Renshaw cell

Renshaw cells are inhibitory interneurons

found in the gray matter of the spinal cord,
and are associated in two ways with an
alpha motor neuron.

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.

Renshaw Cell
Details

Neurotransmitter Glycine

Identifiers

NeuroLex ID nifext_113

Anatomical terms of neuroanatomy

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 synergist motor neurons,
and in turn the Renshaw cell synapses
with multiple neurons, eliciting IPSP in
alpha motor, 1a inhibitory interneurons and
gamma motor neurons. The antidromic
collateral circuit back to the triggering
motor neuron is known as “recurrent
inhibition”. This homonymous inhibition is
not universal. Whereas most initial
experiments have been done on cats, it
has been found that in man that proximal
muscles of the hand and foot do not have
homonymous inhibition. Heteronymous
inhibition has been found to be dominant
in the leg compared to the arm, where
antagonist muscles work simultaneously.
(It must also be noted that Renshaw cells
are activated by gamma motor neurons,
but to a lesser extent). The Renshaw cells
not only synapse with homonymous and
heteronymous nerves, but also with the Ia
interneurones, which are stimulated by the
Ia afferents from the same muscle group
activated by the motor neurons, which
have an inhibitory effect on the antagonist
muscle group. This “recurrent facilitation”
causes reduced inhibition of the reciprocal
inhibition of the Ia interneuron of the
antagonist group (Baret et al.; 2003),
which may in turn also be inhibited by
signals from the corticospinal tract.[2] It
has been shown that:[3][4][5]

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],[6][7] antidromic ventral axons[8]
as well as “descending” inhibition.[9][10]
The hyperpolarization of Renshaw cells by
afferent and descending neurons have
been shown to be caused by the release of
glycine, but GABA may also hyperpolarize
the Renshaw cell - for a prolonged time
relative to glycine. It has also been shown
that glycine is the inhibitory transmitter
released by the Renshaw cells.[11][12]
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 negative
feedback loop, which prevents weakly
excited alpha motor neurons from firing.
Descending spinal cord nerves in turn
regulate the Renshaw cells.

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 gylcine
receptors on the alpha motor neuron and
thus muscles contiually contract and may
prove fatal if the diaphram is involved.

History
The concept of the Renshaw cells was
postulated by Birdsey Renshaw (1911–
1948),[13] when it was discovered that with
antidromic signals from a motor neuron
running collaterally back via the ventral
root into the spinal cord, there were
interneurons firing with a high frequency,
resulting in inhibition. Later work by Eccles
et al.,[14] provided evidence that these
interneurons, which they called “Renshaw
Cells,” are stimulated by acetylcholine
from motor neurons (nicotinic receptor).
Previous work by Renshaw[15] and
Lloyd[16][17] had shown that this antidromic
inhibition resembled direct inhibition from
spinal nerves but resulted in relatively
longer inhibition of 40-50 ms (compared to
15 ms). The antidromic stimulation of the
nerve fiber also resulted in action
potentials in the cell bodies of the motor
neurons along with hyperpolarization of
other groups of motor neurons. In the
event where the initial stimulation of the
motor neuron originated in a spinal tract
the Renshaw cell spike occurred during the
declining phase of the initial motor neuron
soma spike giving an indication of the
source and sequence of stimulation of the
Renshaw cell.

References
1. 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
2. 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
3. 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.
4. 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
5. 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
6. Wilson VJ, Talbot WH, Kato M
Inhibitory convergence upon Renshaw
cells. Journal of neurophysiology.
1964;27:1063-1079.
7. R. W. Ryall, M. F. Piercey, and C.
Polosa. Intersegmental and
intrasegmental distribution of mutual
inhibition of Renshaw cells. J
Neurophysiol 34: 700-, 1971
8. 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
9. 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.
10. 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
11. 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
12. Victor J. Wilson & William H. Talbot.
Integration at an Inhibitory
Interneurone: Inhibition of Renshaw
Cells. Nature 1963 200, 1325–1327
13. Renshaw B. Central effects of
centripetal impulses in axons of spinal
ventral roots. J Neurophysiol 1946
9:191–204
14. 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.
15. Renshaw B. Influence of discharge of
motoneurons upon excitation of
neighboring motoneurons. J
Neurophysiol 1941 4:167
 16. Lloyd, D. P. C.. Facilitation and
inhibition of spinal motoneurons,
J.Neurophysiol.,1946, 9,421.
17. Lloyd, D. P. C., After-currents, after-
potentials, excitability, and ventral root
electrotonus in spinal motoneurons,
J.gen. Physiol..,1951,35 ,289

External links
Diagram at pediatricneuro.com
NIF Search - Renshaw Cell via the
Neuroscience Information Framework

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