Abstract
Glutamic acid (GLU) and/or aspartic acid (ASP) are considered the most likely candidates as the predominant excitatory neurotransmitters in the mammalian brain (Curtis and Johnston, 1974; Cotman et al., 1981; Watkins and Evans, 1981; Fonnum, 1984). Nevertheless, certain reservations about this inference remain because these amino acids are involved in several metabolic pathways, including protein synthesis, and because they exhibit rather uniform excitatory effects on brain neurons. Furthermore, reports of inconsistencies between the pharmacology of ionophoretically applied GLU/ASP and that of the endogenous excitatory neurotransmitter released at putative GLU/ASP synapses have appeared. For example, Hori et al. (1981) demonstrated that a-amino-phosphono-butyric acid (APB) antagonized the effects of the excitatory neurotransmitter released by the lateral olfactory tract (LOT) but not the excitatory effects of ionophoretically applied GLU and ASP, which have been proposed as neurotransmitters for the LOT based upon their selective uptake and evoked release (Bradford and Richards, 1976; Collins, 1978). Shiells et al. (1981) have observed differences in the neurophysiologie effects of GLU on retinal bipolar cells from that of the endogenous neurotransmitter released by the photoreceptors, which is reputed to be GLU.
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© 1986 Plenum Press, New York
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Coyle, J.T. et al. (1986). Acidic Peptides in Brain: Do They Act at Putative Glutamatergic Synapses?. In: Schwarcz, R., Ben-Ari, Y. (eds) Excitatory Amino Acids and Epilepsy. Advances in Experimental Medicine and Biology, vol 203. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-7971-3_28
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DOI: https://doi.org/10.1007/978-1-4684-7971-3_28
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