Presynaptic inhibition and antidromic spikes in primary afferents of the crayfish: a computational and experimental analysis.

Primary afferent depolarizations (PADs) are associated with presynaptic inhibition and antidromic discharges in both vertebrates and invertebrates. In the present study, we have elaborated a realistic compartment model of a primary afferent from the coxobasipodite chordotonal organ of the crayfish based on anatomical and electrophysiological data. The model was used to test the validity of shunting and sodium channel inactivation hypotheses to account for presynaptic inhibition. Previous studies had demonstrated that GABA activates chloride channels located on the main branch close to the first branching point. We therefore focused the analysis on the effect of GABA synapses on the propagation of action potentials in the first axonal branch. Given the large diameters of the sensory axons in the region in which PADs were likely to be produced and recorded, the model indicates that a relatively large increase in chloride conductance (up to 300 nS) is needed to significantly reduce the amplitude of sensory spikes. The role of the spatial organization of GABA synapses in the sensory arborization was analyzed, demonstrating that the most effective location for GABA synapses is in the area of transition from active to passive conduction. This transition is likely to occur on the main branch a few hundred micrometers distal to the first branching point. As a result of this spatial organization, antidromic spikes generated by large-amplitude PADs are prevented from propagating distally.