describe the sequence of events that results in an action potential in a sensory neurone, using a chemoreceptor cell in a human taste bud as an example

Control and Coordination in Mammals – Action Potential in a Taste Bud

Learning Objective (AO1 / AO2)

Describe, step‑by‑step, the sequence of events that leads to an action potential in an afferent sensory neurone, using a chemoreceptor (taste) cell in a human taste bud as a concrete example.

Link to Cambridge International AS & A Level Biology (9700) syllabus

• Topic 15 – Control and coordination (neuronal signalling).
• Assessment Objective 1: recall and use appropriate terminology (ion channels, receptor potential, neurotransmitter, etc.).
• Assessment Objective 2: explain the mechanisms that underlie generation and propagation of an action potential.
• This example illustrates the general principles that apply to all sensory systems (mechanoreceptors, photoreceptors, etc.), not only taste.

1. Where the Taste‑Bud Circuit Fits in the Nervous System

• Specialised epithelial chemoreceptor cells (taste cells) sit on the apical surface of the papillae and detect dissolved chemicals (tastants).
• The taste cell releases a neurotransmitter onto the afferent sensory neurone, the first element of the gustatory pathway.
• The neurone conducts the impulse to the gustatory nucleus of the solitary tract in the brainstem, then to the thalamus and primary gustatory cortex.
• Thus the taste‑bud circuit is a peripheral sensory transduction pathway that converts a chemical stimulus into an electrical signal that can travel in the nervous system – a model for all mammalian sensory systems.

2. Sensory Transduction in a Taste Cell

2.1. Taste Modalities, Receptor Types & Key Messengers

2.2. From Tastant Binding to a Graded (Receptor) Potential

1. Stimulus contact: Tastant molecules dissolve in saliva and reach the apical microvilli of the taste cell.
2. Channel opening or GPCR activation:

   • Ligand‑gated channels (ENaC, PKD2L1) open directly.
   • GPCRs activate G‑protein → phospholipase C → IP₃ → Ca²⁺ release from the endoplasmic reticulum.

3. Ion movements produce a graded depolarisation (receptor potential). The magnitude depends on tastant concentration.
4. Threshold for voltage‑gated Ca²⁺ channels (~ –40 mV): when the receptor potential reaches this value, L‑type Ca²⁺ channels open, allowing Ca²⁺ influx.

2.3. Example – Salty (NaCl) Taste (Step‑by‑Step)

1. Stimulus arrival: Na⁺ ions in saliva contact ENaC on the apical membrane.
2. ENaC opening: Na⁺ flows into the cell (driving force ≈ +60 mV), depolarising the membrane from ≈ –70 mV toward –30 mV.
3. Receptor potential: If the depolarisation reaches ≈ –40 mV, voltage‑gated Ca²⁺ channels open.
4. Ca²⁺ influx: Cytoplasmic Ca²⁺ rises sharply.
5. Neurotransmitter release: Ca²⁺ triggers exocytosis of vesicles containing ATP into the synaptic cleft.

2.4. Quantitative Note (AO2)

• Resting membrane potential of a taste cell ≈ –70 mV (determined by the Nernst/Goldman‑Hodgkin‑Katz equations for Na⁺, K⁺, Cl⁻).
• Threshold for voltage‑gated Ca²⁺ channels ≈ –40 mV; for the afferent neurone’s Na⁺ channels ≈ –55 mV.
• These values illustrate how a graded receptor potential can reach the all‑or‑none threshold of the neurone.

3. Synaptic Transmission to the Afferent Sensory Neurone

1. ATP binding: ATP released from the taste cell binds to ionotropic P2X purinergic receptors on the neurone’s peripheral terminal.
2. Ionic effect: P2X channels open, permitting Na⁺ (and a small amount of Ca²⁺) to flow into the neurone, producing a local depolarisation (postsynaptic receptor potential).
3. Termination: Ectonucleotidases in the cleft hydrolyse ATP → ADP → AMP → adenosine, rapidly removing the stimulus.
4. Alternative transmitters: Some bitter cells release serotonin; the downstream mechanisms are analogous (binding to 5‑HT₃ receptors → Na⁺/Ca²⁺ influx).

4. Generation of an Action Potential in the Sensory Neurone

1. Threshold reached (≈ –55 mV): voltage‑gated Na⁺ channels open en masse.
2. Up‑stroke (all‑or‑none): Massive Na⁺ influx drives the membrane potential rapidly toward +30 mV.
3. Repolarisation:

   • Voltage‑gated K⁺ channels open, K⁺ exits the cell.
   • Na⁺ channels enter the inactivated state.

4. After‑hyperpolarisation & restoration:

   • K⁺ channels close, membrane briefly hyperpolarises (~ –80 mV).
   • Na⁺/K⁺‑ATPase (the sodium‑potassium pump) restores the original Na⁺ and K⁺ gradients, returning the resting potential to ≈ –70 mV.

5. Refractory periods:

   • Absolute refractory period – Na⁺ channels are inactivated; another spike cannot be generated (≈ 1 ms).
   • Relative refractory period – a stronger depolarisation can trigger a spike as some Na⁺ channels recover.

6. Propagation: The spike travels along the axon (myelinated for the facial nerve, unmyelinated for some glossopharyngeal fibres) to the gustatory nucleus of the solitary tract.

5. Summary of Ion Movements & Potentials

6. Key Points to Remember (AO1 / AO2)

• The taste cell generates a graded receptor potential; it does not fire an action potential.
• The afferent sensory neurone is the element that produces the all‑or‑none action potential.
• Critical thresholds: ≈ –40 mV for Ca²⁺ channels in the taste cell; ≈ –55 mV for Na⁺ channels in the neurone.
• ATP is the principal fast neurotransmitter for salty, sour, sweet, umami and most bitter taste cells (serotonin for a subset of bitter cells).
• Rapid clearance of ATP by ectonucleotidases prevents continuous firing of the neurone.
• Na⁺/K⁺‑ATPase restores ionic gradients after each spike, ensuring the neuron is ready for the next stimulus.
• Refractory periods guarantee discrete, unidirectional spikes and set an upper limit to firing frequency.
• This sequence exemplifies the general principles of sensory transduction in mammals, applicable to mechanoreceptors, photoreceptors, and other chemoreceptors.