Nociceptors, fast and slow pain, the capsaicin receptor, the gate control theory, people who feel no pain, chronic pain and the power of placebo — why pain is an experience made by the brain.
Senses & Perception
Intermediate
Pain and How the Brain Feels It
The Editors
November 19, 2025
3 min read
In plain English
Pain starts when special nerve endings detect damage or danger and send signals to the spinal cord and brain. But pain is ultimately an experience the brain creates, shaped by attention, mood and expectations. That's why the same injury can hurt differently in different situations, and why some pain persists after injuries heal.
Intermediate level: Builds on the basics. Introduces the real vocabulary and the mechanisms behind it.
Concepts to know first
The International Association for the Study of Pain defines pain as an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage. Note the word experience: pain is produced by the brain, not simply delivered by the nerves.
Nociceptors
Free nerve endings called nociceptors respond to potentially damaging stimuli: intense pressure, extreme heat or cold, and chemicals released by injured or inflamed tissue. Two kinds of fibre carry the signals. Thin myelinated A-delta fibres give fast, sharp, well-localised "first pain". Unmyelinated C fibres give slower, dull, burning "second pain".
The chilli receptor
In 1997 David Julius's lab identified the receptor for capsaicin, the hot molecule in chilli peppers: an ion channel called TRPV1, which also opens at painfully hot temperatures (above about 43°C). That's why chilli feels hot — it triggers the same sensor as heat. Menthol activates a related cold sensor, TRPM8, which is why mint feels cool. Julius shared the 2021 Nobel Prize.
Gating in the spinal cord
In 1965 Ronald Melzack and Patrick Wall proposed the gate control theory: pain signals entering the spinal cord can be dampened by other inputs, such as touch. Rubbing a bumped elbow helps for this reason. The brain also sends descending signals — via the periaqueductal grey and endorphins — that can turn pain down (during an emergency or sport) or up (when anxious or focused on it).
Living without pain
Rare people are born unable to feel pain, for example because of mutations in SCN9A, which encodes the sodium channel Nav1.7. It sounds like a gift but is dangerous: they injure themselves repeatedly without noticing. Pain is a protective alarm.
When pain becomes the disease
Chronic pain, lasting beyond normal healing, affects a large share of adults worldwide. Nerve circuits can become sensitised so that the alarm fires too easily. Treatment increasingly combines medication with physical activity, psychological approaches and education about how pain works. Expectation matters too: placebo treatments can reduce pain measurably, partly by triggering the brain's own opioids.
Everyday examples & things to try
Try it
Gate control at work
Next time you bump your shin, rub it firmly. The touch signals carried by large fibres partially 'close the gate' on pain signals in your spinal cord, and the pain usually eases.
Real world
Why chilli 'burns'
Capsaicin doesn't damage your tongue — it opens TRPV1, the same channel that responds to scalding heat. Your brain receives a heat alarm with no real heat. Drinking milk helps because fats dissolve capsaicin; water mostly spreads it around.
Key takeaways
- Nociceptors detect potential damage; A-delta fibres give sharp pain, C fibres slow burning pain.
- TRPV1 detects heat and capsaicin; gate control and descending signals modulate pain.
- Pain is a brain-made experience; chronic pain often reflects sensitised circuits.
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Tagssensespainnociceptionchronic pain
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