Renshaw cell
Renshaw cell | |
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Details | |
Neurotransmitter | Glycine |
Identifiers | |
MeSH | D066293 |
NeuroLex ID | nifext_113 |
FMA | 86787 |
Anatomical terms of neuroanatomy |
Renshaw cells are inhibitory
- They receive an excitatory collateral from the alpha neuron's axon as they emerge from the motor root, and are thus "kept informed" of how vigorously that neuron is firing.
- They send an inhibitory axon to synapse with the cell body of the initial alpha neuron and/or an alpha motor neuron of the same motor pool.
In this way, the Renshaw cell action represents a negative feedback mechanism. A Renshaw cell may be supplied by more than one alpha motor neuron collateral and it may synapse on multiple motor neurons.
Function
Although during embryonic development the Renshaw cells lack synapses from the dorsal root, prenatal and postnatal stages show the development of dorsal root originating synapses, which are functional and stimulate action potentials. But these decrease during development while acetylcholine motor axons begin to synapse and proliferate with Renshaw cells, ultimately being primarily stimulated by the motor neurons.[1]
The Renshaw cells are ultimately excited by multiple antidromic motor neuron axons, where the majority of axons originate from
- Recurrent inhibition is depressed during strong voluntary contractions (presumably due to inhibition of the Reshaw cell by descending input).
- Renshaw cells are more inhibited at the same level during a dynamic contraction compared with sustained contraction.
- Renshaw cells are facilitated during weak voluntary contractions.
- Renshaw cells are facilitated during co-activation of antagonists.
The Renshaw cells may also be inhibited by both proprioceptive dorsal root afferents],
In essence the Renshaw cells regulate the firing of the alpha motor neuron leaving the ventral horn. Conceptually they remove “noise” by dampening the firing frequency of over-excited neurons with a
The rate of discharge of the Renshaw cell is broadly proportional to the rate of discharge of the associated motor neuron(s), and the rate of discharge of the motor neuron(s) is broadly inversely proportional to the rate of discharge of the Renshaw cell(s). Renshaw cells thus act as "limiters," or "governors," on the alpha motor neuron system, thus helping to prevent muscular damage from tetanus.
Renshaw cells utilize the neurotransmitter glycine as an inhibitory substance that synapses on the alpha motor neurons.
Clinical significance
Renshaw cells are also the target of the toxin of Clostridium tetani, a Gram positive, spore-forming anaerobic bacterium that lives in the soil, and causes tetanus. When wounds are contaminated with C. tetani, the toxin travels to the spinal cord where it inhibits the release of glycine, an inhibitory neurotransmitter, from Renshaw cells. As a result, alpha motor neurons become hyperactive, and muscles constantly contract.
Strychnine poison also specifically acts on these cell's ability to control alpha motor neuron firing by binding to the glycine receptors on the alpha motor neuron and thus muscles continually contract and may prove fatal if the diaphragm is involved.
History
The concept of the Renshaw cells was postulated by
See also
List of distinct cell types in the adult human body
References
- ^ George Z. Mentis, Valerie C. Siembab, Ricardo Zerda, Michael J. O'Donovan, and Francisco J. Alvarez, Primary Afferent Synapses on Developing and Adult Renshaw Cells. The J.of Neuroscience, 2006, 26(51):13297-13310
- ^ Mazzocchio R, Rossi A, Rothwell JC. Depression of Renshaw recurrent inhibition by activation of corticospinal fibres in human upper and lower limb. J Physiol (Lond) 1994; 481: 487–9
- ^ H. Hultborn, E. Pierrot-Deseilligny.Changes in recurrent inhibition during voluntary soleus contractions in man studied by an H-Reflex Technique. J. Phyeiol. 1979, 297, pp. 229–251.
- ^ Iles JF, Pardoe J. Changes in transmission in the pathway of heteronymous spinal recurrent inhibition from soleus to quadriceps motor neurons during movement in man. Brain 1999; 122: 1757–64
- ^ Nielsen J, Pierrot-Deseilligny E. Evidence of facilitation of soleus-coupled Renshaw cells during voluntary co-contraction of antagonistic ankle muscles in man. J Physiol (Lond) 1996; 493: 603–11
- ^ Wilson VJ, Talbot WH, Kato M Inhibitory convergence upon Renshaw cells. Journal of neurophysiology. 1964;27:1063-1079.
- ^ R. W. Ryall, M. F. Piercey, and C. Polosa. Intersegmental and intrasegmental distribution of mutual inhibition of Renshaw cells. J Neurophysiol 34: 700-, 1971
- ^ RYALL, R. W. Renshaw cell mediated inhibition of Renshaw cells: patterns of excitation and inhibition from impulses in motor axon collaterals. J.Neurophysiol. 1970, 33, 257-270
- ^ R. Granit, J. Haase, and L. T. Rutledge. Recurrent inhibition in relation to frequency of firing and limitation of discharge rate of extensor motoneurones. J. Physiol. 1960 December; 154(2): 308–328.
- ^ J Haase, J van der Meulen. Effects of supraspinal stimulation on Renshaw cells belonging to extensor motoneurones. Journal of neurophysiology. 10/1961; 24:510-20
- ^ D R Curtis, C J Game, D Lodge, and R M McCulloch. A pharmacological study of Renshaw cell inhibition. J. Physiol. 1976 June; 258(1): 227–242
- ^ Victor J. Wilson & William H. Talbot. Integration at an Inhibitory Interneurone: Inhibition of Renshaw Cells. Nature 1963 200, 1325–1327
- ^ Renshaw B. Central effects of centripetal impulses in axons of spinal ventral roots. J Neurophysiol 1946 9:191–204
- ^ Eccles JC, Fatt P, Koketsu K. Cholinergic and inhibitory synapses in a pathway from motor-axon collaterals to motoneurones. J. Physiol. 1954;126:524–562.
- ^ Renshaw B. Influence of discharge of motoneurons upon excitation of neighboring motoneurons. J Neurophysiol 1941 4:167
- ^ Lloyd, D. P. C.. Facilitation and inhibition of spinal motoneurons, J.Neurophysiol.,1946, 9,421.
- ^ Lloyd, D. P. C., After-currents, after-potentials, excitability, and ventral root electrotonus in spinal motoneurons, J.gen. Physiol..,1951,35 ,289