No abstract

1. Triceps surae and plantaris (Pl) motoneurons were recorded intracellularly in chloralose or pentobarbital sodium (Nembutal)-anesthetized cats during unfused tetanic contractions of gastrocnemius medialis muscle (GM) produced by stimulating either a cut branch of the GM nerve or the muscle directly. 2. In alpha-motoneurons, during a series of GM twitches at 10/s, contraction-induced inhibitory potentials, probably the result of input from Golgi tendon organs (autogenetic inhibition), rapidly subsided before the end of the series. In contrast, excitatory potentials, probably the result of the activation of spindle primary endings during relaxation from contraction, persisted. 3. In gastrocnemius lateralis-soleus (GL-S) and Pl motoneurons lacking an excitatory connection with Ia afferents from GM, the sustained contraction of this muscle also elicited a declining inhibition. Rapid reduction of contraction-induced autogenetic inhibition was also observed in homonymous gamma-motoneurons. During unfused tetanic contractions lasting 0.5-4s, inhibitory potentials quickly subsided, but an abrupt increase in contractile force elicited a new series of decreasing inhibitory potentials. 4. The assumption that the inhibition induced by GM unfused tetanic contractions was due to activation of homonymous Ib afferents was supported by observations of the effects of electrical stimulation of the GM nerve. In Pl motoneurons lacking an excitatory connection with Ia afferents from GM, repetitive trains applied to the GM nerve, at a strength just above threshold for group I fibers, elicited rapidly declining inhibitory potentials similar to those produced by GM contraction. It was verified that during such stimulation, the amplitude of the group I afferent volleys did not decrease. 5. Reduction of contraction-induced Ib inhibition during sustained GM contraction was still present after a low spinalization of the preparation. As GM tendon organ discharges were verified to persist throughout prolonged contractions, the observed decline of autogenetic inhibition is likely to depend on a spinal mechanism, possibly involving presynaptic inhibition of Ib afferents and/or mutual inhibition of Ib-inhibitory interneurons.

SUMMARY1. The distribution of fusimotor axons to bag1, bag2 and chain muscle fibres in cat tenuissimus spindles has been studied using a modification of the glycogen-depletion technique of Edstr6m & Kugelberg (1968). Single fusimotor axons were stimulated intermittently at 40-100/sec for long periods (30-90 sec) during blood occlusion. Portions of muscle containing the activated spindles were quick-frozen, fixed in absolute ethanol during freeze-substitution, and then embedded in paraffin wax. Serial transverse sections were stained for glycogen using the periodic acid-Schiff method, and examined for depletion.2. Dynamic y axons (i.e. those that increase the dynamic index of primary-ending responses to ramp stretches of large amplitude) depleted bag1 fibres almost exclusively.3. Static y axons (i.e. those that reduce or abolish the dynamic index) depleted both bag and chain fibres. Bag1 and bag2 fibres were depleted about equally. 4. A single static y axon may activate both bag and chain fibres in one spindle (the most common pattern), chain fibres only in another, and bag fibres only in a third spindle.5. Static y axons with conduction velocities less than 25 m/sec also had a non-selective distribution, but no depletion was observed in bag2 fibres.6. The zones of depletion produced by dynamic y axrons were distributed more or less equally in the intra-and extracapsular parts of spindle poles, whereas those produced by static y axons were mainly intracapsular.7. The results are compared with the glycogen-depletion studies of Brown & Butler (1973 and our own study of the distribution of

Twitch and tetanic contractions of single motor units of the cat peroneus tertius muscle were examined after application of a test allowing their identification as either fast fatigable (f.f.) or fast fatigue‐resistant (f.r.) or fast intermediate (f.i.) or slow units as established by Burke, Levine, Tsairis & Zajac (1973). The test was found to leave two kinds of after‐effects in f.f., f.r. and f.i. units whereas it did not affect slow units. The first after‐effect was an early and brief potentiation of twitch tension occurring in all f.r. and f.i. units and in most f.f. units. The second after‐effect, termed ‘delayed fatigue', was a prolonged depression of tension output, that developed slowly following the early potentiation in all f.f. and f.i. units and more than half of the f.r. units. One hour after the test, unfused tetanic contractions elicited by 20‐40/sec stimulation were deeply depressed in motor units that had been left without stimulation since the end of the test. Recovery took place in 3‐5 hr. Motor units affected by delayed fatigue could nevertheless be made to develop nearly normal tension by gradual build‐up upon prolonged stimulation at 30‐40/sec. Maximal tetanic contractions elicited by 200/sec stimulation were much less depressed during delayed fatigue than unfused tetanic contractions. These observations suggest that contractile mechanism were not impaired by delayed fatigue. Since absence of change in muscle action potential indicated that excitation of muscle fibres was not affected either, delayed fatigue might be due to a temporary failure of excitation‐contraction coupling.