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L-glutamate applied iontophoretically to the extrajunctional membrane of locust muscle produced a biphasic response, depolarization followed by hyperpolarization (i.e. DH-response). Applying L-glutamate and DL-ibotenate from multibarrel micropipettes allowed comparison of their extrajunctional responses. While glutamate produced a two component response, ibotenate produced a single component H-response. 2. The equilibrium values for the H-responses to L-glutamate and DL-ibotenate applied at the same extrajunctional site were very similar. The equilibrium value was 59-5 +/- 5-4 mV indicating an increased Cl- conductance. The H-response was reversed and abolished in Cl- free medium. Picrotoxin 10(-3) M selectively blocked the H-component of the DH-response in a reversible manner. 3. The possibility that the D- and H-responses arose from the activation of two distinct types of extrajunctional glutamate receptors was investigated. Desensitization of the glutamate H-response by ibotenate and vice versa indicated the presence of an extrajunctional H-receptor sensitive to glutamate and ibotenate and an extrajunctional D-receptor sensitive to glutamate and insensitive to ibotenate. The junctional depolarizing response to glutamate was insensitive to ibotenate. 4. The presence of junctionally occurring H-receptors could not be discounted, although, if present, they were not measurably activated by the excitatory transmitter. 5. Double logarithmic plots (coulomb dose vs. response) for the actions of glutamate and ibotenate on H-receptors had values of 0-75, indicating that both drugs act on the same receptors with similar mechanisms. The value for the action of glutamate on the D-receptors was 1-5. 6. While the extrajunctional D-receptors show analogies to the extrajunctional ACh receptors in vertebrate muscle, the significance of the extrajunctional H-receptors remains speculative.

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