Renshaw cell mediated inhibition of Renshaw cells: patterns of excitation and inhibition from impulses in motor axon collaterals.

Ryall, R. W.

doi:10.1152/jn.1970.33.2.257

Cited by 140 publications

(82 citation statements)

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“…It was also shown, however, that the opponently organized Renshaw-la system could automatically compensate for this positional distortion. Thus the model rationalized a formerly mysterious interneuronal connectivity pattern, which was already known to exist in vivo (Baldissera et al, 1981;Pompeiano, 1984;Renshaw, 1946;Ryall, 1970). The present results show some of the dynamics associated with this same connectivity scheme during rapid movement.…”

Section: Tri-phasic Emg Genesissupporting

confidence: 85%

Emergence of tri-phasic muscle activation from the nonlinear interactions of central and spinal neural network circuits

Bullock

Grossberg

1992

Human Movement Science

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Section: Tri-phasic Emg Genesissupporting

confidence: 85%

Emergence of tri-phasic muscle activation from the nonlinear interactions of central and spinal neural network circuits

Bullock

Grossberg

1992

Human Movement Science

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“…Thus, the recurrent axon collaterals have been shown to excite small interneurones, the socalled Renshaw cells (Renshaw, 1946;Eccles, Fatt & Koketsu, 1954), which in S. CULLHEIM AND J.-O. KELLERTH turn inhibit a-motoneurones (Eccles et al 1954), y-motoneurones (Brown, Lawrence & Matthews, 1968;Ellaway, 1968Ellaway, , 1971, Ia-interneurones (Hultborn, Jankowska & Lindstr6m, 1968, 1971, other Renshaw cells (Ryall, 1970) and ventral spinocerebellar tract neurones (Lindstr6m & Schomburg, 1973). Although the full physiological implications of these complex reflex actions still remain to be revealed, it is evident that the activity of a-motoneurones is strongly influenced by the recurrent motor axon collaterals.…”

Section: Introductionmentioning

confidence: 99%

A morphological study of the axons and recurrent axon collaterals of cat alpha‐motoneurones supplying different hind‐limb muscles.

Cullheim¹,

Kellerth²

1978

The Journal of Physiology

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SUMMARY1. Intracellular injections with horseradish peroxidase were performed in cat a-motoneurones supplying various hind-limb muscles.2. Ten a-motoneurones from each of the quadriceps, posterior biceps, gastroenemius-soleus and anterior tibial pools as well as from the pool supplying the short plantar muscles were collected for morphological analysis of the intramedullary axonal systems including the recurrent axon collaterals.3. The diameter of the a-motor axons showed considerable variation within each motoneurone pool, the total range being from 4 6 to 9 0 ,tm. No significant difference in mean axon diameter was obtained between the different pools.4. All a-motoneurones supplying the short plantar muscles and one single amotoneurone supplying the quadriceps muscle lacked collaterals completely, while the remaining motoneurones gave off one to five collaterals.5. The number of axon collateral outbulgings, interpreted as synaptic boutons, which originated from a single a-motoneurone showed large variation within each pool that possessed axon collaterals, the total range being from seventeen to 158. The mean number varied from forty-four (quadriceps) to eighty-two (anterior tibial).6. The axon collateral outbulgings were distributed not only in the Renshaw cell area ventromedial to the main motor nuclei but also in those parts of the motor nuclei which were located in the vicinity of the parent cell bodies. In the rostrocaudal direction, the outbulgings were distributed within a distance of less than 1 mm around the position of the parent cell bodies.7. Some physiological implications of the lack of axon collaterals from a-motoneurones supplying the short plantar muscles were discussed in relation to the functional characteristics of plantar muscles and motor units.

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“…DHI3E did not block excitation by DLH. It does not antagonize a muscarinic component of the excitatory action of acetyl-,-methylcholine (Curtis & Ryall, 1966b) and it facilitates the late discharge of Renshaw cells evoked by antidromic ventral root volleys (Curtis & Ryall, 1966c;Ryall, 1970). It was observed that atropine consistently and selectively blocked the excitatory action of ACh, leaving excitation by DLH unaffected (Figures 1, 2).…”

Section: Agonistsmentioning

confidence: 95%

A Re‐evaluation of Acetylcholine Receptors on Feline Renshaw Cells

King

Ryall

1981

British J Pharmacology

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1 The effects of atropine, methylatropine and lachesine administered by ionophoresis were examined on responses of Renshaw cells to acetylcholine, acetyl-43-methylcholine, nicotine and DL-muscarine in cats anaesthetized with pentobarbitone or chloralose. 2 The antagonists were as effective in antagonizing excitation by nicotine as they were in antagonizing excitation by acetylcholine and were only slightly more effective in antagonizing excitation by acetyl-,3-methylcholine.

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Renshaw cell mediated inhibition of Renshaw cells: patterns of excitation and inhibition from impulses in motor axon collaterals.

Cited by 140 publications

References 0 publications

Emergence of tri-phasic muscle activation from the nonlinear interactions of central and spinal neural network circuits

Emergence of tri-phasic muscle activation from the nonlinear interactions of central and spinal neural network circuits

A morphological study of the axons and recurrent axon collaterals of cat alpha‐motoneurones supplying different hind‐limb muscles.

A Re‐evaluation of Acetylcholine Receptors on Feline Renshaw Cells

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