ISSN:
1471-4159
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
Avermectin B1a, a novel macrocyclic lactone antiparasitic agent, causes a marked and sustained increase of γ-aminobutyric acid release from rat brain synaptosomes. A concentration of 8-10 μM of avermectin B1a produced the maximal effect (310 ± 30% of the control), while the half-maximal level was achieved at 2-3 μM. The drug also stimulated γ-aminobutyric acid release (251 ± 11% of the basal level) from synaptosomes in calcium-free medium, which was 28 ± 4% lower than that in the 1.8 mm-Ca2+ medium. The compound did not, however, affect the synaptosomal release of glutamate. At the lobster neuromuscular junction, avermectin B1a reduced the input resistance of muscle fibers in control Ringer's solution as well as in Ringer's solution in which Co2+ was substituted for Ca2+. This observation is in accord with the Ca2+ independent stimulation of γ-aminobutyric acid release seen with synaptosomes. A good correlation between antiparasitic activity and γ-aminobutyric acid-releasing activity has been found among various derivatives of avermectin B1a, which suggests that the ability of the drug to release this neurotransmitter may be the basis of its antiparasitic action.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1111/j.1471-4159.1980.tb06604.x
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