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1. In the anesthetized and artificially ventilated cat, stimulation of the posterior articular nerve (PAN) with low strengths (1.2-1.4 x T) produced a small negative response (N1) in the cord dorsum of the lumbosacral spinal cord with a mean onset latency of 5.2 ms. Stronger stimuli (> 1.4 x T) produced two additional components (N2 and N3) with longer latencies (mean latencies 7.5 and 15.7 ms, respectively), usually followed by a slow positivity lasting 100-150 ms. With stimulus strengths above 10 x T there was in some experiments a delayed response (N4; mean latency 32 ms). 2. Activation of posterior knee joint nerve with single pulses and intensities producing N1 responses only, usually produced no dorsal root potentials (DRPs), or these were rather small. Stimulation with strengths producing N2 and N3 responses produced distinct DRPs. Trains of pulses were clearly more effective than single pulses in producing DRPs, even in the low-intensity range. 3. Cooling the thoracic spinal cord to block impulse conduction, increased the DRPs and the N3 responses produced by PAN stimulation without significantly affecting the N2 responses. Reversible spinalization also increased the DRPs produced by stimulation of cutaneous nerves. In contrast, the DRPs produced by stimulation of group I afferents from flexors were reduced. 4. Conditioning electrical stimulation of intermediate and high-threshold myelinated fibers in the PAN depressed the DRPs produced by stimulation of group I muscle and of cutaneous nerves. 5. Analysis of the intraspinal threshold changes of single Ia and Ib fibers has provided evidence that stimulation of intermediate and high threshold myelinated fibers in the posterior knee joint nerve inhibits the primary afferent depolarization (PAD) of Ia fibers, and may either produce PAD or inhibit the PAD in Ib fibers, in the same manner as stimulation of cutaneous nerves. In 7/16 group I fibers the inhibition of the PAD was increased during reversible spinalization. 6. The results obtained suggest that intermediate and high-threshold myelinated fibers in the PAN have the same actions on Ia and Ib fibers as intermediate and high-threshold cutaneous afferents and may therefore be considered as belonging to the same functional system. They further indicate that in anesthetized preparations the pathways mediating the PAD of group I fibers, as well as the pathways mediating the inhibition of the PAD, may be subjected to a descending control that is removed by spinalization.

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Auditory brainstem responses (ABRs) were evaluated during the postnatal development (P10–P180) of taiep rats, neurological mutants characterized by early abnormal myelin development and subsequent demyelination of the CNS. The disorder is produced by an autosomal recessive mutation trait that affects the oligodendrocytes but not the Schwann cells. After onset of ABRs (P12–P14), taiep rats and their nonaffected heterozygous littermates that served as controls showed a similar pattern of maturation for wave I. The central waves (In–IV) showed significantly longer latencies in the mutants. By P60–P180, the later waves (III and IV) were frequently difficult to discern. From the onset of ABRs, the interpeak latency I–IV, corresponding to the central conduction time (CCT) of the auditory pathway, showed in taiep rats significantly longer values than controls. After an initial reduction, proportional to that of control rats, the CCT value increased progressively during the second month of the mutants’ lives. The electrophysiological results of the present study strongly support the hypothesis that mutation in the taiep rat impairs neuromaturation of the central auditory pathway in the brainstem by affecting the myelination process in the CNS.