1. 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. 2. The GABA-induced inward current was fast (1.5 ± 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. 3. The agonist effects (GABA and muscimol) indicated the involvement of GABAA receptors and Cl-permeability changes in activating inward current. Picrotoxin (10 −5-10 −4 M) and Cd 2+ 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. 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. 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. 6. The results are in agreement with the data obtained on cloned Lymnaea GABA receptors.