Abstract
As Kravitz et al.1 have pointed out, glutamic acid is at present the only candidate for the excitatory transmitter at crustacean neuromuscular junctions. The evidence is that1,2 glutamic acid is the most potent excitatory substance present in the crustacean central nervous system (CNS), whole peripheral nerves and isolated excitatory axons1,3–5; that the glutamic acid content in nerve extracts accounts for the whole of their excitatory activity on crustacean muscles1, and that the receptors to glutamate are localised at the same junctional spots as the receptors to the natural excitatory transmitter6. Also, both glutamic acid and the natural transmitter produce similar changes in the permeability of the postjunctional muscle membrane7–9 and in spite of a large background leakage, a significant release of glutamic acid can be evoked by stimulation of excitatory nerves1. There is also a selective uptake of glutamic acid at the neuromuscular junction which could provide an inactivation mechanism10. There is, however, no information on whether glutamate receptors have the same pharmacological properties as the receptors of the natural excitatory transmitter.
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References
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LOWAGIE, C., GERSCHENFELD, H. Glutamate antagonists at a crayfish neuromuscular junction. Nature 248, 533–535 (1974). https://doi.org/10.1038/248533a0
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DOI: https://doi.org/10.1038/248533a0
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