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
Control and Coordination in Mammals
Objective
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.
Synaptic cleft: narrow gap between the taste cell and the afferent sensory neurone.
Sensory neurone (afferent fibre): carries the signal from the taste bud to the brainstem.
Ion channels and pumps: Na⁺, K⁺, Ca²⁺ channels and the Na⁺/K⁺‑ATPase maintain the resting membrane potential.
Sequence of Events Leading to an Action Potential
Binding of tastant: A dissolved substance (e.g., NaCl) contacts the apical surface of a taste cell and binds to specific receptors (e.g., ENaC for salty taste).
Opening of ligand‑gated ion channels: The receptor activation opens Na⁺ channels, allowing Na⁺ influx into the taste cell.
Depolarisation of the taste cell: The influx of Na⁺ reduces the negative membrane potential (e.g., from –70 m \cdot to –30 mV).
Opening of voltage‑gated Ca²⁺ channels: When the membrane potential reaches the threshold (~ –40 mV), voltage‑gated Ca²⁺ channels open, and Ca²⁺ enters the cell.
Neurotransmitter release: The rise in intracellular Ca²⁺ triggers exocytosis of vesicles containing the neurotransmitter (e.g., ATP).
Activation of the sensory neurone: ATP binds to purinergic P2X receptors on the afferent neurone, opening Na⁺ channels in the neurone membrane.
Local depolarisation of the neurone: Na⁺ influx depolarises the neurone membrane to its threshold (≈ –55 mV).
Generation of an action potential: Voltage‑gated Na⁺ channels open rapidly, producing the up‑stroke of the action potential; subsequent opening of voltage‑gated K⁺ channels repolarises the membrane.
Propagation: The action potential travels along the sensory neurone to the gustatory nucleus of the brainstem.
Ion Movements During the Process
Step
Primary Ion(s) Involved
Direction of Movement
Resulting Change
1 – Tastant binding
Na⁺ (via ENaC)
Into taste cell
Depolarisation of taste cell
4 – Voltage‑gated Ca²⁺ channel opening
Ca²⁺
Into taste cell
Triggers neurotransmitter release
6 – Purinergic receptor activation
Na⁺ (through P2X)
Into sensory neurone
Depolarisation of neurone
8 – Action potential up‑stroke
Na⁺ (voltage‑gated)
Into neurone
Rapid rise to +30 mV
8 – Repolarisation
K⁺ (voltage‑gated)
Out of neurone
Return to resting potential
Key Points to Remember
The taste cell does not generate an action potential; it converts chemical information into a graded depolarisation that leads to neurotransmitter release.
The sensory neurone is the element that fires the all‑or‑none action potential.
Threshold potentials are crucial: ~–40 m \cdot for Ca²⁺ channel opening in the taste cell and ~–55 m \cdot for Na⁺ channel opening in the neurone.
ATP is the primary neurotransmitter for many taste modalities (sweet, umami, bitter).
Suggested diagram: Schematic of a taste bud showing a chemoreceptor cell, synaptic cleft, and the afferent sensory neurone with the sequence of ion movements indicated.