Abstract
Cyclodiene insecticides release labeled neurotransmitter in striatal and cortical synaptosome preparations under nondepolarizing conditions, typically showing half-maximal potencies for release in the low micromolar range. This level of potency is similar to those reported for inhibition of 36Cl− influx at the γ-aminobutyric acid (GABA)A receptor, their consensus target site. A wide variety of other GABAA antagonists, including picrotoxinin and bicuculline, did not cause significant dopamine release, which obviated direct involvement of the GABAA receptor as a possible site of action. Release assays with different transmitters indicated that striatal dopaminergic terminals are severalfold more sensitive to release than other neurotransmitter types. The selective sensitivity of nigrostriatal dopaminergic nerve terminals to insecticidal organochlorines provides biochemical evidence supporting an epidemiological linkage between exposure to environmental toxicants and Parkinsonism.
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