What is the primary mechanism by which local anesthetics achieve nerve blockade?

What is the primary mechanism by which local anesthetics achieve nerve blockade?

• A. They increase depolarization
• B. They decrease depolarization
• C. They block calcium channels
• D. They stimulate nerve impulses

Answer: (B)

Local anesthetics block nerve conduction by preventing the nerve from depolarizing. They achieve this by inhibiting voltage-gated sodium channels in the axon membrane. When a nerve impulse would normally open these channels and allow sodium to rush in, the anesthetic binds from the inside of the neuron and keeps the channels from opening or staying inactivated. This reduces sodium influx, raises the threshold for action potential generation, and slows or stops the propagation of the impulse along the fiber. As a result, the nerve cannot carry pain signals to the brain. In addition, local anesthetics are weak bases that cross the membrane in their nonionized form and then become ionized inside the cell to bind the channel. In acidic or inflamed tissue, more of the drug is ionized outside, which can lessen diffusion into the nerve and reduce effectiveness. Why the other ideas don’t fit: increasing depolarization would promote nerve signaling rather than block it; blocking calcium channels mainly affects neurotransmitter release at synapses rather than the ability of the axon to propagate an action potential; stimulating nerve impulses would clearly not produce blockade.

Local anesthetics block nerve conduction by preventing the nerve from depolarizing. They achieve this by inhibiting voltage-gated sodium channels in the axon membrane. When a nerve impulse would normally open these channels and allow sodium to rush in, the anesthetic binds from the inside of the neuron and keeps the channels from opening or staying inactivated. This reduces sodium influx, raises the threshold for action potential generation, and slows or stops the propagation of the impulse along the fiber. As a result, the nerve cannot carry pain signals to the brain.

In addition, local anesthetics are weak bases that cross the membrane in their nonionized form and then become ionized inside the cell to bind the channel. In acidic or inflamed tissue, more of the drug is ionized outside, which can lessen diffusion into the nerve and reduce effectiveness.

Why the other ideas don’t fit: increasing depolarization would promote nerve signaling rather than block it; blocking calcium channels mainly affects neurotransmitter release at synapses rather than the ability of the axon to propagate an action potential; stimulating nerve impulses would clearly not produce blockade.