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Submitted to: Dr. Shifaat Yaar Khan
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Table of Content: page#
1. Nociceptor:
Types of pain and their qualities 2
Slow pain and fast pain 3
2. Thermal receptors: 3
Cold and worm receptors 4
Mechanism of stimulation of thermal receptors 4
3. Mechanoreceptors: 4
Meissner’s corpuscle 5
Merkel disc 5
Free Nerve endings 5
Pacinian corpuscles 4
Ruffini endings 5
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Nociceptors: receptors which sense the pain. These receptors are present in skin
Pain is protective Mechanism: when tissue get damaged we sense pain and then we
unconsciously try to remove or reduce pain stimulus. Skin cells get damaged during long sitting
because blood supply to skin is stopped and we get pain. We try to shift our body weight
unconsciously.
Fast pain: pain is sensed within in 0.1 second after pain stimulus is applied. Other names of fast
pain are sharp pain, acute pain, pricking pain and electric pain. This type of pain occurs when
skin is cut with a knife, pricked by needle and given a electric shock to skin. We can’t sense this
pain in deeper tissues.
Slow pain: pain is sensed after 1 second or more and increases gradually with a time. We often
use other names for slow pain are slow burning pain, aching pain, throbbing pain, nauseous
pain, chronic pain. This pain occurs for long time and situation unbearable due to tissue
destruction. Normally this pain is sensed in skin, deeper tissue and in organ
Pain receptors: these are free nerve endings which superficial widespread in skin and in internal
tissues such as periosteum, the arterial walls and joint surfaces and in tentorium cranial vault.
Generally pain receptors are excited by Mechanical ,Chemical and Thermal stimuli. Fast pain is
usually initiated by mechanical and thermal stimuli and slow pain by all three stimuli.
Chemical stimuli are bradykinin, acetylcholine, serotonin, histamine, potassium ions and
proteolytic enzymes. Some chemicals enhance the nerve ending sensitivity, not directly excite
them, are prostaglandins and substance P. chemicals mostly involve in slow pain which are
secreted after injury.
Some researcher suggest that bradykinin is responsible for pain and intensity of pain is correlated
with potassium ions concentration or with proteolytic enzymes. Because these enzymes directly
attack on nerve endings and make more permeable for ions concentrations.
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Tissue Ischemia as a cause of pain:
Ischemia is restriction of blood supply, causing shortage of oxygen supply needed for cellular
metabolism. (Merck)
Due to ischemia tissue becomes painful and pain intensity is directly related to tissue metabolism.
High metabolism rate involve more pain and due to ischemia cell death occurs along with pain.
Cause of pain during ischemia is accumulation of lactic acid due to anaerobic respiration. In
addition bradykinin and proteolytic enzymes are released because of damage tissue with are
responsible for pain and pain intensity.
Spasms of Muscle are most common and due to overuse and muscle fatigue, dehydration and
electrolytes abnormalities. (Wedro)
It is common cause of pain. Direct cause of spasm is stimulation mechanosensitive pain receptors
and indirect cause is compression of blood vessel which cause ischemia.
Thermal Receptors:
These are also free nerve endings which are responsible for the detection of changes in
temperature. They respond according to temperature. Thermoreceptors are also present in
epidermis or dermis. Distribution of cold and warm receptors are different. These areas called
warm or cold spots. A spot refer to small area of skin which is responsible for the sensation of cold
and warmth. E.g. Rattle snakes and vipers have well developed heat sensitive pit organ between
eye and nostril on both side which are responsible for the detection of warm-blooded pery.
3 to 10 times cold receptors are more than warm receptors. No of these receptors in different area
varies like 15 to 25 cold spots per square centimeter in lips, 3 to 5 cold spots/cm 2 and less than 1
spots/cm2 in broad surfaces of trunk.
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These fibers respond differently at different level of temperature. Pain-cold fibers are stimulated
by very cold temperature (5℃) and stimulation fade out at 13℃. If temperature is even colder,
nearly freezing or freezes then cold-pain receptors can’t respond.
Cold receptors begins to stimulate around 14℃ as cold-pain receptor cease to respond. These
receptors show peak response around 24C℃ and fade out slightly above 40℃.
Warm receptors are stimulated and fade out around 30℃ and 49℃ respectively.
Heat pain receptors begins to be stimulated above 45℃. This temperature cause damage of cold-
pain receptors ending so both receptors show sensation of pain. So every kind of receptor has
temperature limit for stimulation and fading out.
It is believed that cold or warmth receptors are stimulated by changes in metabolic rates. Metabolic
changes are direct effect of temperature like two fold metabolic reaction changes by every 10℃
changes. Temperature indirectly stimulate nerve endings.
Mechanoreceptors:
A receptor excited by mechanical pressures and distortion. e.g. sound, touch, and muscular
contractions. These are naked dendritic endings which surrounds the hair follicles. Some nerve
endings are encapsulated by connective tissue layers also sense pressure and touch are called
Pacinian corpuscles and Meissner’s corpuscles. Some are expanded by dendritic endings called
Merkel’s disc
Mechanoreceptors types:
1) Pacinian corpuscles (2) Meissner’s corpuscles (3) Merkel’s disc (4) Ruffini Corpuscles
(5) bare nerve endings
1) Pacinian corpuscles: these dendritic endings are encased within 30 to 50 connective tissue
layers.
Structure: dendrites are encapsulated by concentric lamellae of connective tissue structure
Sensation: deep pressure, fast vibrations
Location: these are present beneath the skin and deep in dermis
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2) Meissner’s corpuscles(Rapidly adapting RA types) (Talbot WH, Darian-Smith I,
Kornhuber HH, Mountcastle VB, 1968)
Structure: dendrites encapsulated in connective tissue
Sensation: changes in texture and slow vibrations
Location: upper dermis and mostly in finger tips
3) Merkel’s disc(slowly adapting type SA1) (Johnson KO): these are often grouped together
in a receptor organ called Iggo dome receptors
Structure: expanded dendritic endings
Sensation: sustained touch and pressure
Location: base of epidermis (stratum base)
4) Ruffini Corpuscles (Slowly adapting type SA2) (Torebjörk HE, 1980)
Structure: enlarged dendritic endings with open elongated capsule
Sensation: sustained pressure
Location: deep in dermis and hypodermis
5) Free nerve endings (slow adapting, intermediate and rapidly adapting)
Structure: unmyelinated dendrites of sensory neurons
Sensation: light touch, hot, cold and pain
Location: around hair follicles, throughout skin
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References
Johnson KO, H. S. (n.d.). mechano receptors. Neural mechanisms of tactual form and texture
perception.
Talbot WH, Darian-Smith I, Kornhuber HH, Mountcastle VB. (1968). mechano receptors. Journal
of Neurophysiology.
Torebjörk HE, O. J. (1980). Mechano receptors. Specific sensations evoked by activity in single
identified sensory units in man.
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