Abdominal ganglion cells of an Aplysia contain a characteristic GABA-receptor, the activation of which induces a marked hyperpolarization due to a specific increase in the membrane permeability of Cl-. The GABA-receptor of this type was named an Hcl-type. A two-minutes exposure to 10-3M lidocaine (LIDO) had little effect on resting membrane potential with a receptor of the GABAHcl-type but significantly depressed the response to 10-3M GABA. The depressing effect of LIDO on this type of response was completely reversible after 15 miniutes of rinsing with normal Aplysia blood. The dose-inhibition curves, with relative responses to given doses (GABA) plotted against log (LIDO), showed no shift in either direction with increase in GABA. These findinigs suggest that LIDO depresses the GABA receptor in a noncompetitive manner.
Treatment with 10-4M diazepam (DZ) also reversively depressed the same type of response to 10-3M GABA. The dose-inhibition curves, in which relative responses to given doses of GABA were plotted against DZ, showed no shift in either direction, and this indicated that the mode of depression of the GABA-receptor was also noncompetitive.
Further, the interaction between LIDO and DZ on GABA-receptor was studied. 10-6M DZ restores the response to 10-3M GABA which was depressed by 10-3M of LIDO when applied simultaneously. The 10-3M GABA-induced response was reduced to 70% of the control by 10-3M LIDO, but this was restored to 40% of the control by 10-6M DZ, however when pretreated with l10-6M DZ, the blocking effect of 10-3M LIDO was decreased to only 10% of the control.
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