures of rat cortical neurons in a dose‐dependent manner. The rank order of potency calculated from the dose‐response curves was quisqualate > glutamate = NMDA > kainate, with EC 50 values of 0.4, 20, and 40 μ M , respectively. Alanine, glutamine, and glycine did not modify the release of somatostatin. The stimulation of somatostatin release elicited by L‐glutamate was Ca 2+ dependent, was decreased by Mg 2+ , and was blocked by DL‐amino‐5‐phosphonovaleric acid (APV) and thienyl‐phencyclidine (TCP), two specific antagonists of NMDA receptors. The NMDA stimulatory effect was strongly inhibited by APV in a competitive manner (IC 50 = 50 μ M ) and by TCP in a noncompetitive manner (IC 50 = 90 n M ). The release of somatostatin induced by the excitatory amino acid agonists was not blocked by tetrodotoxin (1 μ M ), a result suggesting that tetrodotoxin‐sensitive, sodium‐dependent action potentials are not involved in the effect. Somatostatin release in response to NMDA was potentiated by glycine, but the inhibitory strychnine‐sensitive glycine receptor did not appear to be involved. Our data suggest that glutamate exerts its stimulatory action on somatostatin release essentially through an NMDA receptor subtype.