Abstract
1. 1. Glutamate at 10 −3 M induced a 100% stimulation of the calcium efflux from locust hindgut visceral muscle strips but was without effect on calcium efflux from foregut visceral muscle. 2. 2. Dopamine at 10 −4 M caused a 60% stimulation of calcium efflux from foregut visceral muscle but was without significant effect on the hindgut visceral muscle. 3. 3. 5-Hydroxytryptamine at 10 −4 M caused over 200% stimulation of calcium efflux from the foregut muscle and caused a very small stimulation of calcium efflux from the hindgut. 4. 4. In the case of all three agonist actions, the stimulatory effects on calcium efflux and the related contractile responses were abolished in calcium-free and lanthanum-containing media. 5. 5. Caffeine was able to induce contractures and to stimulate calcium efflux in muscles subjected to calcium-free media or lanthanum treatment which were otherwise unresponsive to glutamate, dopamine and 5-hydroxytryptamine. 6. 6. Locust foregut and hindgut visceral muscles show a clear neurochemical dichotomy in response to these agonists, both in terms of contractile response and cellular calcium translocation. 7. 7. It is concluded that the effects of these agonists on contractile activity results from a rise in cellular free calcium. The mechanism for elevating activator calcium during excitation-contraction coupling appears to be an agonist-induced influx of calcium from the external medium via voltage-dependent slow calcium channels. This inward calcium signal is secondarily amplified by the triggering of calcium release from cellular storage sites.
Published Version
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