Figure 6.

The functional effects of the delayed IPSP in motor neurons. A, Summary diagram showing the proposed circuitry underlying the direct EPSP and delayed IPSP and the methods used to examine the influence of the delayed IPSP. Open circles are excitatory inputs, and filled circles are inhibitory inputs. The letters refer to the treatments shown in B-D. The output of the disynaptic pathway could be blocked with strychnine, whereas the activation of this pathway could be blocked using high-calcium Ringer's solution to raise the spike threshold in the interposed neuron or using low-calcium Ringer's solution or glutamate receptor antagonists to reduce EIN-evoked EPSP amplitudes. Note that the latter treatments will affect the amplitude of direct EIN inputs to motor neurons (MN) and to the SiINs. The direct input will persist, but the delayed IPSP will be blocked because the reduced EPSP amplitude will not be able to evoke spiking in the SiIN. B, Blocking the output of the proposed disynaptic pathway with strychnine (1 μm) converted the depression of the direct EPSP into facilitation. C, High-calcium Ringer's solution blocked the delayed IPSP during the spike train, presumably by preventing the SiIN from reaching spike threshold, and also abolished the depression of the direct EPSP. D, The non-NMDA glutamate receptor antagonist DNQX (2 μm) reduced the amplitude of the direct EPSP in motor neurons and abolished the delayed IPSP, presumably by reducing the amplitude of the EIN-evoked EPSP in the SiIN. All traces are averages of at least five sweeps. Black traces show the control response, and gray traces show the effects of the different treatments. Graphs showing the amplitude (E) and half-width (F) of the direct EPSP in a motor neuron evoked by EIN stimulation at 20 Hz in control in the presence of the glycine receptor antagonist strychnine (1 μm), high-calcium Ringer's solution, and the non-NMDA receptor antagonist DNQX (2 μm).