Characterization of the GABA response on identified dialysed Lymnaea neurons

1. The effect of gamma-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 (1.5 +/- 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 (tau = 0.7 sec) and slow (tau = 3.6 sec) time constants. The outward current component was slow and activated at more positive Vh(-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.