Name: pain signaling and inflammation
Uploaded: 2025-10-23T11:49:14.000Z
Duration: 1 min 44 s
Channel: JoVE

Nociception, generally referred to as pain, is the process through which a noxious stimulus is transmitted through the peripheral and central nervous systems to warn off potential harm or injury.

When a damaging signal is detected, nociceptors, free nerve endings, are activated. Nearby mast cells release chemicals, such as histamines, while macrophages secrete cytokines, small proteins that are critical factors in immune signaling.

Simultaneously, the axons of the nociceptors transmit the signal to the dorsal horn of the spinal cord, mainly via two different pain fibers.

The first ones to be activated are the thinly myelinated A-delta fibers, which conduct immediate sharp and well-localized pain at a very fast speed, to allow the body to withdraw from the harmful stimulus.

The other type of axons are C fibers, which conduct slowly as they are unmyelinated and transmit prolonged burning pain.

From the spinal cord the pain signals cross over and travel to the brain stem, followed by the thalamus and somatosensory cortex where the pain signals are interpreted to determine the location of injury.

Additional brain regions process the pain, notably corticolimbic structures, including the amygdala and prefrontal cortex that relate to emotional memories and cognition. Ultimately, the multiple interactions within the brain contribute to the subjective perception that individuals experience.

nociception

Nociception

Nociception&#8212;the ability to feel pain&#8212;is essential for an organism&#8217;s survival and overall well-being. Noxious stimuli such as piercing pain from a sharp object, heat from an open flame, or contact with corrosive chemicals are first detected by sensory receptors, called nociceptors, located on nerve endings. Nociceptors express ion channels that convert noxious stimuli into electrical signals. When these signals reach the brain via sensory neurons, they are perceived as pain. Thus, pain helps the organism avoid noxious stimuli.

The immune system plays an essential role in pain pathology. Upon encountering noxious stimuli, immune cells such as mast cells and macrophages present at the site of injury release inflammatory chemicals such as cytokines, chemokines, histamines, and prostaglandins. These chemicals attract other immune cells such as monocytes and T cells to the injury site. They also stimulate nociceptors, resulting in hyperalgesia&#8212;a more intense response to a previously painful stimulus, or allodynia&#8212;a painful response to a normally innocuous stimulus such as light touch. Such pain sensitization helps protect the injured site during healing.

In some cases, pain outlives its role as an acute warning system if sensitization fails to resolve over time. Chronic pain&#8212;persistent or recurrent pain lasting longer than three months&#8212;often accompanies inflammatory conditions such as rheumatoid arthritis. Non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin and ibuprofen reduce pain by inhibiting the synthesis of the inflammatory molecules prostaglandins. However, NSAIDs and opioids currently used to combat pain suffer from severe side effects and the potential for addiction. Therefore, understanding the mechanisms underlying pain pathology can help develop more effective drugs to suppress pain perception with less severe negative side effects.

Nociception&#8212;the ability to feel pain&#8212;is essential for an organism&#8217;s survival and overall well-being. Noxious stimuli such as piercing ...

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pain signaling and inflammation

Pain signaling begins when the body detects a harmful stimulus. Sharp objects, open flames, and corrosive chemicals can trigger this response. Sensory receptors called nociceptors, which sit on nerve endings, detect these noxious stimuli and use ion channels to turn them into electrical signals.

Those electrical signals travel through sensory neurons to the brain, where they are experienced as pain. This warning system helps an organism avoid damage and stay safe. Pain is therefore an important part of survival and overall well-being.

The immune system also shapes pain after an injury. Mast cells and macrophages at the injury site release inflammatory chemicals such as cytokines, chemokines, histamines, and prostaglandins. These signals attract more immune cells, including monocytes and T cells, and they also stimulate nociceptors.

This immune response can increase pain sensitivity. Hyperalgesia is a stronger response to a stimulus that was already painful. Allodynia is pain caused by something that is usually not painful, such as light touch. These changes help protect the injured area during healing.

Pain can become a problem when sensitization does not fade. Chronic pain is persistent or recurring pain that lasts longer than three months. It often occurs with inflammatory diseases such as rheumatoid arthritis. NSAIDs, including aspirin and ibuprofen, reduce pain by blocking the production of prostaglandins. However, NSAIDs and opioids can cause serious side effects and may lead to addiction, so researchers continue to study pain mechanisms to find safer drugs.

Pain Signaling and Inflammation

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Pain signaling begins when the body detects a harmful stimulus. Sharp objects, open flames, and corrosive chemicals can trigger this response. Sensory receptors called nociceptors, which sit on nerve endings, detect these noxious stimuli and use ion channels to turn them into electrical signals. Those electrical signals travel through sensory neurons to the brain, where they are experienced as pain. This warning system helps an organism avoid damage and stay safe. Pain is therefore an...

key terms and concepts

Learn how nociceptors detect harmful stimuli, how inflammation boosts pain sensitivity, and why chronic pain can persist after injury.

Pain Signaling and Inflammation | JoVE K12

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Pain Signaling and Inflammation

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