Richard E. Doolin

GABA-mediated inhibition of primary olfactory receptor neurons.

Applying GABA (1 μM–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 μM 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.

Properties and Functional Role of a Sodium-Activated Nonselective Cation Channel in Lobster Olfactory Receptor Neurons

Research on lobster olfactory receptor cells has implicated a novel sodium-activated nonselective cation channel in olfactory transduction. In addition to providing some of the first evidence for a functional role for sodium-activated channels, these studies provide a possible explanation as to how the sensitivity of these channels to sodium could be much greater in intact cells than in excised patches.