Calcium accumulation precedes the degenerative effects of L-glutamate on locust muscle fibres.

Agonist-induced degeneration of locust muscle occurs only when desensitization of the excitatory glutamate receptors present on this tissue is inhibited. It has been suggested that an increase in intracellular Ca2+ is responsible for this degeneration. To test this proposal the accumulation of 45Ca by locusts muscle has been studied under various conditions, including those under which receptor desensitization was inhibited. Retractor unguis muscles from the metathoracic leg of locusts (Schistocerca gregaria) were used in these studies. All muscles exposed to L-glutamate exhibited an early increase in intracellular radioactivity but this was 2-3 times greater in muscle pretreated with concanavalin A (Con A) to block receptor desensitization. In the desensitizing system the increase in muscle radioactivity was not maintained, intracellular Ca2+-levels declining to control values after 30 min in 45Ca-saline-containing glutamate. In Con A-treated muscles intracellular Ca2+-levels plateaued well above control levels within 5 min of exposure to glutamate and were maintained at these levels throughout the period of glutamate treatment. These results support the contention that agonist-induced degeneration of locust muscle is triggered by entry of Ca2+ and a rise in intracellular concentration of this cation to a toxic level.