Q1
LONG ANSWER
10M
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Define action potential. Describe its phases and ionic basis. Add a note on the refractory period.
Definition
Action potential = a rapid, transient, self-propagating reversal of membrane potential that occurs when an excitable cell is stimulated at or above threshold.
Phases
| Phase | Potential change | Ionic basis |
|---|---|---|
| Resting | −70 mV | K+ leak; Na+–K+ pump |
| Latent period | — | Stimulus artefact to onset |
| Depolarisation (ascending limb) | −70 → +35 mV | Na+ influx through voltage-gated channels |
| Overshoot | 0 to +35 mV | Reversal of polarity |
| Repolarisation (descending limb) | +35 → −70 mV | Na+ channel inactivation + K+ efflux |
| After-depolarisation | Slow return | Slowed K+ efflux |
| After-hyperpolarisation | Below −70 mV | Excess K+ efflux (channels close slowly) |
Ionic Basis
Stimulus → Membrane depolarises to firing level (−55 mV) → Voltage-gated Na+ channels open → Na+ influx → further depolarisation → positive feedback → spike to +35 mV → Na+ channels inactivate; K+ channels open → K+ efflux → repolarisation
- Na+ channel has two gates — an activation gate (outer, opens fast) and an inactivation gate (inner, closes slowly). This explains the refractory period
- Total duration in nerve 1–2 ms; in skeletal muscle 2–4 ms; in cardiac muscle 200–300 ms
- Actual ion movement is minute — 1 in 100,000 ions; the Na+–K+ pump restores it later
Properties of Action Potential
- All-or-none law — a subthreshold stimulus produces no response; at or above threshold the response is maximal and of constant amplitude, regardless of stimulus strength
- Propagated without decrement — amplitude does not fall along the fibre
- Self-propagating — local circuit currents depolarise the adjacent segment
- Refractory period follows
- Stimulus strength is coded by frequency, not amplitude
Refractory Period
| Absolute refractory period | Relative refractory period | |
|---|---|---|
| Timing | Depolarisation + first third of repolarisation | Rest of repolarisation + after-depolarisation |
| Duration (nerve) | 0.4 ms | 0.5 ms |
| Response | No stimulus, however strong, can excite | A stronger than normal stimulus can excite |
| Cause | Na+ channels inactivated | Some Na+ channels recovered; K+ efflux continues |
- Significance — limits the maximum firing frequency (about 2500/s in nerve) and ensures one-way conduction
- In cardiac muscle the long refractory period prevents tetanus — essential for the pumping action
Electrotonic Potential and Local Response
- Subthreshold stimulus → local, graded, non-propagated change
- Catelectrotonus — depolarisation at the cathode → ↑ excitability
- Anelectrotonus — hyperpolarisation at the anode → ↓ excitability
- Local response — at 7–15% below threshold; graded and can summate
Strength–duration Curve
| Term | Definition |
|---|---|
| Rheobase | The minimum strength of stimulus that can excite when applied for an infinite (long) duration |
| Utilisation time | The minimum time for which a rheobasic stimulus must act |
| Chronaxie | The minimum time for which a stimulus of twice rheobase must act |
- Chronaxie is inversely proportional to excitability — a short chronaxie means a highly excitable tissue
- Chronaxie values — nerve 0.0001–0.001 s; skeletal muscle 0.001–0.01 s; cardiac muscle 0.001–0.003 s
- Denervated muscle has a greatly prolonged chronaxie — used to detect denervation
Compound Action Potential
- Recorded from a whole nerve trunk, not a single fibre
- Does not obey the all-or-none law — amplitude increases with stimulus strength as more fibres are recruited
- Shows multiple peaks (A, B, C waves) because fibres conduct at different velocities
Applied Aspects
- Local anaesthetics (lignocaine) → block voltage-gated Na+ channels from within → no action potential → loss of sensation. Small unmyelinated pain fibres are blocked first
- Tetrodotoxin (puffer fish) → blocks Na+ channels; tetraethylammonium blocks K+ channels
- Hypocalcaemia → ↑ Na+ permeability → firing level approaches RMP → spontaneous discharge → tetany
- Hyperkalaemia → sustained depolarisation → Na+ channels inactivated → cardiac arrest
- Multiple sclerosis → demyelination → conduction block or slowing → visual and motor deficits
- Epilepsy → abnormal synchronous high-frequency discharge of cortical neurones; phenytoin acts by prolonging Na+ channel inactivation
- Hyperventilation → alkalosis → ↓ ionised calcium → tetany with carpopedal spasm
All questions in Nerve & Muscle Physiology
- Q1Define action potential. Describe its phases and ionic basis. Add a note on the refractory period. ★
- Q2Describe the structure of the neuromuscular junction and the steps of neuromuscular transmission. Add a note on the drugs acting on it. ★
- Q3Describe the sliding filament mechanism of skeletal muscle contraction. Explain excitation–contraction coupling and the role of calcium. ★
- Q4Classify nerve fibres. Describe the mechanism of impulse conduction and compare saltatory with continuous conduction. Add a note on nerve degeneration and regeneration. ★
- Q5Compare the structure and properties of skeletal, cardiac and smooth muscle. Describe the mechanism of smooth muscle contraction. ★
- SN1Write a short note on myasthenia gravis. ★
- SN2Write a short note on rigor mortis. ★
- SN3Define motor unit. Describe the innervation ratio and the size principle. ★
- SN4Differentiate between isotonic and isometric contraction.
- SN5Describe the changes following section of a peripheral nerve. Add a note on regeneration. ★
- SN6Describe the length–tension relationship of skeletal muscle and give its significance.
- SN7Write a short note on muscle fatigue. Add a note on oxygen debt.