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Accumulation of 3 H‐Phosphoinositides Mediated by Muscarinic Receptors in the Developing Chick Retina: Inhibition of Carbachol‐Induced Response by Glutamate Receptors
Author(s) -
Calvet Guilherme Amaral,
Marques Ventura Ana Lucia
Publication year - 1995
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 - 10.1046/j.1471-4159.1995.64031064.x
Subject(s) - carbachol , muscarinic acetylcholine receptor , biology , endocrinology , retina , medicine , glutamate receptor , microbiology and biotechnology , stimulation , receptor , chemistry , neuroscience , biochemistry
In the present work we show the development of carbachol‐induced accumulation of 3 H‐inositol phosphates ( 3 H‐InsPs) in the chick embryonic retina and its regulation by glutamate receptors. Although basal levels of 3 H‐InsPs increased during development, the retinal response to carbachol was high in the early developing stages and decreased after synaptogenesis in the retina. Eserine also stimulated the turnover of phosphoinositides in the embryonic but not in the mature retina. The effect of eserine could be blocked by atropine, suggesting that acetylcholine could be released from developing retina cells and further stimulate the turnover of InsPs in the embryonic tissue. Our data also show that muscarinic stimulation of turnover of 3 H‐InsPs could be blocked by stimulation of glutamatergic ionotropic receptors. Moreover, the effect of glutamate agonists did not seem to be mediated by the release of other neurotransmitters such as GABA, glycine, adenosine, or dopamine from the tissue because these neurotransmitters did not interfere with the retinal response to carbachol. These results suggest that muscarinic activation of phosphoinositide turnover occurs mainly in the embryonic retina and that activation of glutamate receptors can inhibit directly the muscarinic stimulation of hydrolysis of 3 H‐InsPs in this tissue.