Questions: Synaptic Transmission

Question 1

What is the direct role of Ca²⁺ influx at the axon terminal when an action potential arrives?

• A. It opens Na⁺ channels to depolarize the postsynaptic cell
• B. It triggers exocytosis of neurotransmitter-filled vesicles
• C. It hyperpolarizes the axon terminal to reset it for the next signal
• D. It binds to postsynaptic receptors to generate an EPSP

Answer: (B)

Voltage-gated Ca²⁺ channels open when the action potential reaches the terminal, and the resulting Ca²⁺ influx is the direct trigger for vesicle docking and fusion (exocytosis), releasing neurotransmitter into the synaptic cleft. Ca²⁺ does not itself cross the cleft or bind postsynaptic receptors — it acts inside the presynaptic terminal as the coupling signal between electrical arrival and chemical release.

Question 2

An inhibitory postsynaptic potential (IPSP) is produced when the postsynaptic neuron stops receiving electrical input and goes passive.

• T. True
• F. False

Answer: False

An IPSP is an active process: inhibitory neurotransmitters (like GABA binding GABA-A receptors) open Cl⁻ channels, causing chloride to flow into the cell, actively hyperpolarizing the membrane potential further from threshold. The neuron does not simply go passive — it is pushed away from firing. This distinction matters clinically: drugs that enhance GABA-A activity (like benzodiazepines) actively suppress neural firing rather than just reducing excitation.

Question 3

How can the same neurotransmitter produce excitatory effects at some synapses and inhibitory effects at others?

Model answer: The effect depends on which receptor the neurotransmitter binds, not on the neurotransmitter itself. Different receptor types open different ion channels: if the channel conducts Na⁺ (inward), the membrane depolarizes (excitatory); if it conducts Cl⁻ or K⁺ (outward), the membrane hyperpolarizes (inhibitory). GABA is typically inhibitory, but in early development when Cl⁻ gradients are reversed, GABA-A activation causes Cl⁻ to flow outward, producing depolarization instead.

This is a fundamental principle: a chemical signal's effect is determined by the receiver, not the signal itself. The receptor defines what ion channel opens or what G-protein cascade activates. This gives the nervous system enormous flexibility — the same neurotransmitter released from different neurons can have opposite effects in different target cells or developmental stages.