Receptors detect stimulus and convert it into a form that neurons can understand and transmit—either as a graded potential or by modulating synaptic transmission.
Receptors are specialized proteins (or receptor cells) that respond selectively to:
Chemical signals (neurotransmitters, hormones)
Mechanical forces (stretch, pressure)
Thermal changes (heat, cold)
Light (photons)
Painful stimuli (nociception)
This specificity is what allows precise signaling.
This is called sensory transduction.
The receptor converts the stimulus into a change in membrane potential
This produces a receptor potential (graded, not all-or-none)
If large enough, it triggers an action potential in the afferent neuron
📌 Example:
Stretching a muscle spindle opens mechanosensitive ion channels → Na⁺ influx → depolarization → action potential.
At synapses, receptors determine how neurons talk to each other.
Ligand-gated ion channels
Neurotransmitter binding directly opens a channel
Produces EPSPs or IPSPs
Millisecond response
📌 Examples:
AMPA (glutamate → Na⁺ influx → excitation)
GABA_A (Cl⁻ influx → inhibition)
G-protein–coupled receptors
Activate second messenger cascades
Modulate ion channels, gene expression, synaptic strength
Slower but longer-lasting effects
📌 Examples:
Muscarinic ACh receptors
Dopamine receptors
β-adrenergic receptors
The same neurotransmitter can have different effects depending on the receptor:
| Neurotransmitter | Receptor | Effect |
|---|---|---|
| Acetylcholine | Nicotinic | Excitatory |
| Acetylcholine | Muscarinic (M2) | Inhibitory |
| Glutamate | AMPA | Fast excitation |
| Glutamate | NMDA | Plasticity, Ca²⁺ entry |
| GABA | GABA_A | Inhibitory |
➡️ Receptors, not neurotransmitters alone, determine function.
Different receptor types encode different modalities:
| Modality | Receptor type |
|---|---|
| Touch/pressure | Mechanoreceptors |
| Pain | Nociceptors |
| Temperature | Thermoreceptors |
| Vision | Photoreceptors |
| Taste | Chemoreceptors |
| Hearing | Hair cell mechanoreceptors |
They also encode:
Intensity (firing frequency)
Duration (adaptation)
Location (receptive fields)
Local anesthetics block Na⁺ channels → action potentials fail
Antidepressants alter receptor signaling and sensitivity
Myasthenia gravis targets nicotinic ACh receptors
Parkinson’s disease involves dopamine receptor signaling
Benzodiazepines enhance GABA_A receptor function
Receptors detect stimuli or neurotransmitters and convert them into electrical or biochemical signals that determine whether, when, and how neurons communicate.
If you want, I can:
Contrast receptor potentials vs action potentials
Link this to synaptic integration
Apply this to USMLE-style questions or clinical cases
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Here is a clean, high-yield contrast between receptor potentials and action potentials, the way it is expected in physiology exams and clinical reasoning.
A graded change in membrane potential produced when a receptor detects a stimulus
Occurs in sensory receptor endings or specialized receptor cells
Reflects stimulus strength
A regenerative, all-or-none electrical signal used for long-distance transmission
Occurs in axons
Encodes information by frequency, not size
| Feature | Receptor Potential | Action Potential |
|---|---|---|
| Nature | Graded | All-or-none |
| Amplitude | Variable | Fixed |
| Threshold | No | Yes |
| Summation | Yes (temporal & spatial) | No |
| Propagation | Decremental (local) | Non-decremental |
| Direction | Local | One direction |
| Refractory period | None | Absolute & relative |
| Ion channels | Stimulus-gated (mechanical, chemical, thermal) | Voltage-gated Na⁺ & K⁺ |
| Location | Sensory receptors / dendrites | Axon |
| Encodes | Stimulus intensity | Information via firing rate |
Stimulus activates receptor
Receptor potential forms
If depolarization reaches threshold at the trigger zone:
→ Action potentials fire
Stronger stimulus → larger receptor potential → higher AP frequency
📌 Key point:
Stimulus intensity is coded by the size of the receptor potential but by the frequency of action potentials.
Light touch → small receptor potential → few APs
Firm pressure → large receptor potential → many APs
Light causes hyperpolarization, not depolarization
Still graded → modulates neurotransmitter release
Strong noxious stimulus → large receptor potential
Leads to high-frequency firing → perceived as severe pain
| Condition | Effect |
|---|---|
| Demyelination (MS) | AP propagation fails |
| Local anesthetics | Block AP generation |
| Neuropathy | Reduced receptor potentials |
| Hyperkalemia | Alters AP threshold |
| Na⁺ channel mutations | AP abnormalities (epilepsy, pain syndromes) |
Receptor potentials can summate; action potentials cannot
Action potentials do not decrease in size with distance
Frequency ≠ amplitude for APs
Blocking Na⁺ channels abolishes APs but not receptor potentials
Receptor potentials are graded local signals that detect stimulus strength, while action potentials are all-or-none signals that transmit information over distance by changing firing frequency.
If you want, I can:
Walk through a USMLE-style MCQ
Explain adaptation (phasic vs tonic receptors)
Link this to EEG vs nerve conduction studies