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Neuron: Renshaw Cell
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The concept of the Renshaw cells was postulated by B. Renshaw [6], when it was discovered that with antidromic signals from a motor neuron running collaterally back via the ventral horn into the spinal cord, there were interneuron’s firing with a high frequency, resulting in inhibition. Later work by Eccles et al [7], gave evidence that these interneurones which they labelled as “Renshaw Cells” were stimulated by acetylcholine from motor neurons. Previous work by Renshaw [8] and Lloyd [9,10] had show that this antidromic inhibition resembled direct inhibition from spinal nerves but resulted in relatively longer inhibition of 40-50msec (compared to 15msec). The stimulation of the antidromic nerve fiber also resulted in action potentials of the central part of the motoneurones that would generate the original impulse, along with hyperpolarization of other groups of motor neurons. In the event where the initial stimulation of the motoneuron originated in the spinal track, these impulses occurred after the initial stimulation, and where the Renshaw cell spike occurred during the declining phase of the initial motoneuron soma spike had thus giving an indication of the source and sequence of stimulation of the Renshaw cell.

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 [11]. 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, Ia inhibitory interneurones 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. Where as 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” results in 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 [12]. It has been shown that [13, 14, 15]: • 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 week voluntary contractions. • Renshaw cells are facilitated during co-activation of antagonists.

The Renshaw cells may also be inhibited by both proprioceptive dorsal root afferents [16,17], antidromic ventral axons [6,17,18] as well as “descending” inhibition [19, 20]. 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 be show that glycine is the inhibitory transmitter released by the Renshaw cells [21,22].

In essence the Renshaw cells regulate the firing of the alpha motor neuron leaving the ventral horn. Conceptually removing “noise”; this is done by dampening the firing frequency of over excited neurons by a negative feedback loop and preventing the firing of those weakly excited. The Renshaw cells are in-turn regulated descending nerves of the spinal cord.

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.
Next, they send their own inhibitory axon to synapse with the cell body of the initial alpha neuron.

In this way, Renshaw cell inhibition represents a negative feedback mechanism. A Renshaw cell may be supplied by more than one alpha motor neuron collaterals and it may synapse on multiple motor neurons.

The rate of discharge of the Renshaw cell is broadly proportional to the rate of discharge of the associated motor neuron, and the rate of discharge of the motor neuron is broadly inversely proportional to the rate of discharge of the Renshaw cell. 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 fibers. Strychnine specifically acts on these cell's ability to control alpha motor neuron firing by binding to the glycine receptors on the motor neuron. This antagonistic poison will thus predispose someone to tetanic contractions, and can prove fatal if the diaphragm becomes involved.

Renshaw cells are also the target of the toxin of Clostridium tetani, a spore-forming anaerobic bacterium that lives in the soil. When wounds are contaminated with C. tetani, the toxin travels to the spinal cord where it inhibits the release of glycine from Renshaw cells. As a result, alpha motor neurons become hyperactive, and muscles constantly contract.

[6] Renshaw B. Central effects of centripetal impulses in axons of spinal ventral roots. J Neurophysiol 1946 9:191–204 [7] 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. [8] Renshaw B. Influence of discharge of motoneurons upon excitation of neighboring motoneurons. J Neurophysiol 1941 4:167 [9] Lloyd, D. P. C.. Facilitation and inhibition of spinal motoneurons, J.Neurophysiol.,1946, 9,421. [10] Lloyd, D. P. C., After-currents, after-potentials, excitability, and ventral root electrotonus in spinal motoneurons, J.gen. Physiol..,1951,35 ,289 [11] 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 [12] 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 [13] 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. [14] 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 [15] 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 [16] Wilson VJ, Talbot WH, Kato M Inhibitory convergence upon Renshaw cells. Journal of neurophysiology. 1964;27:1063-1079. [17] R. W. Ryall, M. F. Piercey, and C. Polosa. Intersegmental and intrasegmental distribution of mutual inhibition of Renshaw cells. J Neurophysiol 34: 700-, 1971 [18] 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 [19] 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. [20] 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 [21] 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 [22] Victor J. Wilson & William H. Talbot. Integration at an Inhibitory Interneurone: Inhibition of Renshaw Cells. Nature 1963 200, 1325 - 1327

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