A dorsal spinal neural network in cat. II. Changes in responsiveness initiated by single conditioning impulses in single type 1 cutaneous input fibers

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Abstract
In 22 adult cats the time course of changes in excitability of the lamina 4:type 1 network resulting from single-impulse conditioning stimuli (CS) was studied. The impulse output of the lamina 4 neuron to test stimuli (TS) was used to measure network excitabilty. Both the CS and TS were single action potentials introduced into the network via single type 1 afferent fibers emerging from the skin receptive field of the dorsal spinal gray neuron. The CS were either introduced via the same type 1 fiber input channel (temporal interaction) via a neighboring type 1 fiber channel (spatiotemporal interaction) or consisted of an ongoing discharge produced by the lamina 4 neuron. Conditioning-test stimulus intervals (CTSI) ranged from 3-200 ms. A single CS is a potent initiator of long-lasting (> 200 ms) changes in network excitability, and the early response is usually facilitated initially (3-15 ms). In approximately 1/2 of the cases the facilitation rapidly disappears during the 16- to 33-ms period following the CS (rapid recovery) and in others, it slowly wanes, sometimes not disappearing by 50 ms (slow recovery). In the majority of cases, from 51 ms on, there is sustained inhibition regardless of the type of earlier recovery. In contrast, the initial 15 ms of the late response are equally divided between inhibition and facilitation. For > 1/2 the cases, when the early response recovers rapidly from facilitation, the late response is inhibited initially, and when the recovery is slow, the late response is facilitated initially. The later portions of both responses usually displayed prolonged inhibition regardless of the initial form of the excitability curve. The rapid and slow recovery patterns of the early response and character of the late response varied with the specific input channel; often both kinds of input channel were connected to the same principal neuron. Two models are suggested to explain these results: the rapid-recovery pattern may reflect primary afferent depolarization (PAD) initiated by the CS and the slow-recovery pattern may reflect that absence of PAD, i.e., there may be 2 kinds of type 1 input channel, one activating the PAD mechanism (PAD+) and one not activating the mechanism (PAD-); and/or the rapid-recovery pattern may reflect an early short-lived selective postsynaptic inhibition initiated by some input channels and not by others. The prolonged later inhibition may be due to postsynaptic inhibition. Similar patterns of excitability were observed for the spatiotemporal interaction studies. The ongoing discharge used as CS almost always produced a sustained facilitation, suggesting that the ongoing impulse or the process causing it does not trigger the same network mechanisms as those engaged by the peripheral CS. The possibility that the early and late responses are mediated via the axodendritic synapses between the type 1 fibers and the dorsal dendrites of the lamina 4 neurons, synapses that are formed within the glomerular complexes of this region is discussed.