GABA-Mediated Inhibition of Primary Olfactory Receptor Neurons

Applying GABA (1 (mu)M-1 mM) to the soma of cultured lobster olfactory receptor neurons evokes an inward current (Vm = -60 mV) accompanied by an increase in membrane conductance, with a half-effect of 487 (mu)M GABA. The current-voltage relationship of this current is linear between -100 and 100 mV and reverses polarity at the equilibrium potential for Cl-. The current is blocked by picrotoxin and bicuculline methiodide, and is evoked by trans-aminocrotonic acid, isoguvacine, muscimol, imidazole-4-acetic acid, and 3-amino-1-propanesulfonic acid, but not by the GABAC-receptor agonist cis-4-aminocrotonic acid and the GABAB-receptor agonist 3-aminopropylphosphonic. Applying GABA to the soma of the cells in situ reversibly suppresses the spontaneous discharge and substantially decreases the odor-evoked discharge. The effects of GABA on the cell soma in situ are antagonized by both picrotoxin and bicuculline methiodide. Taken together with evidence that GABA directly activates a chloride channel in outside-out patches excised from the soma of these neurons, we conclude that lobster olfactory receptor neurons express an ionotropic GABA receptor that can potentially regulate the output of these cells.