Are sensory mechanoreceptors and mechanical nociceptors the same type of neurons or are they different?

Are sensory mechanoreceptors and mechanical nociceptors the same type of neurons or are they different?

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I always supposed the neurons / receptors which transmitted touch and pain were the same, since they react to stimulus which are the same but with different intensity, and they just sent a stronger signal in the case of something that has to be interpreted as pain. Though recently I've read some articles that imply they aren't, even so they don't say it directly. Reading more information I found this,

A nociceptor ("pain receptor") is a sensory neuron that responds to damaging or potentially damaging stimuli by sending “possible threat” signals.

Types and functions

Mechanical nociceptors respond to excess pressure or mechanical deformation.



Are sensory receptors neurons?

Receptor cells are specialized neurons

Are sensory receptors neurons?

And finally,

Sensory receptors are primarily classified as chemoreceptors, thermoreceptors, mechanoreceptors, or photoreceptors.

Mechanoreceptors detect mechanical forces.

Sensory receptors

This doesnt give me a definitive answer, but it tells me both "sensory mechanoreceptors" and "mechanical nocireceptors" are neurons which responds to pressure/ mechanical forces. Are they supposed to be the same types of neurons named differently by different authors, or are they different types of neurons?

Short answer
Nociceptors are different from mechanoreceptors.

Mechanoreceptors in the skin have specialized dendritic regions that facilitate their specific role in sensing different types of mechanical force, e.g., pressure receptors (Merkel's disks) versus vibration receptors (Pacinian corpuscles and Meissner's corpuscles). See Fig. 1 for schematic representations of these types of receptors (Iheanacho et al). By contrast, pain receptors (or nociceptors) do not have specialized dendritic regions and consist of free nerve endings that respond to harmful mechanical forces (Purves et al., 2001).

Fig. 1. Skin receptors. source: Teach Me Phsyiology

- Iheanacho et al., Mechanoreceptors. In: StatPearls. Treasure Island (FL): StatPearls Publishing (2020)
- Purves et al., eds. In: Neuroscience 2nd ed. Sunderland (MA): Sinauer Associates; 2001. Nociceptors

I don't know if this directly answers your questions, but I think some confusion may stem from an underlying misconception of receptor vs receptor cell.

In most contexts (though not this one), 'receptors' do not refer to cells. Receptors are proteins on the cell membrane that transduct some signal/stimulus to the cell. Sometimes a "normal" peripheral neuron will have end processes that contain receptors that pass the signal directly to the neuron. Other times, a special 'receptor cell' is present. These cells are labeled as mechanoreceptors or nociceptors. The difference here is that a "standard" neuron is responsible for signal gating and propagation, whereas a receptor (cell) is primarily responsible for converting an external stimulus into a chemo or electrical signal recognized by "normal" neurons (or other cells).

Edit: As noted by AliceD's answer, different receptors have different proteins and thus have different mechanisms. To add, "nociceptor" and "mechanoreceptor" are categories. There are many different receptors that are nociceptors and many different receptors that are mechanoreceptors. Furthermore, nociceptor is a category of 'function' - it describes that the receptor responds to a pain/damage stimulus. A mechanoreceptor is a category of 'mechanism' - it describes how the receptor works. These categories are not mutually exclusive, and there are indeed nociceptors that are ALSO mechanoreceptors. (E.g. "Joint nociceptors are classified as high threshold mechanoreceptors" (source)) But not all nociceptors are mechanoreceptors and not all mechanoreceptors are nociceptors.

Are sensory mechanoreceptors and mechanical nociceptors the same type of neurons or are they different? - Biology

There are various types of tactile mechanoreceptors that work together to signal and process “touch.”

Learning Objectives

Describe the structure and function of mechanoreceptors

Key Takeaways

Key Points

  • The four major types of tactile mechanoreceptors include: Merkel’s disks, Meissner’s corpuscles, Ruffini endings, and Pacinian corpuscles.
  • Merkel’s disk are slow-adapting, unencapsulated nerve endings that respond to light touch they are present in the upper layers of skin that has hair or is glabrous.
  • Meissner’s corpuscles are rapidly-adapting, encapsulated neurons that responds to low-frequency vibrations and fine touch they are located in the glabrous skin on fingertips and eyelids.
  • Ruffini endings are slow adapting, encapsulated receptors that respond to skin stretch and are present in both the glabrous and hairy skin.
  • -Pacinian corpuscles are rapidly-adapting, deep receptors that respond to deep pressure and high-frequency vibration.

Key Terms

  • dendrite: branched projections of a neuron that conduct the impulses received from other neural cells to the cell body
  • glabrous: smooth, hairless, bald

Somatosensory Receptors

Sensory receptors are classified into five categories: mechanoreceptors, thermoreceptors, proprioceptors, pain receptors, and chemoreceptors. These categories are based on the nature of the stimuli that each receptor class transduces. Mechanoreceptors in the skin are described as encapsulated or unencapsulated. A free nerve ending is an unencapsulated dendrite of a sensory neuron they are the most common nerve endings in skin. Free nerve endings are sensitive to painful stimuli, to hot and cold, and to light touch. They are slow to adjust to a stimulus and so are less sensitive to abrupt changes in stimulation.


There are three classes of mechanoreceptors: tactile, proprioceptors, and baroreceptors. Mechanoreceptors sense stimuli due to physical deformation of their plasma membranes. They contain mechanically-gated ion channels whose gates open or close in response to pressure, touch, stretching, and sound. There are four primary tactile mechanoreceptors in human skin: Merkel’s disks, Meissner’s corpuscles, Ruffini endings, and Pacinian corpuscle two are located toward the surface of the skin and two are located deeper. A fifth type of mechanoreceptor, Krause end bulbs, are found only in specialized regions.

Primary mechanoreceptors: Four of the primary mechanoreceptors in human skin are shown. Merkel’s disks, which are unencapsulated, respond to light touch. Meissner’s corpuscles, Ruffini endings, Pacinian corpuscles, and Krause end bulbs are all encapsulated. Meissner’s corpuscles respond to touch and low-frequency vibration. Ruffini endings detect stretch, deformation within joints, and warmth. Pacinian corpuscles detect transient pressure and high-frequency vibration. Krause end bulbs detect cold.

Merkel’s disks are found in the upper layers of skin near the base of the epidermis, both in skin that has hair and on glabrous skin that is, the hairless skin found on the palms and fingers, the soles of the feet, and the lips of humans and other primates. Merkel’s disks are densely distributed in the fingertips and lips. They are slow-adapting, unencapsulated nerve endings, which respond to light touch. Light touch, also known as discriminative touch, is a light pressure that allows the location of a stimulus to be pinpointed. The receptive fields of Merkel’s disks are small, with well-defined borders. That makes them very sensitive to edges they come into use in tasks such as typing on a keyboard.

Meissner’s corpuscles, also known as tactile corpuscles, are found in the upper dermis, but they project into the epidermis. They are found primarily in the glabrous skin on the fingertips and eyelids. They respond to fine touch and pressure, but they also respond to low-frequency vibration or flutter. They are rapidly- adapting, fluid-filled, encapsulated neurons with small, well-defined borders which are responsive to fine details. Merkel’s disks and Meissner’s corpuscles are not as plentiful in the palms as they are in the fingertips.

Meissner corpuscles: Meissner corpuscles in the fingertips, such as the one viewed here using bright field light microscopy, allow for touch discrimination of fine detail.

Deeper in the dermis, near the base, are Ruffini endings, which are also known as bulbous corpuscles. They are found in both glabrous and hairy skin. These are slow-adapting, encapsulated mechanoreceptors that detect skin stretch and deformations within joints they provide valuable feedback for gripping objects and controlling finger position and movement. Thus, they also contribute to proprioception and kinesthesia. Ruffini endings also detect warmth. Note that these warmth detectors are situated deeper in the skin than are the cold detectors. It is not surprising, then, that humans detect cold stimuli before they detect warm stimuli.

Pacinian corpuscles, located deep in the dermis of both glabrous and hairy skin, are structurally similar to Meissner’s corpuscles. They are found in the bone periosteum, joint capsules, pancreas and other viscera, breast, and genitals. They are rapidly-adapting mechanoreceptors that sense deep, transient (not prolonged) pressure, and high-frequency vibration. Pacinian receptors detect pressure and vibration by being compressed which stimulates their internal dendrites. There are fewer Pacinian corpuscles and Ruffini endings in skin than there are Merkel’s disks and Meissner’s corpuscles.

Pacinian corpuscles: Pacinian corpuscles, such as these visualized using bright field light microscopy, detect pressure (touch) and high-frequency vibration.

Nociceptors were discovered by Charles Scott Sherrington in 1906. In earlier centuries, scientists believed that animals were like mechanical devices that transformed the energy of sensory stimuli into motor responses. Sherrington used many different experiments to demonstrate that different types of stimulation to an afferent nerve fiber's receptive field led to different responses. Some intense stimuli trigger reflex withdrawal, certain autonomic responses, and pain. The specific receptors for these intense stimuli were called nociceptors. [5]

In mammals, nociceptors are found in any area of the body that can sense noxious stimuli. External nociceptors are found in tissue such as the skin (cutaneous nociceptors), the corneas, and the mucosa. Internal nociceptors are found in a variety of organs, such as the muscles, the joints, the bladder, the visceral organs, and the digestive tract. The cell bodies of these neurons are located in either the dorsal root ganglia or the trigeminal ganglia. [6] The trigeminal ganglia are specialized nerves for the face, whereas the dorsal root ganglia are associated with the rest of the body. The axons extend into the peripheral nervous system and terminate in branches to form receptive fields.

Nociceptors develop from neural-crest stem cells. The neural crest is responsible for a large part of early development in vertebrates. It is specifically responsible for development of the peripheral nervous system (PNS). The neural-crest stem cells split from the neural tube as it closes, and nociceptors grow from the dorsal part of this neural-crest tissue. They form late during neurogenesis. Earlier forming cells from this region can become non-pain sensing receptors, either proprioceptors or low-threshold mechanoreceptors. All neurons derived from the neural crest, including embryonic nociceptors, express the TrkA, which is a receptor to nerve-growth factor (NGF). However, transcription factors that determine the type of nociceptor remain unclear. [7]

Following sensory neurogenesis, differentiation occurs, and two types of nociceptors are formed. They are classified as either peptidergic or nonpeptidergic nociceptors, each of which express a distinct repertoire of ion channels and receptors. Their specializations allow the receptors to innervate different central and peripheral targets. This differentiation occurs in both perinatal and postnatal periods. The nonpeptidergic nociceptors switch off the TrkA and begin expressing Ret, which is a transmembrane signaling component that allows the expression of glial-cell-derived growth factor (GDNF). This transition is assisted by Runx1 which is vital in the development of nonpeptidergic nociceptors. On the contrary, the peptidergic nociceptors continue to use TrkA, and they express a completely different type of growth factor. There currently is a lot of research about the differences between nociceptors. [7]

The peripheral terminal of the mature nociceptor is where the noxious stimuli are detected and transduced into electrical energy. [8] When the electrical energy reaches a threshold value, an action potential is induced and driven towards the central nervous system (CNS). This leads to the train of events that allows for the conscious awareness of pain. The sensory specificity of nociceptors is established by the high threshold only to particular features of stimuli. Only when the high threshold has been reached by either chemical, thermal, or mechanical environments are the nociceptors triggered. The majority of nociceptors are classified by which of the environmental modalities they respond to. Some nociceptors respond to more than one of these modalities and are consequently designated polymodal. Other nociceptors respond to none of these modalities (although they may respond to stimulation under conditions of inflammation) and are referred to as sleeping or silent.

Nociceptors have two different types of axons. The first are the Aδ fiber axons. They are myelinated and can allow an action potential to travel at a rate of about 20 meters/second towards the CNS. The other type is the more slowly conducting C fiber axons. These only conduct at speeds of around 2 meters/second. [9] This is due to the light or non-myelination of the axon. As a result, pain comes in two phases. The first phase is mediated by the fast-conducting Aδ fibers and the second part due to (Polymodal) C fibers. The pain associated with the Aδ fibers can be associated to an initial extremely sharp pain. The second phase is a more prolonged and slightly less intense feeling of pain as a result of the acute damage. If there is massive or prolonged input to a C fiber, there is a progressive build up in the spinal cord dorsal horn this phenomenon is similar to tetanus in muscles but is called wind-up. If wind-up occurs there is a probability of increased sensitivity to pain. [10]

Thermal Edit

Thermal nociceptors are activated by noxious heat or cold at various temperatures. There are specific nociceptor transducers that are responsible for how and if the specific nerve ending responds to the thermal stimulus. The first to be discovered was TRPV1, and it has a threshold that coincides with the heat pain temperature of 43 °C. Other temperature in the warm–hot range is mediated by more than one TRP channel. Each of these channels express a particular C-terminal domain that corresponds to the warm–hot sensitivity. The interactions between all these channels and how the temperature level is determined to be above the pain threshold are unknown at this time. The cool stimuli are sensed by TRPM8 channels. Its C-terminal domain differs from the heat sensitive TRPs. Although this channel corresponds to cool stimuli, it is still unknown whether it also contributes in the detection of intense cold. An interesting finding related to cold stimuli is that tactile sensibility and motor function deteriorate while pain perception persists.

Mechanical Edit

Mechanical nociceptors respond to excess pressure or mechanical deformation. They also respond to incisions that break the skin surface. The reaction to the stimulus is processed as pain by the cortex, just like chemical and thermal responses. These mechanical nociceptors frequently have polymodal characteristics. So it is possible that some of the transducers for thermal stimuli are the same for mechanical stimuli. The same is true for chemical stimuli, since TRPA1 appears to detect both mechanical and chemical changes. Some mechanical stimuli can cause release of intermediate chemicals, such as ATP, which can be detected by P2 purinergic receptors, or nerve growth factor, which can be detected by Tropomyosin receptor kinase A (TrkA). [11]

Chemical Edit

Chemical nociceptors have TRP channels that respond to a wide variety of spices. The one that sees the most response and is very widely tested is capsaicin. Other chemical stimulants are environmental irritants like acrolein, a World War I chemical weapon and a component of cigarette smoke. Apart from these external stimulants, chemical nociceptors have the capacity to detect endogenous ligands, and certain fatty acid amines that arise from changes in internal tissues. Like in thermal nociceptors, TRPV1 can detect chemicals like capsaicin and spider toxins and acids. [7] [11] Acid-sensing ion channels (ASIC) also detect acidity. [11]

Sleeping/silent Edit

Although each nociceptor can have a variety of possible threshold levels, some do not respond at all to chemical, thermal or mechanical stimuli unless injury actually has occurred. These are typically referred to as silent or sleeping nociceptors since their response comes only on the onset of inflammation to the surrounding tissue. [6]

Polymodal Edit

Many neurons perform only a single function therefore, neurons that perform these functions in combination are given the classification "polymodal." [12]

Ascending Edit

Afferent nociceptive fibers (those that send information to, rather than from the brain) travel back to the spinal cord where they form synapses in its dorsal horn. This nociceptive fiber (located in the periphery) is a first order neuron. The cells in the dorsal horn are divided into physiologically distinct layers called laminae. Different fiber types form synapses in different layers, and use either glutamate or substance P as the neurotransmitter. Aδ fibers form synapses in laminae I and V, C fibers connect with neurons in lamina II, Aβ fibers connect with lamina I, III, & V. [6] After reaching the specific lamina within the spinal cord, the first order nociceptive project to second order neurons that cross the midline at the anterior white commissure. The second order neurons then send their information via two pathways to the thalamus: the dorsal column medial-lemniscal system and the anterolateral system. The former is reserved more for regular non-painful sensation, while the latter is reserved for pain sensation. Upon reaching the thalamus, the information is processed in the ventral posterior nucleus and sent to the cerebral cortex in the brain via fibers in the posterior limb of the internal capsule.

Descending Edit

As there is an ascending pathway to the brain that initiates the conscious realization of pain, there also is a descending pathway which modulates pain sensation. The brain can request the release of specific hormones or chemicals that can have analgesic effects which can reduce or inhibit pain sensation. The area of the brain that stimulates the release of these hormones is the hypothalamus. [13] This effect of descending inhibition can be shown by electrically stimulating the periaqueductal grey area of the midbrain or the periventricular nucleus. They both in turn project to other areas involved in pain regulation, such as the nucleus raphe magnus which also receives similar afferents from the nucleus reticularis paragigantocellularis (NPG). In turn the nucleus raphe magnus projects to the substantia gelatinosa region of the dorsal horn and mediates the sensation of spinothalamic inputs. This is done first by the nucleus raphe magnus sending serotoninergic neurons to neurons in the dorsal cord, that in turn secrete enkephalin to the interneurons that carry pain perception. [14] Enkephalin functions by binding opioid receptors to cause inhibition of the post-synaptic neuron, thus inhibiting pain. [11] The periaqueductal grey also contains opioid receptors which explains one of the mechanisms by which opioids such as morphine and diacetylmorphine exhibit an analgesic effect.

Nociceptor neuron sensitivity is modulated by a large variety of mediators in the extracellular space. [15] Peripheral sensitization represents a form of functional plasticity of the nociceptor. The nociceptor can change from being simply a noxious stimulus detector to a detector of non-noxious stimuli. The result is that low intensity stimuli from regular activity, initiates a painful sensation. This is commonly known as hyperalgesia. Inflammation is one common cause that results in the sensitization of nociceptors. Normally hyperalgesia ceases when inflammation goes down, however, sometimes genetic defects and/or repeated injury can result in allodynia: a completely non-noxious stimulus like light touch causes extreme pain. Allodynia can also be caused when a nociceptor is damaged in the peripheral nerves. This can result in deafferentation, which means the development of different central processes from the surviving afferent nerve. With this situation, surviving dorsal root axons of the nociceptors can make contact with the spinal cord, thus changing the normal input. [10]

Nociception has been documented in non-mammalian animals, including fish [16] and a wide range of invertebrates, including leeches, [17] nematode worms, [18] sea slugs, [19] and larval fruit flies. [20] Although these neurons may have different pathways and relationships to the central nervous system than mammalian nociceptors, nociceptive neurons in non-mammals often fire in response to similar stimuli as mammals, such as high temperature (40 degrees C or more), low pH, capsaicin, and tissue damage.

Due to historical understandings of pain, nociceptors are also called pain receptors. Although pain is real, psychological factors can strongly influence subjective intensity. [21]

2. Meissner Corpuscles

Meissner corpuscles, like Pacinian corpuscles, adapt quickly to a sustained stimulus but are activated again when the stimulus is removed. Thus they are especially sensitive to movement across the skin.

They are situated closer to the surface of the skin than Pacinian corpuscles where they respond to the gentlest of touches. However, they have poor two-point discrimination.

They form synapses with A&beta sensory neurons leading back to the CNS.

Phases of Pain Perception

When an injury occurs (such accidentally cutting your finger with a knife), the stimulated nociceptors activate the A fibers, causing a person to experience sharp, prickling pain. This is the first phase of pain, known as fast pain, because it is not especially intense but comes right after the painful stimulus.

During the second phase of pain, the C fibers are activated, causing a person to experience an intense, burning pain that persists even after the stimulus has stopped.

The fact that burning pain is carried by the C fibers explains why upon touching a hot stove, there is a short delay before feeling the burn. Aching, sore pain is also carried by the C fibers and arises from organs within the body (for example, a sore muscle or stomachache).  


Proprioception is our "body sense". It enables us to unconsciously monitor the position of our body. It depends on receptors in the muscles, tendons, and joints. If you have ever tried to walk after one of your legs has "gone to sleep," you will have some appreciation of how difficult coordinated muscular activity would be without proprioception.

Four Mechanoreceptors

1: The Pacinian Corpuscle

Pacinian corpuscles are pressure receptors. They are located in the skin and also in various internal organs. Each is connected to a sensory neuron. Because of its relatively large size, a single Pacinian corpuscle can be isolated and its properties studied. Mechanical pressure of varying strength and frequency is applied to the corpuscle by the stylus. The electrical activity is detected by electrodes attached to the preparation.

Deforming the corpuscle creates a generator potential in the sensory neuron arising within it. This is a graded response: the greater the deformation, the greater the generator potential. If the generator potential reaches threshold, a volley of action potentials (also called nerve impulses) are triggered at the first node of Ranvier of the sensory neuron. Once threshold is reached, the magnitude of the stimulus is encoded in the frequency of impulses generated in the neuron. So the more massive or rapid the deformation of a single corpuscle, the higher the frequency of nerve impulses generated in its neuron.

2: Adaptation

When pressure is first applied to the corpuscle, it initiates a volley of impulses in its sensory neuron. However, with continuous pressure, the frequency of action potentials decreases quickly and soon stops. This is the phenomenon of adaptation. Adaptation occurs in most sense receptors. It is useful because it prevents the nervous system from being bombarded with information about insignificant matters like the touch and pressure of our clothing. Stimuli represent changes in the environment. If there is no change, the sense receptors soon adapt. But note that if we quickly remove the pressure from an adapted Pacinian corpuscle, a fresh volley of impulses will be generated. This is why Pacinian corpuscles respond especially well to vibrations.

The speed of adaptation varies among different kinds of receptors. Receptors involved in proprioception such as spindle fibers adapt slowly if at all.

3: Meissner Corpuscles

Meissner corpuscles, like Pacinian corpuscles, adapt quickly to a sustained stimulus but are activated again when the stimulus is removed. Thus they are especially sensitive to movement across the skin.

4: Merkel Cells

Merkel cells are transducers of light touch, responding to the texture and shape of objects indenting the skin. Unlike Pacinian and Meissner corpuscles, they do not adapt rapidly to a sustained stimulus that is, they continue to generate nerve impulses so long as the stimulus remains. They are found in the skin often close to hairs. They form synapses with A&beta sensory neurons leading back to the CNS.

In the rat, light movement of a hair triggers a generator potential in a Merkel cell. If this reaches threshold, an influx of Ca ++ ions through voltage-gated calcium channels generate action potentials in the Merkel cell. These cause the release of neurotransmitters at the synapse with its A&beta sensory neuron. (This neuron may also have its own mechanically-gated ion channels able to directly generate action potentials more rapidly than Merkel cells can.)

The knee jerk is a stretch reflex. Your physician taps you just below the knee with a rubber-headed hammer. You respond with an involuntary kick of the lower leg.

  • The hammer strikes a tendon that inserts an extensor muscle in the front of the thigh into the lower leg.
  • Tapping the tendon stretches the thigh muscle.
  • This activates stretch receptors within the muscle called muscle spindles. Each muscle spindle consists of
    • sensory nerve endings wrapped around
    • special muscle fibers called spindle fibers (also called intrafusal fibers)
    • Some of the branches of the I-a axons synapse directly with alpha motor neurons (Pacinian Corpuscle). These carry impulses back to the same muscle causing it to contract. The leg straightens.
    • Some of the branches of the I-a axons synapse with inhibitory interneurons in the spinal cord (Meissner Corpuscles). These, in turn, synapse with motor neurons leading back to the antagonistic muscle, a flexor in the back of the thigh. By inhibiting the flexor, these interneurons aid contraction of the extensor.
    • Still other branches of the I-a axons synapse with interneurons leading to brain centers, e.g., the cerebellum, that coordinate body movements (Merkel Cells).

    Sensory System


    The initialization of sensation stems from the action of a specific receptor to a physical stimulus. The receptors which react to the stimulus and start the procedure of sensation are commonly defined in four distinct categories: chemoreceptors, photoreceptors, mechanoreceptors, and thermoreceptors. All receptors receive unique physical stimuli and transduce the signal into an electrical action capacity. This action potential then travels along afferent neurons to specific brain areas where it is processed and translated.


    • Chemoreceptors, or chemosensors, detect specific chemical stimuli and transduce that signal into an electrical action capacity. The two primary types of chemoreceptors are:
    • Distance chemoreceptors are essential to receiving stimuli in the olfactory system through both olfactory receptor neurons and neurons in the vomeronasal organ.
    • Direct chemoreceptors consist of the taste buds in the gustatory system as well as receptors in the aortic bodies which identify alterations in oxygen concentration.


    • Photoreceptors are capable of phototransduction, a method which converts light (electromagnetic radiation) into, other kinds of energy, a membrane capacity.
    • The three primary kinds of photoreceptors are: Cones are photoreceptors which respond substantially to color. In human beings the three different kinds of cones refer a primary reaction to short wavelength (blue), medium wavelength (green), and long wavelength (yellow/red).
    • Rods are photoreceptors which are really sensitive to the intensity of light, enabling vision in dim lighting. The concentrations and ratio of rods to cones is highly associated with whether an animal is diurnal or nocturnal.
    • In human beings rods outnumber cones by around 20:1, while in nighttime animals, such as the tawny owl, the ratio is more detailed to 1000:1. Ganglion Cells live in the adrenal medulla and retina where they are involved in the sympathetic response. Of the


    Mechanoreceptors are sensory receptors which react to mechanical forces, such as pressure or distortion. While mechanoreceptors exist in hair cells and play an essential function in the vestibular and auditory systems, most of mechanoreceptors are cutaneous and are grouped into four categories:

    • Slowly adapting type 1 receptors have small responsive fields and react to static stimulation. These receptors are mostly used in the sensations of form and roughness.
    • Slowly adapting type 2 receptors have large receptive fields and react to extend. Similarly to type 1, they produce sustained reactions to an ongoing stimulus.
    • Rapidly adjusting receptors have small receptive fields and underlie the understanding of slip.
    • Pacinian receptors have large receptive fields and are the predominant receptors for high-frequency vibration.


    • Thermoreceptors are sensory receptors which react to varying temperature levels. While at the same time the systems through which these receptors run is uncertain, recent discoveries have shown that mammals have at least two distinct kinds of thermoreceptors:
    • The end-bulb of Krause, or bulboid corpuscle, detects temperatures above body temperature.
    • Ruffini’s end organ identifies temperatures below body temperature level.


    Nociceptors respond to possibly destructive stimuli by sending signals to the spinal cord and brain. This procedure, called nociception, generally causes the understanding of pain. They are found in internal organs, and also on the surface of the body. Nociceptors detect various type of harmful stimuli or actual damage. Those that only respond when tissues are damaged are called “sleeping” or “quiet” nociceptors.

    • Thermal nociceptors are activated by poisonous heat or cold at numerous temperature levels.
    • Mechanical nociceptors respond to excess pressure or mechanical contortion.
    • Chemical nociceptors respond to a wide array of chemicals, some of which are indications of tissue damage. They are associated with the detection of some spices in food.


    • The sensory systems create our mental images of the external world. These representations offer us with details and cues that guide the motor systems to create movements produced by the collaborated contractions and relaxations.
    • The motor systems are hierarchically organized in the central nervous system (CNS) as the spinal neuronal circuits that control the automatic stereotypic reflexes.
    • Higher centers in the brainstem moderate postural regulated and balanced locomotor movements. The highest centers, consisting of the motor areas of the cerebral cortex, initiate and regulate intricate skilled voluntary movements.

    The major components of the somatic motor system are arranged and longitudinally oriented along the neuraxis as two path systems:

    (1) The phylogenetically new direct pathways that fine-tune and control voluntary movements namely the corticospinal tract and the corticobulbar tract coming from the cerebral cortex and project to end in the anterior horn of the spinal cord and nuclei of the brainstem.

    When Normal Touch Becomes Painful, the Same Neurons Are Involved

    Ruth Williams
    Oct 10, 2018

    I t shouldn’t hurt to put on socks, wash hands, or walk about, but for some people with damaged nerves, certain innocuous actions can be agony—a condition called mechanical allodynia. Now, researchers have discovered in mice that, regardless of whether such nondamaging activities are actually perceived as painless or painful (as in allodynia), the very same cells—those containing high levels of the protein Piezo2—transmit the tactile information to the central nervous system. The results, presented by two independent research groups, appear in Science Translational Medicine today (October 10).

    “Put these two papers together as a unit and you’ve got it all,” says Jeffrey Mogil of McGill University in Montreal who studies the genetics of pain, but who did not participate in either project. “They used completely different techniques to address the same question . . . and they make a pretty compelling case” for the importance of Piezo2.

    When injury or inflammation occurs in a part of the body, sensations that would normally not hurt—such as a hug, a handshake, or getting dressed—can become painful. Imagine, for example, the tenderness of a badly sunburned back, against which a soft cotton shirt may feel like sandpaper.

    In the short term, such pain from normally painless stimuli is thought to encourage safeguarding of the injured area “so that it heals faster,” says Swetha Murthy, a postdoc in the laboratory of Ardem Patapoutian at Scripps Research in La Jolla, California, and a coauthor of one of the papers. But for some unlucky patients, nerve damage—caused by, among other things, chemotherapy, surgery, or injury—can lead to a permanent state of allodynia, where everyday gestures and actions cause misery.

    Touch and pain—the sensations felt by pushing on the right and wrong end of a thumbtack, respectively—are detected by discreet subsets of sensory neurons: nociceptors for pain and low-threshold mechanoreceptors (LTMRs) for touch. LTMRs are characterized by high levels of the transmembrane ion channel Piezo2, which transduces mechanical pressure into electrical signals. Whether these cells signal pressure stimuli in allodynia, when touch is felt as pain, was unknown.

    To find out, Murthy and colleagues examined mice genetically engineered to lack Piezo2 and compared their behaviors with wildtype animals. The team gave the mice allodynia in their hind paws by either injecting them with capsaicin, causing local inflammation, or by surgically severing a nerve. Both injuries caused the wildtype animals to show signs of pain, withdrawing their paws and licking, when the area was gently brushed. Mice lacking Piezo2, on the other hand, showed a dramatically reduced response to the paw touching, whether they had allodynia or not. The response of the engineered mice to a painful pinprick, by contrast, was only slightly muted compared to that of the control animals.

    In the accompanying study, neuroscientist Alexander Chesler of the National Center for Complementary and Integrative Health in Bethesda and colleagues also engineered mice to lack Piezo2. In these animals, in vivo calcium imaging of neural activity confirmed a lack of cellular activity in response to touch (whether by brushing or vibration of the skin), while cellular activity in response to a painful pinch appeared similar to that of wildtype animals. Cells of the Piezo2-lacking animals also did not respond to touch stimuli under three different conditions of localized allodynia.

    “The major take away for me is that mechanical allodynia . . . is driven by sensory afferents that have Piezo2 as their transducer. I think that is now confirmed and is very clear in the two papers,” says neurologist Clifford Woolf of Boston Children’s Hospital and Harvard Medical School who was not involved in either paper.

    In rare cases, PIEZO2 mutations can occur in people, where they are associated with deficits in touch sensation and coordinated mobility, but the patients can still feel pain. When Chesler and colleagues gave four such PIEZO2-lacking patients capsaicin injections into their forearms to induce local allodynia, their sense of touch at the inflamed site remained deficient compared with that of healthy controls, who in contrast felt pain.

    Together with the mouse studies, these results indicate that PIEZO2 transmits the sense of touch, specifically, mechanical pressure, regardless of whether it is perceived in the brain as painful or painless. An inability to transmit this pressure sensation because of the missing transducer thus fails to produce a pain sensation in allodynia.

    “[It’s] quite gratifying . . . how much these two studies agree with one another,” says Chesler, considering “there was no coordination between our labs.”

    With the data from humans supporting the results seen in the mouse models, “the results are a stepping stone to start looking at treatments for clinical pain,” says Murthy.

    A Piezo2-inhibiting treatment could not be used systemically to treat patients with chronic allodynia because the sense of touch throughout the body would be affected. If a locally administered treatment, such as a topical cream, could be developed, says Woolf, a patient’s “sense of touch and tactile allodynia would be diminished,” while their normal sense of pain would remain intact. That’s important, he adds, “because you need that information to protect yourself.”

    S.E. Murthy et al., “The mechanosensitive ion channel Piezo2 mediates sensitivity to mechanical pain in mice,” Science Translational Medicine, 10:eaat9897, 2018.

    M. Szczot et al., “PIEZO2 mediates injury-induced tactile pain in mice and humans,” Science Translational Medicine, 10:eaat9892, 2018.

    Types of Sensory Receptors

    For a signal to be sent down the sensory nerve, it must first be transduced from an external stimulus into action potential. This occurs at the site of the sensory receptors. There are different kinds of sensory receptors that respond to different stimuli. These sensory receptors include chemorecptors, photoreceptors, mechanoreceptors, thermoreceptors, and nociceptors. The different receptors respond to the different stimuli exist and transduce the energies into action potentials that are generated at the sensory neuron.


    Chemoreceptors, or chemosensors, detect certain chemical stimuli and transduce that signal into an electrical action potential. There are two primary types of chemoreceptors:

    • Distance chemoreceptors are integral to receiving stimuli in the vomeronasal organ.
    • Direct chemoreceptors include the taste buds in the gustatory system as well as receptors in the aortic bodies which detect changes in oxygen concentration. [3]


    Photoreceptors are capable of phototransduction, a process which converts light (electromagnetic radiation) into, among other types of energy, a membrane potential. There are three primary types of photoreceptors: Cones are photoreceptors that respond significantly to color. In humans the three different types of cones correspond with a primary response to short wavelength (blue), medium wavelength (green), and long wavelength (yellow/red). [4] Rods are photoreceptors that are very sensitive to the intensity of light, allowing for vision in dim lighting. The concentrations and ratio of rods to cones is strongly correlated with whether an animal is diurnal or nocturnal. In humans, rods outnumber cones by approximately 20:1, while in nocturnal animals, such as the tawny owl, the ratio is closer to 1000:1. [4] Ganglion Cells reside in the adrenal medulla and retina where they are involved in the sympathetic response. Of the

    1.3 million ganglion cells present in the retina, 1-2% are believed to be photosensitive. [5]


    Mechanoreceptors are sensory receptors which, respond to mechanical forces, such as pressure or distortion. [6] While mechanoreceptors are present in hair cells and play an integral role in the vestibular and auditory system, the majority of mechanoreceptors are cutaneous and are grouped into four categories:

    • Slowly Adapting type 1 Receptors have small receptive fields and respond to static stimulation. These receptors are primarily used in the sensations of form and roughness.
    • Slowly Adapting type 2 Receptors have large receptive fields and respond to stretch. Similarly to type 1, they produce sustained responses to a continued stimuli.
    • Rapidly Adapting Receptors have small receptive fields and underlie the perception of slip.
    • Pacinian Receptors have large receptive fields and are the predominant receptors for high frequency vibration.


    Thermoreceptors are sensory receptors, which respond to varying temperatures. While the mechanisms through which these receptors operate is unclear, recent discoveries have shown that mammals have at least two distinct types of thermoreceptors: [7]

    • The End-Bulb of Krause, or bulboid corpuscle, detects temperatures above body temperature
    • Ruffini’s end organ detects temperatures below body temperature


    Nociceptors respond to potentially damaging stimuli by sending signals to the spinal cord and brain. This process, called

    • Thermal nociceptors are activated by noxious heat or cold at various temperatures.
    • Mechanical nociceptors respond to excess pressure or mechanical deformation.
    • Chemical nociceptors respond to a wide variety of chemicals, some of which are signs of tissue damage. They are involved in the detection of some spices in food.

    Spinal Cord Entry

    Sensory information carried by the afferent axons of the spinal nerves enters the spinal cord via the dorsal roots, and motor commands carried by the efferent axons leave the cord via the ventral roots. Once the dorsal and ventral roots join, sensory and motor axons (with some exceptions) travel together in the segmental spinal nerves). [1]

    Input into the CNS

    Information from the sensory receptors in the head enters CNS through cranial nerves. Information from receptors below the head enters the spinal cord and passes towards the brain through the 31 spinal cord nerves. [9] The sensory information traveling through the spinal cord follows well-defined pathways. The nervous system codes the differences among the sensations in terms of which cells are active.

    Generalized hydrostatic pressure

    Several types of aquatic animals are sensitive to small changes of hydrostatic, or water, pressure. Among fish, this applies particularly to the superorder Ostariophysi, which includes about 70 percent of all freshwater species of fishes. The swimbladder in these animals is connected with the labyrinth (sacculus) of the inner ear through a chain of movable tiny bones, or ossicles ( weberian apparatus). Alterations in hydrostatic pressure change the volume of the swimbladder and thus stimulate the sacculus. These fish can easily be trained to respond selectively to minute increases or decreases in pressure (for example, to a few millimetres of water pressure), indicating that they have a most refined sense of water depth. Such fish are known as physostomes, which means that they have a swimbladder duct through which rapid gas exchange with the atmosphere can occur many live in relatively shallow water. The hydrostatic pressure sense can function to inform the animals about their distance from the surface or about the direction and velocity of their vertical displacement. It also appears that improvement and refinement of the sense of hearing arises through the swimbladder’s connections via the weberian apparatus with the labyrinth.

    The sensitivity of several kinds of crustaceans to relatively small hydrostatic pressure changes (as low as 5 to 10 cm [2 to 4 inches] of water pressure) is most remarkable because these animals have no gas-filled cavity whatsoever. The mechanism by which the stimuli are detected remains unclear, although information about changing water depth during tidal ebb and flow would seem to have adaptive value.

    Watch the video: 2-Minute Neuroscience: Touch Receptors (September 2022).


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