Reduction of Ib autogenetic inhibition in motoneurons during contractions of an ankle extensor muscle in the cat

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.

Heterogeneity of contraction‐induced effects in neurons of the cat dorsal spinocerebellar tract.

“…Altogether, fifteen DSCT neurons (20% of the contraction-sensitive sample) displayed signs of declining excitation during TS contractions (see Table 1). Figure 4 illustrates the most frequently observed effect of an unfused TS tetanus on contraction-sensitive DSCT cells, that is, a declining inhibition, similar to those previously observed in motoneurons (Zytnicki et al 1990). Figure 4A shows a record from a DSCT neuron in which inputs A 2 mV 100 gf generated by TS contractions first induced an hyperpolarization of 0 4 mV amplitude.…”

“…A priori, such contraction-induced inhibition could be ascribed to I b inputs because tendon organs are activated by contraction and Ib afferents produce di-or trisynaptic inhibition in homonymous and synergic motoneurons (see . In support of this assumption, repetitive electrical stimulation of Ib afferents in the muscle nerve did elicit declining inhibitions resembling those induced by contraction in motoneurons, and this suggested further that the decline was due to a central mechanism (Zytnicki et al 1990). Intra-axonal recordings of primary afferent depolarizations in Ib afferent fibres from the contracting muscle later pointed to a contribution of presynaptic inhibition of Ib afferents to this mechanism (Lafleur, Zytnicki, Horcholle-Bossavit & Jami, 1992).…”

Indications for GABA-Immunoreactive Axo-Axonic Contacts on the Intraspinal Arborization of a Ib Fiber in Cat: A Confocal Microscope Study

“…Our results, therefore, suggest that each collateral might be contacted by several tens of GABAimmunoreactive contacts and, because a Ib fiber usually has Ͼ10 collaterals in the lumbosacral spinal cord (Brown and Fyffe, 1979), the whole fiber might bear up to several hundreds of axo-axonic synapses. The present results indicate that segmental Ib collaterals possess adequate synaptic equipment to receive a significant presynaptic inhibition that might account for the filtering out of Ib input during contraction as observed in previous studies (Zytnicki et al, 1990;Lafleur et al, 1992).…”

Low frequency fatigue in human quadriceps is fatigue dependent and not task dependent

“…Fuglevand and colleagues did not induce similar levels of fatigue across tasks, thus the lower initial force task (20% MVC) induced over 80% fatigue compared to higher force contractions (65% MVC). Mechanisms that contribute to EMG amplitude not reaching prefatigue levels include: increased peripheral inhibitory feedback from metabolite-sensitive muscle receptors (Bigland-Ritchie, 1981), a reduction in muscle spindle gain (Macefield et al, 1991), an increase in Golgi tendon organ (Zytnicki et al, 1990) afferent input, an increase in recurrent inhibition (Mcnabb et al, 1988), and neuromuscular propagation failure (Fuglevand et al, 1993). Although it is impossible to identify which of these processes is responsible, our findings that EMG amplitude at end point was similar across both contractions (35% and 65%) suggests that these mechanisms are also fatigue dependent, rather than intensity/duration dependent for the tasks examined in this study.…”