U. Garcia et al., EXCITATORY ACTION OF GAMMA-AMINOBUTYRIC-ACID (GABA) ON CRUSTACEAN NEUROSECRETORY-CELLS, Cellular and molecular neurobiology, 14(1), 1994, pp. 71-88
1. Intracellular and voltage-clamp recordings were obtained from a sel
ected population of neuroscretory (ns) cells in the X organ of the cra
yfish isolated eyestalk. Pulses of gamma-aminobutyric acid (GABA) elic
ited depolarizing responses and bursts of action potentials in a dose-
dependent manner. These effects were blocked by picrotoxin (50 mu M) b
ut not by bicuculline. Picrotoxin also suppressed spontaneous synaptic
activity. 2. The responses to GABA were abolished by severing the neu
rite of X organ cells, at about 150 mu m from the cell body. Responses
were larger when the application was made at the neuropil level. 3. T
opical application of Cd2+ (2 mM), while suppressing synaptic activity
, was incapable of affecting the responses to GABA. 4. Under whole-cel
l voltage-clamp, GABA elicited an inward current with a reversal poten
tial dependent on the chloride equilibrium potential. The GABA effect
was accompanied by an input resistance reduction up to 33% at a -50 mV
holding potential. No effect of GABA was detected on potassium, calci
um, and sodium currents present in X organ cells. 5. The effect of GAB
A on steady-state currents was dependent on the intracellular calcium
concentration. At 10(-6) M [Ca2+](i), GABA (50 mu M) increased the mem
brane conductance more than threefold and shifted the zero-current pot
ential from -25 to -10 mV. At 10(-9) M [Ca2+](i), GABA induced only a
1.3-fold increase in membrane conductance, without shifting the zero-c
urrent potential. 6. These results support the notion that in the popu
lation of X organ cells sampled in this study, GABA acts as an excitat
ory neurotransmitter, opening chloride channels.