The glutamate uptake blocker p-chloromercuriphenylsulphonic acid (PCMS) (100 mumol l-1) does not block any of the membrane potential changes induced by the application of L-glutamate to the adaxonal Schwann cells of the giant axon of the tropical squid Sepioteuthis sepioidea. This indicates that these potential changes are not due to the activation of an electrogenic glutamate uptake system and supports the idea that they are due to the activation of specific glutamate receptors. The presence of PCMS (100 mumol l-1) reduces the activity of the glutamate uptake system sufficiently for the extracellular level of axonally released glutamate to exceed the threshold for the activation of the NMDA-type glutamate receptors in this preparation.

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