In typical GABAergic signaling, what effect do chloride ions have on the postsynaptic membrane potential?

In typical GABAergic signaling, what effect do chloride ions have on the postsynaptic membrane potential?

• A. They enter the neuron to produce depolarization.
• B. They exit the neuron to produce depolarization.
• C. They are pumped out by Na+/K+ ATPase to terminate inhibition.
• D. They enter the neuron to produce hyperpolarization.

Answer: (D)

Opening GABA_A receptor channels creates a chloride conductance. In mature neurons, the intracellular Cl− concentration is kept low, so the Cl− equilibrium potential is more negative than the resting membrane potential. When these channels open, Cl− flows into the cell, pulling the membrane potential toward this negative reversal potential. The result is hyperpolarization, making it harder for the neuron to reach threshold and fire an action potential. In other words, chloride entering the neuron under typical mature conditions produces an inhibitory postsynaptic potential. (Note: in some developing neurons, intracellular Cl− can be higher, which can make GABAergic signaling depolarizing, but the standard scenario described here is chloride influx causing inhibition.)

Opening GABA_A receptor channels creates a chloride conductance. In mature neurons, the intracellular Cl− concentration is kept low, so the Cl− equilibrium potential is more negative than the resting membrane potential. When these channels open, Cl− flows into the cell, pulling the membrane potential toward this negative reversal potential. The result is hyperpolarization, making it harder for the neuron to reach threshold and fire an action potential. In other words, chloride entering the neuron under typical mature conditions produces an inhibitory postsynaptic potential. (Note: in some developing neurons, intracellular Cl− can be higher, which can make GABAergic signaling depolarizing, but the standard scenario described here is chloride influx causing inhibition.)