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Free nerve endings
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Free nerve endings are branching terminal parts of afferent nerve fibers that function as sensory receptors. They are the most abundant type of receptor, located in numerous tissues throughout the body and are responsible for a wide range of sensations, such as pain, temperature, itching, tickling, and genital sensations.
Key facts about free nerve endings |
|
| Definition | Unencapsulated branching terminal parts of sensory (afferent) neurons that act as sensory receptors. |
| Location | Skin: between epithelial layers, within the dermis's connective tissue, and at the base of hair follicles Cornea Gastrointestinal tract Joints Muscles Tendons Dura mater Bones and periosteum Viscera Connective tissues |
| Function | Somatosensory functions: nociception (pain), temperature sensation, itch, tickle, genital sensations, and sensory input from internal organs (visceral sensation). |
- Structure of free nerve endings
- Where are free nerve endings located?
- Function
- Clinical notes
- Sources
Structure of free nerve endings
Free nerve endings are unencapsulated; they are not surrounded by any special type of structure like other types of receptors (e.g., Pacinian corpuscles). The pseudounipolar sensory nerve fibers branching into the free nerve endings are either type Aδ or C. Type Aδ fibers are small-diameter (2-5μm) with a thin layer of myelination and conduction velocity of 6-30 m/sec. Type C fibers have even slower conduction velocity of 0.5-2 m/sec, because they are unmyelinated and have the smallest diameter (<2 μm) of all types of nerve fibers.
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Where are free nerve endings located?
Free nerve endings are the most numerous and widespread receptors, located in various tissues, including the:
- Skin: between epithelial layers, within the dermis's connective tissue, and at the base of hair follicles
- Cornea
- Gastrointestinal tract
- Joints
- Muscles
- Tendons
- Dura mater
- Bones and periosteum
- Viscera
- Connective tissues
This widespread distribution enables them to detect a range of stimuli across multiple organ systems.
Sensory nerve endings are grouped by whether a capsule surrounds the terminal. The table below compares free (unencapsulated) endings with encapsulated endings.
| Free nerve endings | Encapsulated nerve endings | |
| Capsule | Absent (unencapsulated) | Present (connective tissue capsule) |
| Nerve fiber type | Aδ and C | Mainly Aβ (large myelinated) |
| Threshold | Often high (nociception) | Low (discriminative touch) |
| Main modalities | Pain, temperature, itch, crude touch | Fine touch, vibration, pressure, stretch |
| Examples | Nociceptors, thermoreceptors, J-receptors | Meissner, Pacinian, Ruffini corpuscles |
| Distribution | Widespread: skin, cornea, viscera, joints | Skin, deep tissue, joints |
Function
Free nerve endings function as somatosensory receptors (nociceptors, mechanoreceptors or chemoreceptors) responsible for the senses of pain, temperature, itching, tickling, and genital sensations. Free nerve endings vary in what they detect. Some are modality-specific, such as the separate warm and cold thermoreceptors. Others are polymodal nociceptors that respond to mechanical, thermal and chemical stimuli through the same ending. Most polymodal nociceptors are C fibers. Upon a stimulus, ion channels in the nerve ending membrane open, generating a receptor potential. If this potential reaches the threshold, it triggers an action potential that travels along the nerve fiber to the sensory neuron’s cell body in the dorsal root ganglion. From there, the signal is relayed to a second-order neuron located in the dorsal horn of the spinal cord. The axon of this second-order neuron then transmits the signal to the central nervous system (CNS) via the anterolateral (spinothalamic) pathway.
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Free nerve endings as nociceptors
Nociceptors, responding to potential harmful stimuli are free nerve endings.
When tissue damage is caused by mechanical forces, it activates specific ionotropic channels, such as Piezo and TRPV4. Mechanical stress applied to the cell membrane alters the stereochemistry of these channels, causing them to open. In this context, free nerve endings act as high-threshold mechanoreceptors, detecting damaging pressure or stretch.
Other harmful stimuli, such as chemical or thermal insults, lead to the release of inflammatory mediators that bind to receptors like TRP channels, ASICs, and P2X receptors, triggering their activation and increasing their sensitivity. These mediators include prostaglandins, leukotrienes, bradykinin, histamine, serotonin, ATP, hydrogen ions (H⁺), and substance P. In this case, free nerve endings function as chemoreceptors, sensing chemical changes that signal tissue injury.
Free nerve endings as thermoreceptors
Free nerve endings can also be stimulated by temperature changes, triggering responses such as sweating and shivering to maintain homeostasis. They contain TRP ion channels that open in response to either increase or decrease in temperature, but not both. Therefore there are distinct warm receptors and cold receptors.
Free nerve endings in organ function
Free nerve endings play a vital role in the function of a lot of organs by detecting harmful stimuli and initiating protective responses.
The corneal epithelium is densely innervated by free nerve endings that detect touch, pain, and temperature, contributing to the blink reflex and tear production and secretion.
In internal organs, free nerve endings act as sensory receptors that detect pain, mechanical and chemical stimuli, contributing to reflexes like coughing, vomiting, or changes in heart rate. For example, pulmonary J-receptors and irritant receptors are free nerve endings of vagal afferents that respond to lung inflation, irritants, and congestion, triggering rapid shallow breathing and cough. (The slowly adapting stretch receptors behind the Hering-Breuer reflex are a separate population in airway smooth muscle, served by myelinated vagal fibers rather than free nerve endings.) The ability to sense internal disturbances makes free nerve endings essential for maintaining homeostasis.
Clinical notes
Hyperalgesia is characterized by extreme sensitivity to pain, meaning that a painful stimulus is interpreted as being much more painful than it actually is. It is defined as “primary” when it is caused by hypersensitivity of nociceptors (free nerve endings). This can result from reduced activation threshold, leading to an easier creation of action potentials. Another cause of hypersensitivity of nociceptors is the facilitation of the transmission of pain signals due to prolonged exposure to painful stimuli. This exposure leads to the nerve fibers adapting by sprouting more branches. Therefore, a painful stimulus activates an increased number of nerve endings, leading to an exaggerated painful sensation.
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