2′,4′-Dimethylbenzamiloride (DMB), an inhibitor of Na+-Ca++ antiporter dose-dependently (10-100 μM) inhibited Na+-dependent 45Ca++ efflux from brain synaptosomes. This compound was also able to stimulate basal release of [3H]DA from superfused TIDA neurons. Another amiloride analogue, 5-N-methyl-N-guanidinocarbonylmethylamiloride (MGCMA, 100-300 μM), which lacks of inhibitory properties on the Na+-Ca++ antiporter, failed to modify basal [3H]DA release from TIDA neurons. In addition, when the antiporter operates as a Ca++-influx pathway, DMB dose-dependently inhibited Na+-dependent 45Ca++ uptake in brain synaptosomes, whereas it did not prevent K+-induced 45Ca++ uptake, which reflects the activation of voltage-operated Ca++ channels. Finally DMB inhibited ouabain-induced [3H]DA release, which depends on the activation of the Na+-Ca++ exchanger due to the inhibition of the Na+/K+-ATPase pump.
ASJC Scopus subject areas
- Cell Biology
- Molecular Biology
- Cellular and Molecular Neuroscience