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Renshaw cells

NeurologyNervousMusculoskeletal

Summary

Renshaw cells are inhibitory interneurons in the ventral horn of the spinal cord that receive collaterals from alpha motor neurons and feed back inhibition onto them. They mediate recurrent inhibition, and their loss underlies the spasms of tetanus.

Detail

An alpha motor neuron sends an axon collateral to a Renshaw cell, which releases glycine and GABA back onto that same motor neuron and its neighbours, damping and smoothing motor output and sharpening the contrast between agonist and antagonist activation. Two classic toxins target this circuit. Tetanospasmin, produced by Clostridium tetani, is a zinc protease that cleaves SNARE proteins in inhibitory Renshaw interneurons, preventing glycine and GABA release; loss of inhibition produces sustained co-contraction of agonists and antagonists, giving trismus, risus sardonicus, and opisthotonus with a fully conscious patient. Strychnine acts on the same pathway pharmacologically by competitively antagonizing the postsynaptic glycine receptor, producing similar convulsive rigidity. This contrasts with botulinum toxin, which cleaves SNAREs at the neuromuscular junction and at cholinergic autonomic synapses, blocking excitatory acetylcholine release and producing flaccid paralysis. The clinically useful mnemonic is that tetanus blocks inhibition causing rigidity, while botulism blocks excitation causing flaccidity.

Sources

  • First Aid for the USMLE Step 1
  • Kandel Principles of Neural Science

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