Inhibitory post-synaptic potentials (IPSPs) are generated by which mechanism?

• A Increased Na+ conductance, depolarising the membrane beyond threshold
• B Decreased Ca2+ conductance at the presynaptic terminal, reducing neurotransmitter release
• C Activation of metabotropic receptors that increase intracellular cGMP
• D Increased Cl- conductance (via GABA-A receptors) or increased K+ conductance, hyperpolarising the membrane ✓

Explanation

IPSPs are generated by postsynaptic membrane hyperpolarisation, moving the membrane potential away from threshold. The two main mechanisms are: (1) GABA-A receptor activation increases Cl- conductance — Cl- enters the cell (or K+ leaves) depending on the Cl- equilibrium potential, hyperpolarising the membrane; (2) glycine (inhibitory interneurons) and some GABA-B receptors increase K+ conductance, allowing K+ to exit and hyperpolarise the cell. The equilibrium potential for Cl- in mature neurons is more negative than the resting potential, so opening Cl- channels clamps the membrane near E_Cl (around -70 mV), resisting depolarisation even if excitatory input occurs ('shunting inhibition').

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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