Question:hard
Which combination of the following statements about presynaptic inhibition is TRUE?
- Axoaxonal synapse mediated
- Prolongs IPSP
- Prolonged by anaesthesia
- Not affected by pharmacological agents
- It affects motor endplate potential
- Decreased by strychnine
- Decreased by picrotoxin
Which combination of the following statements about presynaptic inhibition is TRUE?
- Axoaxonal synapse mediated
- Prolongs IPSP
- Prolonged by anaesthesia
- Not affected by pharmacological agents
- It affects motor endplate potential
- Decreased by strychnine
- Decreased by picrotoxin
Show Hint
Presynaptic inhibition is axo-axonal and GABA mediated: blocked by picrotoxin (not strychnine), prolonged by anaesthesia.
Updated On: Jul 8, 2026
- a, d, f
- b, e, f
- a, c, f
- a, c, g
Show Solution
The Correct Option is D
Solution and Explanation
Step 1: Set up a two column comparison.
It helps to compare presynaptic inhibition against postsynaptic (direct) inhibition side by side, since most of the statements are really testing that contrast.
Step 2: Anatomy.
Postsynaptic inhibition uses an axo-somatic or axo-dendritic synapse and hyperpolarises the cell body, producing a clear IPSP. Presynaptic inhibition instead uses an axo-axonal synapse, sitting on another axon terminal, so option (a) fits presynaptic inhibition.
Step 3: Electrical signature.
Because presynaptic inhibition works by cutting down transmitter release rather than hyperpolarising the postsynaptic membrane, it does not produce or prolong a postsynaptic IPSP. So option (b) does not belong to presynaptic inhibition.
Step 4: Drug sensitivity.
General anaesthetics boost GABA-A receptor function at the axo-axonal terminal, so they prolong presynaptic inhibition, making option (c) correct. Since GABA-A receptors are the target here, presynaptic inhibition is clearly drug sensitive, so option (d) is wrong.
Step 5: Site of action.
The motor endplate potential belongs to the neuromuscular junction, a site with no axo-axonal GABA synapse, so option (e) does not apply to presynaptic inhibition.
Step 6: Pharmacological block.
Glycine receptor blockers such as strychnine remove postsynaptic inhibition, while GABA-A receptor blockers such as picrotoxin remove presynaptic inhibition. So option (f), strychnine, is wrong for presynaptic inhibition, and option (g), picrotoxin, is right.
Step 7: Collect the correct set.
Putting the correct items together gives (a), (c), and (g).
\[ \boxed{a,\ c,\ g} \]
It helps to compare presynaptic inhibition against postsynaptic (direct) inhibition side by side, since most of the statements are really testing that contrast.
Step 2: Anatomy.
Postsynaptic inhibition uses an axo-somatic or axo-dendritic synapse and hyperpolarises the cell body, producing a clear IPSP. Presynaptic inhibition instead uses an axo-axonal synapse, sitting on another axon terminal, so option (a) fits presynaptic inhibition.
Step 3: Electrical signature.
Because presynaptic inhibition works by cutting down transmitter release rather than hyperpolarising the postsynaptic membrane, it does not produce or prolong a postsynaptic IPSP. So option (b) does not belong to presynaptic inhibition.
Step 4: Drug sensitivity.
General anaesthetics boost GABA-A receptor function at the axo-axonal terminal, so they prolong presynaptic inhibition, making option (c) correct. Since GABA-A receptors are the target here, presynaptic inhibition is clearly drug sensitive, so option (d) is wrong.
Step 5: Site of action.
The motor endplate potential belongs to the neuromuscular junction, a site with no axo-axonal GABA synapse, so option (e) does not apply to presynaptic inhibition.
Step 6: Pharmacological block.
Glycine receptor blockers such as strychnine remove postsynaptic inhibition, while GABA-A receptor blockers such as picrotoxin remove presynaptic inhibition. So option (f), strychnine, is wrong for presynaptic inhibition, and option (g), picrotoxin, is right.
Step 7: Collect the correct set.
Putting the correct items together gives (a), (c), and (g).
\[ \boxed{a,\ c,\ g} \]
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