Anesthetics nerve agent interactions

Both the inhaled and the intravenous anesthetics can depress spontaneous and evoked activity of neurons in many regions of the brain. Older concepts of the mechanism of anesthesia evoked nonspecific interactions of these agents with the lipid matrix of the nerve membrane (the so-called Meyer-Overton principle)—interactions that were thought to lead to secondary changes in ion flux. More recently, evidence has accumulated suggesting that the modification of ion currents by anesthetics results from more direct interactions with specific nerve membrane components. The ionic mechanisms involved for different anesthetics may vary, but at clinically relevant concentrations they appear to involve interactions with members of the ligand-gated ion channel family. 

Receptor interactions bupivacaine binds to the intracellular portions of sodium channels and blocks sodium influx into nerve cells which therefore prevents nerve cell depolarization. Since pain-transmitting nerve fibers tend to be thinner (small diameter) and either unmyelinated or only lightly myelinated (myelin is non-polar and lipophilic), the local anesthetic agent can diffuse more readily into them than into thicker and more heavily myelinated nerve fibers such as touch and proprioception. 

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