Abstract
Afferent neurons from a proprioceptor [the femoral chordotonal organ (FCO)] at the femoro-tibial joint of a locust hindleg carry patterns of spikes to the CNS in which information is coded about the positions and movements of the tibia. Intracellular recordings from the afferents of this organ as they enter the CNS reveal spikes and depolarizing post- synaptic potentials (PSPs) during voluntary or imposed movements of the joint. Some of these PSPs are generated as a result of spikes in other FCO afferents, and can be evoked experimentally by electrical stimulation of the nerve from the organ. One afferent does not appear to synapse directly on another, but instead activates reliable pathways involving other central neurons. Current clamping of individual afferents in isolated ganglia shows that the PSPs are increased in amplitude by hyperpolarizing currents injected into an afferent, and decreased by depolarizing ones. They reverse at about -68 mV (n = 5). At the normal resting potential of the afferents, -72 mV (+/- 0.42 SE, n = 57), the PSPs are therefore depolarizing, and are associated with an increased conductance of the membrane. The changes in membrane potential and conductances associated with the PSPs can be mimicked by pressure injection of GABA into the regions of neuropil that contain the terminals of the afferents. The potential evoked by GABA is associated with an increased conductance of the membrane and reverses at the same potential as the PSPs. GABA also reduces the PSPs evoked in the terminals, either by movements of the FCO or by electrical stimulation of its nerve. The PSPs and the effects of the GABA-evoked potentials are mimicked by the GABA agonist muscimol. The PSPs are blocked reversibly by picrotoxin. The PSPs and the GABA-evoked potentials both alter the excitability of an afferent terminal by reducing the ability of the membrane to support an action potential. It is suggested that the PSPs are depolarizing, inhibitory potentials generated in the terminals of the afferents by central neurons that release GABA, and that their role is to change the efficacy of the afferent spikes at their first output synapses in the CNS. These interactions could form a graded, gain control mechanism for synaptic transmission at the afferent output synapses that is directly dependent on the features of the mechanical movements of the joint.
