Regeneration of afferent and efferent fibres to muscle spindles after nerve injury in adults cats.

Brown, M. Christian; Butler, Richard

doi:10.1113/jphysiol.1976.sp011514

Cited by 65 publications

(48 citation statements)

References 16 publications

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“…On the one hand, it is clear that recovery is not complete (Brown and Butler, 1976;Gregory et al, 1982;Banks and Barker, 1989;Lewin and McMahon, 1991). The number of innervated spindle receptors is reduced to as few as 75% of normal (Table 1) (Banks et al, 1984;Barker et al, 1985Barker et al, , 1988Scott, 1987;Dieler and Schroder, 1990), and there is indirect evidence that those receptors that are reinnervated may be supplied by the wrong class of afferents (Collins et al, 1986;Banks and Barker, 1989).…”

Section: Response Of Regenerated Spindle Afferents To Muscle Stretchmentioning

confidence: 99%

“…Group differences in both length threshold and background firing might be explained by the incomplete recovery of ␥-motoneuron influences on spindle afferents described in previous studies of reinnervated muscle (Brown and Butler, 1976;Gregory et al, 1982). To test this possibility, we eliminated all ␥-motoneuron input to muscle spindles by sectioning the ventral roots acutely at the time of data collection in three rats with unoperated MG muscle nerves.…”

Section: Response Properties Of Regenerated Muscle Spindle Afferentsmentioning

confidence: 99%

“…In contrast with the nearly complete motor recovery, there is only partial recovery in sensory encoding of muscle stretch. Abnormalities reported for spindle afferents in response to stretch of a reinnervated muscle include firing rates that are slower at the peak of ramp stretch and/or slower or unsustained during static stretch (Brown and Butler, 1976;Gregory et al, 1982;Banks and Barker, 1989;Lewin and McMahon, 1991). These and other aberrations (Decherchi et al, 2001) focus attention on incomplete recovery of proprioceptive feedback as the basis for stretch areflexia.…”

Section: Introductionmentioning

confidence: 99%

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Central Suppression of Regenerated Proprioceptive Afferents

Haftel¹,

Bichler²,

Wang³

et al. 2005

J. Neurosci.

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Long after a cut peripheral nerve reinnervates muscle and restores force production in adult cats, the muscle does not respond reflexively to stretch. Motivated by the likelihood that stretch areflexia is related to problems with sensing and controlling limb position after peripheral neuropathies, we sought to determine the underlying mechanism. Electrophysiological and morphological measurements were made in anesthetized rats having one of the nerves to the triceps surae muscles either untreated or cut and immediately rejoined surgically many months earlier. First, it was established that reinnervated muscles failed to generate stretch reflexes, extending observations of areflexia to a second species. Next, multiple elements in the sensorimotor circuit of the stretch reflex were examined in both the PNS and CNS. Encoding of muscle stretch by regenerated proprioceptive afferents was remarkably similar to normal, although we observed some expected abnormalities, e.g., increased length threshold. However, the robust stretch-evoked sensory response that arrived concurrently at the CNS in multiple proprioceptive afferents produced synaptic responses that were either smaller than normal or undetectable. Muscle stretch failed to evoke detectable synaptic responses in 13 of 22 motoneurons, although electrical stimulation generated monosynaptic excitatory postsynaptic potentials that were indistinguishable from normal. The ineffectiveness of muscle stretch was not attributable therefore to dysfunction at synapses made between regenerated Ia afferents and motoneurons. Among multiple candidate mechanisms, we suggest that centrally controlled neural circuits may actively suppress the sensory information encoded by regenerated proprioceptive afferents to prevent recovery of the stretch reflex.

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Section: Response Of Regenerated Spindle Afferents To Muscle Stretchmentioning

confidence: 99%

Section: Response Properties Of Regenerated Muscle Spindle Afferentsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Central Suppression of Regenerated Proprioceptive Afferents

Haftel¹,

Bichler²,

Wang³

et al. 2005

J. Neurosci.

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“…If the cut peripheral nerve is allowed to regenerate into a muscle, most sensory fibres recover their normal responsiveness to muscle stretch (Fukami, 1972;Brown & Butler, 1976;Ip, Vrbova & Westbury, 1977). On the other hand, the maximum amplitude of monosynaptic e.p.s.p.s recorded from the homonymous motoneurones remains about half the normal size even several hundred days after reunion of a sectioned muscle nerve (Eccles, Eccles & Shealy, 1962).…”

Section: Introductionmentioning

confidence: 99%

Enhancement of synaptic function in cat motoneurones during peripheral sensory regeneration

Gallego

Kuno

Núñez

et al. 1980

The Journal of Physiology

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SUMMARY1. Monosynaptic excitatory post-synaptic potentials (e.p.s.p.s) were recorded from medial (m.g.) and lateral gastrocnemius (1.g.) motoneurones in the cat 2-30 weeks after crushing the m.g. nerve.2. The mean amplitudes of homonymous and heteronymous e.p.s.p.s evoked from the m.g. nerve were initially depressed (2-3 weeks after injury) and subsequently reached levels greater than normal for a period (8-12 weeks) before slowly declining to about 70 % of the normal values (by week 30).3. Monosynaptic e.p.s.p.s evoked in m.g. motoneurones from the intact 1.g. nerve showed neither initial depression nor subsequent alterations following crush of the m.g. nerve.4. By the eighth week after nerve crush, about 70 % of Group I and Group II sensory fibres in the m.g. nerve responded to muscle stretch, about 15 % had regenerated into the muscle but did not respond to muscle stretch, and the remainder failed to regenerate across' the neuroma formed by the nerve crush.5. Homonymous, monosynaptic e.p.s.p.s produced by impulses in single sensory fibres responding to stretch of the m.g. muscle were recorded 8 weeks after crush of the m.g. nerve. Their amplitude distribution was indistinguishable from that obtained in normal, unoperated cats. Thus, there was no evidence that functionally reinnervated sensory fibres are responsible for the enhanced phase of composite e.p.s.p.s observed during peripheral regeneration.6. When the m.g. nerve had been sectioned and prevented from regenerating into the muscle for 8 weeks, the amplitudes of homonymous and heteronymous e.p.s.p.s evoked from the m.g. nerve were significantly smaller than those observed in control animals. Thus, there was no evidence that non-regenerating sensory fibres are responsible for the enhanced phase of composite e.p.s.p.s after nerve crush.7. It is suggested that the sensory fibres responsible for abnormally large composite e.p.s.p.s following nerve crush are those that regenerate into the muscle but do not achieve functional reinnervation. This possibility is discussed in relation to the increase in central synaptic efficacy observed after prolonged disuse of the sensory pathway.

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“…Although effects of androgens at the neuromuscular junction and on the muscle fibres cannot be excluded, it appears that the central nervous system plays an important role in the maintenance of amplexus in Xenopus. During the early stages of regeneration following crush injury to a muscle nerve the spindle primary afferent innervation is often physiologically (Brown & Butler, 1976) and histologically abnormal (Barker & Boddy, 1980).…”

Section: Ppproceedings Of Thementioning

confidence: 99%

Communications

1981

The Journal of Physiology

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Neurology, Queen Square, LondonBiochemical data suggest that L-glutamate (L-glu) and L-aspartate (L-asp) could be the neurotransmitters of the parallel and the climbing fibres respectively in the mammalian cerebellum. We have now used in vitro sagittal slices of adult rat cerebellum to study the responses of Purkinje cells (PCs) to ionophoretic applications of L-glu and L-asp in the molecular layer.Extra-and intra-cellular recordings were made from eighty PCs and L-glu and L-asp were released into their dendritic fields by short current pulses (5 to 100 msec) through a separate multibarelled electrode filled with 0 5 M salt solutions of the drugs.In the nineteen cells recorded from intracellularly, transient depolarizations up to 17 mV in amplitude and with depolarizing slopes up to 0 4 mV/msec were evoked by 2 to 10 nC L-glu or L-asp applied in the molecular layer. Maximum sensitivities were 8 mV/nC for L-glu and 6-4 mV/nC for L-asp. These depolarizations were accompanied by no change in cell input resistance, whereas steady applications of high doses of L-asp or L-glu decreased the membrane resistance.In the extracellularly recorded cells, the lowest threshold for L-glu or L-asp mediated excitations of PCs was as low as 25 pC, with a latency for the response as short as 7 msec. The mapping of these excitatory responses confirmed that the sensitivity of the dendrites for L-glu was greater than that of the soma (Chujo, Yamada & Yamamoto, 1975), and we showed in addition that the same was true for L-asp. No differential sensitivity of PC dendrites for L-asp and L-glu was detected in 66 0 of the tested cells; in the remainder, the sensitivity for L-asp declined markedly in the upper third of the molecular layer, whereas it remained high for L-glu.Finally, the agonist quisqualic acid was a much more potent excitant of PCs than L-glu or L-asp when applied in their dendritic fields, whereas the other major agonist N-methyl DL-aspartate (Sigma) only produced a very weak excitatory effect under the same conditions. The excitatory effects of L-asp, L-glu and quisqualic acid on PCs were antagonized by L-glutamic acid diethyl ester more consistently than by D-a amino adipate, suggesting, together with the previous observations, that L-asp and L-glu act on PCs via quisqualic acid receptors rather than via N-methyl D-aspartate receptors.

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Regeneration of afferent and efferent fibres to muscle spindles after nerve injury in adults cats.

Cited by 65 publications

References 16 publications

Central Suppression of Regenerated Proprioceptive Afferents

Central Suppression of Regenerated Proprioceptive Afferents

Enhancement of synaptic function in cat motoneurones during peripheral sensory regeneration

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