Renshaw Cell - Physiology

Physiology

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.

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. It has been shown that:

• 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], antidromic ventral axons as well as “descending” inhibition. 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.

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. 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 predispose someone to tetanic contractions, and can prove fatal if the diaphragm becomes involved.