In the spinal cord, an axo-axonic interneuron forms a synapse onto the terminal of a primary afferent fiber carrying pain input. Activation of this interneuron reduces transmitter release from the afferent terminal without changing the afferent's membrane potential significantly. What is the underlying mechanism?

• A Reduced calcium entry into the terminal during the action potential ✓
• B Glycine-mediated opening of postsynaptic chloride channels on the terminal
• C GABA-mediated increase in potassium efflux from the terminal
• D Enzymatic degradation of the transmitter within the synaptic cleft

Explanation

Presynaptic inhibition is mediated by GABA-B receptors on the afferent terminal. GABA closes pre-existing calcium channels and opens potassium conductance slightly, so the action potential arriving at the terminal produces less calcium influx and fewer vesicles fuse. The key point is that the afferent action potential itself still fires and conducts normally; only the release step is dampened. Postsynaptic glycine receptors mediate reciprocal inhibition between motor neurons, a distinct circuit.

Reference: Ganong's Review of Medical Physiology, 27th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.