Thus Renshaw cell inhibition is a negative feedback inhibition. Moreover a Renshaw cell may be supplied by more than one alpha motor neuron collaterals and that it may synapse on multiple motor neurons.
The rate of discharge of the Renshaw cell is thus 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.
Recent findings in central nervous system described by researchers from National Institute of Neurological Disorders and Stroke.
Jul 05, 2010; A new study, 'Mechanisms regulating the specificity and strength of muscle afferent inputs in the spinal cord,' is now available....