Characterization of the GABA response on identified dialysed Lymnaea neurons

1. The effect of γ-aminobutyric acid has been studied on identified, internally perfused dialysed neurons of Lymnaea stagnalis L. (Pulmonata, Basommatophora). It was shown that: On the majority of neurons GABA (10^-8-10^-3 M) depolarized the membrane with a decrease in input resistance and activated a Cl^- dependent inward current with -20±4 mV E(GABA). In some cells, the outward current with - 67±8 mV E(GABA) was also recorded. 2. The GABA induced inward current was fast (1.51±0.3 sec, n=4) or slow (3.2±0.2 sec, n=3) peaking in a voltage independent manner, The inactivation phase could be fitted by one or two exponentials characterized with fast (τ=0.7 sec) and slow (τ=3.6 sec) time constants. The outward current component was slow and activated at more positive V(h)(-30-20 mV). 3. The agonist effects (GABA and muscimol) indicated the involvement of GABA(A) receptors and Cl-permeability changes in activating inward current. Picrotoxin (10^-5-10^-4 M) and Cd²⁺ completely inhibited the GABA activated inward current also affecting E(GABA) Furosemide was without effect on the peak value of GABA induced inward current, but slightly modified the slope of inactivation. 4. High concentrations of Ca-ions and their substitution with Ba-ions in extracellular saline failed to alter the GABA induced inward current. However, omission of Cl-ions from extracellular media shifted E(GABA) to the right by 18±8 mV (n=4). 5. Omission of Cl-ions from intracellular saline led to inhibition of the fast component of GABA induced inward current. Full recovery followed readdition of Cl-ions. 6. The results are in agreement with the data obtained on cloned Lymnaea GABA receptors.