Shunting versus inactivation: simulation of GABAergic inhibition in spider mechanoreceptors suggests that either is sufficient.

Afferent neurons entering the central nervous systems of vertebrates and invertebrates receive presynaptic inhibition on their axon terminals. This usually involves an increase in membrane conductance (shunting) and depolarization (primary afferent depolarization, PAD). In arachnids and crustaceans the peripherally located parts of afferent neurons also receive efferent synapses. GABA (gamma-aminobutyric acid) plays a major role in both central and peripheral inhibition, activating chloride channels that depolarize the membrane and increase its conductance. Although both central and peripheral inhibition have been widely investigated, debate continues about the mechanisms involved, especially concerning the relative contributions of shunting versus inactivation of sodium channels by depolarization. Sensory neurons innervating spider VS-3 slit sensilla are accessible to intracellular recordings during mechanical or electrical stimulation. These neurons are inhibited by GABA, and both the electrophysiology and pharmacology of this inhibition have been studied previously. Here, we developed a Hodgkin-Huxley style model to simulate VS-3 neuron activity before and after GABA treatment. The model indicates that GABA-activated chloride current can entirely account for action potential suppression, and that either shunting or inactivation are sufficient to produce inhibition. This model also demonstrates that slowing of sodium current contributes to inhibition.