Pre- and postsynaptic inhibition of identified giant interneurons in the cricket (Acheta domesticus)

Summary

• 1. The neuronal pathways responsible for the cerecl-mediated inhibition of three cricket giant sensory interneurons were investigated.

• 2. Two interneurons which had not previously been studied in detail were found to be influenced markedly by inhibitory inputs. Sensory interneuron 10-3 (SI 10-3) received excitatory synaptic input from longitudinally vibrating sound receptive hairs (L-hairs) on the cercus contralateral, and transversely vibrating hairs (T-hairs) on the cercus ispilateral to its axon. It was inhibited by contralateral T-hairs and ipsilateral L-hairs (Figs. 3 and 4). This pattern of receptor inputs imparts directional sensitivity upon SI 10-3. The inhibitory inputs increased the intensity range over which this directionality was observed (Figs. 4 and 5). SI 10-2 was also directionally selective and received similar cerecl inputs. The relative strength of inhibition, however, was much stronger. SI 10-2 was therefore primarily inhibited by sound (Fig. 6).

• 3. The long latency of inhibition suggested that the pathway from cerecl receptors to the sensory interneurons was polysynaptic. The inhibitory potential could be reversed by injection of hyperpolarizing current (Fig. 7). Furthermore, the inhibitory pathway was capable of blocking action potentials produced by injection of current into the sensory interneurons (Fig. 8). The inhibition was therefore due, at least in part, to synapses impinging directly upon the sensory interneurons.

• 4. The lateral giant interneuron (L.G.I.), also received cerecl inputs capable of producing an inhibitory postsynaptic conductance increase (Fig. 10). In addition, the cerecl receptor-to-giant interneuron pathway was inhibited presynaptically. The excitatory synaptic inputs from cerecl receptors to the L.G.I. were “protected” against decrement by prior activation of the inhibitory pathway (Figs. 12 and 13).

• 5. Intracellular recordings from cerecl afferent axons revealed a primary afferent depolarization (P.A.D.), in response to activation of the cerecl receptors responsible for inhibition (Fig. 14). The latency of the P.A.D. suggested that the pathway involved was indirect. Action potentials occurring in the afferent axon during the P.A.D. had a reduced base-to-peak amplitude (Fig. 14).