What part of the body holds the most pain receptors?

What part of the body holds the most pain receptors?

We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

What part of the body holds the most pain receptors or is likely to cause someone to feel the most intense pain?

I thought it was the eyes but I can't find that source anymore.

There is anecdotal evidence that the cornea is indeed the most sensitive tissue. Just think of it: our eyes well up with tears when slicing an onion. A tiny insect who flew into our eye feels enormous, and a corneal injury, say a scratch, can leave us severely compromised for a number of days. Luckily, the cornea has rapid healing powers.

The cornea is so sensitive that part of determining the amount of brain injury one has sustained is by measuring the corneal reflex. The way this is done is to take a cotton swab and pull off some cotton fibers and twist them into a tiny tail (so to speak), and tough the cotton fibers to the cornea. If there is no reaction, that's a bad sign.

The Sensitivity of the Cornea in Normal Eyes
Evidence-based guideline update: Determining brain death in adults Report of the Quality Standards Subcommittee of the American Academy of Neurology

The Science of Itching and Why Scratching Feels So Good

Humans and other animals itch for a variety of reasons. Scientists believe the underlying purpose of the annoying sensation (called pruritus) is so we can remove parasites and irritants and protect our skin. However, other things can lead to itching, including drugs, diseases, and even a psychosomatic response.

Key Takeaways: Science of Itching

  • Itching is a sensation the produces a desire to scratch. The technical name for an itch is pruritus.
  • Itching and pain use the same unmyelinated nerve fibers in the skin, but pain causes a withdrawal reflex rather than a scratching reflex. However, itching can originate in the central nervous system as well as the peripheral nervous system (skin).
  • Itch receptors only occur in the top two skin layers. Neuropathic itching can result from damage anywhere in the nervous system.
  • Scratching an itch feels pleasurable because the scratch fires pain receptors, causing the brain to release the feel-good neurotransmitter serotonin.

Understanding the effect of pain and how the human body responds

A thorough understanding of the effect of pain on the different body systems helps nurses to choose the most effective pain management strategies. This article is accompanied by a self-assessment questionnaire so you can test your knowledge after reading it


Pain sends a signal that the body needs protection and healing. However, if the physiological changes triggered by pain persist, harm will ensue, and acute pain may become chronic, so pain must be contained and/or relieved. The mechanisms through which pain interacts with the body provide health professionals with various routes of entry and modes of intervention. This article discusses the intricacies of the adaptive response to pain and how they can be used to combat pain.

Citation: Swift A (2018) Understanding pain and the human body’s response to it. Nursing Times [online] 114: 3, 22-26

Author: Amelia Swift is senior lecturer in nursing, University of Birmingham. She has updated a 2003 article, Understanding the physiological effects of unrelieved pain, written by Carolyn Middleton, clinical nurse specialist at Gwent Healthcare Trust.

  • This article has been double-blind peer reviewed
  • Scroll down to read the article or download a print-friendly PDF here
  • Assess your knowledge and gain CPD evidence by taking the Nursing Times Self-assessment test


Pain, which is caused by an unpleasant (noxious) stimulus, is a stressor that can threaten homoeostasis. The body’s adaptive response to pain involves physiological changes, which are useful and potentially life-saving in the initial stages. If the adaptive response persists, harmful and life-threatening effects may ensue. Pain is noxious, which makes it a powerful protective force: indeed the inability to feel pain is associated with a shortened life expectancy (Shin et al, 2016). After injury, pain encourages us to adopt behaviours that help the healing process for example, resting the painful part of the body. This article describes the physiological response to pain, its clinical relevance and its wide-ranging effects on the body. It also explains how nurses can provide effective pain relief to their patients.

Transmission of pain

The initial physiological changes taking place in the body after a pain stimulus are concerned with the transmission of pain, which involves four stages: transduction, transmission, perception and modulation.


During transduction, the pain stimulus is transformed into a nerve impulse. Receptors on the surface of the nerve endings, called nociceptors, respond to noxious stimuli, which can be thermal (temperature above 40°C), mechanical (extreme pressure over a small area) or chemical (strong acid or alkali).

The stimulus interacts with receptors, causing chemical changes that lead the nerve to create an electrical signal (action potential). The sensory nerve fibre will only create an action potential if the stimulus is strong enough. A large stimulus creates a higher frequency of action potentials, which is eventually perceived as more severe pain.

The stimulus causes the nerve and nearby mast cells to release chemical pain mediators such as prostaglandin, bradykinin, serotonin, substance P and histamine, which:

  • Activate more receptors on the nerve fibre, increasing the likelihood that the threshold for an action potential will be reached – this is called primary sensitisation
  • Provoke changes in the walls of local blood vessels, increasing blood supply and allowing white cells to move into the extracellular fluid – this is the inflammatory response, an essential part of healing.

Pain can be alleviated by reducing the sensitisation and activation of nerve endings for example, non-steroidal anti-inflammatory drugs (NSAIDs) can inhibit the production of prostaglandin, one of the main sensitising mediators, while opioids can make it harder for the nerve to create an action potential. Precautions must be taken with both NSAIDs and opioids (Box 1).

Box 1. Precautions with NSAIDs and opioids

  • Non-steroidal anti-inflammatory drugs (NSAIDs) can lead to slower and poorer bone and tendon healing (Su and O’Connor, 2013) and are linked to gastric irritation and ulceration, renal failure and increased risk of thrombosis (Eccleston et al, 2017), particularly in older people. NSAIDs should only be administered for short periods and after a careful assessment of the risks and benefits (Zingler et al, 2016)
  • Opioids can cause sedation and respiratory depression, especially in the first 24 hours of use and when the dose is increased. The risk is increased in people with sleep apnoea or who had respiratory difficulties during surgery (Weingarten et al, 2015). Morphine should be given at the lowest effective dose and patients should be monitored for signs of opioid-induced sedation, which usually precedes respiratory depression (Jarzyna et al, 2011)


During transmission, the nerve impulse travels from the site of transduction to the brain in three stages: from nociceptors to spinal cord, from spinal cord to brain stem, and from brain stem to other parts of the brain.

The electrical signal is conducted along the nerve by cycling of sodium and potassium ions between the extracellular and intracellular fluid. Transmission is quickest along fibres that are myelinated: A-delta fibres are lightly myelinated, so they transmit pain signals more quickly than C fibres. A-delta fibres transmit ‘first pain’ – the sharp sensation felt immediately after injury. C fibres transmit ‘second pain’ – the duller, burning sensation that follows.

Once the signal reaches the end of the long axon of the primary afferent fibre (PAF), which stretches from the periphery to the spinal cord, it needs to cross a small fluid-filled gap – the synapse. This is achieved by the release of neurotransmitters, which diffuse across the synapse and activate receptors on the next neuron in the chain (secondary neuron), as well as on nearby glial cells and interneurons. A strong pain signal causes the release of enough neurotransmitters to activate the secondary neuron, and the signal then travels onwards to the brain, where it stimulates cells in the brainstem, thalamus and cortex.

The transmission of the pain signal can be stopped by applying a local anaesthetic close to the nerve bundle, and it can be slowed down by administering an anticonvulsant, such as gabapentin or pregabalin. There is some evidence that these drugs help reduce neuropathic pain (Griebeler et al, 2014), but there is a growing concern that some people can become addicted to them, especially if they have a history of opioid addiction (Evoy et al, 2017).


Perception, which is when pain becomes a conscious experience, involves recognising, defining and responding to pain. It takes place in the cortex (location and motor response), the limbic system (emotional response) and the reticular system (arousal response). As part of a wider pain management strategy, distraction can be an effective technique to take the mind off pain it has proven helpful in reducing the need for opioids in people with severe trauma pain (Sullivan et al, 2016).


During modulation, the last stage of pain transmission, pain is reduced or increased by the body through descending (from brain to spinal cord) and ascending (from spinal cord to brain) mechanisms.

Pain signals activate the brainstem, which triggers descending nerve fibres to release endogenous opioids (endorphin and encephalin), serotonin, noradrenaline, gamma-aminobutyric acid (GABA) and neurotensin. These chemical mediators activate receptors on the PAF and secondary neuron to inhibit the release of neurotransmitters and make it more difficult for the secondary neuron to create an action potential. This process, known as descending pain inhibition, is activated by the cortex when pain suppression is important – for example, when in danger.

Descending pain inhibition can be stimulated or enhanced by the administration of synthetic versions of the molecules produced by the body for example, the opiate morphine, the antidepressant duloxetine or the anticonvulsant gabapentin. Descending pain inhibition can also be stimulated by hypnosis (deep relaxation), which has been used with good effect in acute and long-term pain, as well as in patients with needle phobia (Brugnoli, 2016, Uman et al, 2013). The production of endogenous opioids can be stimulated by acupuncture, exercise and transcutaneous electrical nerve stimulation (TENS) (Claydon et al, 2011).

Pain can also be modulated by ascending mechanisms. Activated by touch or pressure, A-beta fibres trigger the same secondary neurons as C fibres. When a C fibre activates the secondary neuron, the signal created represents pain, but when an A beta fibre activates the secondary neuron, the signal created represents touch. A beta fibres and C fibres compete to activate the secondary neuron, and only one of them can win. If many A beta fibres are activated, pain signalling is reduced this is the principle of the gate control theory (Melzack and Wall, 1965).

In TENS, the sensation produced competes with pain signals, which reduces the onward signalling of pain from the dorsal horn of the spinal cord (Sluka and Walsh, 2003). This effect is like that obtained when rubbing the painful area.

When pain signals enter the dorsal horn with high frequency, or with a low frequency over a prolonged period, local changes further increase the pain signal. High-frequency inputs to the dorsal horn stimulate the release of not only the short-acting transmitter glutamate, but also longer-acting transmitters substance P and calcitonin gene-related peptide (CGRP). These longer-acting transmitters stay on the receptors of the secondary neuron for a longer period, allowing summation to take place (Woolf and Salter, 2000). This is where a pain signal is amplified as each change in electrical potential of the secondary neuron is added to others to create a larger stimulation. It leads to an enhanced responsiveness of the secondary dorsal horn neuron, known as central sensitisation.

At the same time nearby cells called glia are stimulated to produce more mediators that can sensitise and activate the secondary neuron. The system usually reverts to normal once the noxious stimulus is removed inappropriate persistence of this sensitisation is one of the main causes of chronic pain.

Pain can also be amplified by the release of serotonin from the rostroventral medulla (RVM). Serotonin increases pain signalling when released in low quantities, but in higher quantities it has an inhibitory effect (Zhuo, 2017). The facilitation of pain caused by serotonin happens when the NMDA receptor is active – during central sensitisation – so when pain signals are high frequency or prolonged, the brainstem can amplify pain even further.

Responses to pain

The body responds to pain through numerous and interconnected physiological processes via the sympathetic nervous system (SNS), neuro-endocrine system and immune system, but also via emotions. The effects of these changes on body systems are summarised in Table 1.

Sympathetic nervous system

The SNS is involved in the body’s immediate response to emergencies, including severe and acute pain its reaction to pain or fear is known as the ‘fight or flight’ response. When activated, the SNS stimulates brainstem cells that control descending pain mechanisms to release noradrenaline, serotonin and endogenous opioids into the dorsal horn.

The SNS is concerned with the regulation of vascular tone, blood flow and blood pressure, as sympathetic nerves have stimulating effects on the heart (improving circulation) and respiratory system (increasing oxygen intake). Pain therefore increases heart rate, blood pressure and respiratory rate. If these physiological responses are prolonged, especially in a person with poor physiological reserves, it can lead to ischaemic damage (Wei et al, 2014).

The SNS also has an inhibiting effect on digestion, reducing or preventing the secretion of digestive enzymes in the alimentary canal and the peristaltic action in the gut wall. Pain can therefore lead to a reduced ability to digest food, which can in turn cause nausea, vomiting or constipation (Singh et al, 2016).

Neuro-endocrine system

The endocrine and nervous systems are linked via the pituitary gland at the base of the hypothalamus. Some of the body’s responses to pain are mediated by the nervous and endocrine systems, primarily via the hypothalamic-pituitary-adrenocortical (HPA) axis and the sympathomedullary pathway, and involve the release of mediators such as cortisol, adrenaline and noradrenaline, growth factor and cytokines.

Adrenaline, noradrenaline and cortisol
Pain triggers a response in the amygdala, which drives the hypothalamus to produce corticotrophin-releasing hormone (CRH) this is transmitted to the anterior pituitary gland, where it activates the SNS and stimulates the production of adrenocorticotrophin (ACTH). The SNS also stimulates the adrenal medulla to release adrenaline and noradrenaline, which have various effects (Table 2).

ACTH is carried in the blood to the adrenal cortex, where it stimulates the production of cortisol this mobilises glucose to increase the energy available for the ‘fight or flight’ response, and acts as an anti-inflammatory by inhibiting prostaglandin (Hannibal, 2014). The level of cortisol in the blood provides a feedback mechanism to the hypothalamus, thereby preventing over-release.

When functioning well, this mechanism reduces pain and stops the inflammatory response getting out of control. However, long-term pain and stress can reduce the body’s ability to dampen inflammation. In long-term stress and/or pain, the constant production of cortisol leads to resistance in the glucocorticoid receptors. Consequently, feedback to the hypothalamus is impaired and cortisol loses its ability to keep inflammation under control. Some people with long-term pain have higher levels of inflammatory mediators in their blood, and these can contribute to depression, anxiety and sleep problems (Gerdle et al, 2017).

Growth hormone
Secreted by the anterior pituitary gland, growth hormone (GH) has a direct effect on cellular activity and the metabolism of protein, carbohydrate and fat. Pain increases the secretion of GH, which contributes to the increase in blood glucose levels and insulin resistance (Greisen et al, 2001). A deficiency in GH causes muscle weakness and fatigue, which are also symptoms of a pain syndrome called fibromyalgia. People with fibromyalgia have been found to have lower levels of GH, and GH treatment has improved pain and quality of life (Cuatrecasas et al, 2012).

Cytokines are produced in response to injury and pain by a variety of peripheral cells local to the injury (including macrophages, fibroblasts and monocytes) and by cells in the dorsal horn of the spinal cord and brain (glial cells). Pro-inflammatory cytokines include tumour necrosis factor alpha (TNFα), nerve growth factor (NGF), interleukin 6 (IL-6) and interleukin 1 beta (IL-1β). Anti-inflammatory cytokines include interleukin 10 (IL-10) and interferon alpha (IFNα).

Immediately after an injury, TNFα and IL-1β sensitise sensory nerve endings and stimulate the production of noxious mediators (for example, substance P). In the spinal cord, they encourage the production of pain neurotransmitters (for example, substance P, CGRP, glutamate) and increase the number of receptors for these molecules on the secondary neuron.

At the same time, TNFα and IL-1β inhibit the activity of cells that contribute to the suppression of pain (interneurons that produce GABA and glycine). They are therefore important in the amplification of pain. Pro-inflammatory cytokines also stimulate the hypothalamus, triggering the HPA axis and causing fever their activity is balanced by the activity of anti-inflammatory cytokines such as IL-10 and IFNα. This is a complex relationship partly determined by the circumstances of the pain (Uceyler et al, 2009).

Blocking the activity of pro-inflammatory cytokines can have dramatic effects on pain the first clinical trials of anti-TNFα drugs were conducted in the 1990s (Elliott et al, 1994). A range of drugs called monoclonal antibodies and biologics have been shown to be effective in a number of painful conditions (Zheng et al, 2016 Chessell et al, 2012) – a major step forward in the management of difficult pain.

Immune system

Damage to tissues, whether mechanical or due to infection, triggers an immune response. Macrophages and mast cells produce immune mediators, such as NGF, that stimulate sensory nerve endings and provoke pain. As well as transmitting the pain signal to the dorsal horn, the sensory nerve ending also conducts signals from the cell back along the axon to the periphery, leading to the release of substances such as CGRP and substance P. These increase vasodilation and vascular permeability, stimulating blood flow and helping the translocation of immune cells from the bloodstream to the site of injury.

NGF and other substances important to pain signalling are useful biomarkers to measure pain (Goto et al, 2016). Auto-antibodies (antibodies that act against the self) are involved in a variety of pain states such as rheumatoid arthritis, Guillain-Barré syndrome and complex regional pain syndrome (McMahon et al, 2015). Immunotherapies that target autoantibodies are emerging (Lahoria et al, 2017) and there is hope that these new therapies will help manage complex, hard-to-treat pain.

Effects on mood

Pain also triggers emotional responses orchestrated by various regions of the cortex, the amygdala, the hypothalamus, various brain stem structures, and nerves in the descending modulatory system. Depending on the circumstances, anxiety and depression can either increase or reduce pain (Wiech and Tracey, 2009). A high threat level induces strong emotions such as fear or intense anxiety, leading to a state of high arousal, awareness and/or vigilance, which in turn reduces sensitivity to pain. A low or moderate threat level causes a less intense response, such as low-level anxiety or depression, which induces a low-to-moderate state of arousal in which pain is more easily felt.

Assessing mood is therefore an important part of holistic pain assessment. Anxiety, and depression make both acute and chronic pain harder to manage. Pre-operative assessment and psychological support to help patients develop effective coping strategies will help alleviate post-operative pain (Wood et al, 2016).

Implications for practice

Pain induces a cascade of interrelated changes in several body systems. In the acute phase, most are adaptive and helpful, but in the longer term all are potentially harmful, especially in patients whose reserves are already low. Containing and relieving pain is therefore crucial.

Pain often causes recognisable physiological and behavioural changes, but the absence of these changes does not mean the absence of pain. Typically, people experiencing acute pain will have an elevated heart rate, blood pressure and respiratory rate they may shake or shiver, have goose bumps and pale skin. The more intense the pain, the more visible these signs and symptoms are. Chronic pain is not usually accompanied by physiological or behavioural changes, but these will appear during exacerbations. Such changes can also be related to the person’s condition and treatment, which makes them unreliable indicators, so it is vital to regularly assess patients’ pain using validated tools.

The complexity of pain physiology makes some pains more difficult to manage than others. Acute post-operative pain normally responds well to analgesia, but this should be complemented by strategies such as comfortable positioning, distraction, TENS and reassurance. If poorly managed, post-operative pain is more likely to become chronic (Sansone et al, 2015), so needs to be dealt with effectively.

Good pain management, based on a sound understanding of the physiological effects of pain, is an essential element of nursing care. Understanding the physiology of pain will help you to select and combine the most effective interventions, and appreciate the value of holistic assessment. Not all pain is the same, not all patients are the same, and not all possess effective coping strategies. You can help by getting to know your patients and tailor your support to their needs.

Key points

  • The body reacts to pain with a complex adaptive response
  • Pain is transmitted from the site of injury to the brain by electrical signals
  • Physiological changes triggered by pain are initially useful but become harmful if they persist
  • Understanding pain physiology allows health professionals to act on pain mechanisms
  • Key nursing interventions to contain or relieve pain include holistic pain assessments

  • Test your knowledge with Nursing Times Self-assessment after reading this article. If you score 80% or more, you will receive a personalised certificate that you can download and store in your NT Portfolio as CPD or revalidation evidence.

Brugnoli MP (2016) Clinical hypnosis for palliative care in severe chronic diseases: a review and the procedures for relieving physical, psychological and spiritual symptoms. Annals of Palliative Medicine 5: 4, 280-297.

Chessell IP et al (2012) Biologics: the next generation of analgesic drugs? Drug Discovery Today 17: 875-879.

Claydon LS (2011) Dose-specific effects of transcutaneous electrical nerve stimulation (TENS) on experimental pain: a systematic review. Clinical Journal of Pain 27: 7, 635-647.

Cuatrecasas G et al (2012) Growth hormone treatment for sustained pain reduction and improvement in quality of life in severe fibromyalgia. Pain 153: 7, 1382-1389.

Elliott MJ et al (1994) Randomised double-blind comparison of chimeric monoclonal antibody to tumour necrosis factor alpha (cA2) versus placebo in rheumatoid arthritis. Lancet 344: 1105-1110.

Evoy KE et al (2017) Abuse and misuse of pregabalin and gabapentin. Drugs 77: 4, 403-426.

Gerdle B et al (2017) Signs of ongoing inflammation in female patients with chronic widespread pain: a multivariate, explorative, cross-sectional study of blood samples. Medicine 96: 9, e6130.

Goto T et al (2016) Can wound exudate from venous leg ulcers measure wound pain status? A pilot study. PloS One 11: 12, e0167478.

Greisen J et al (2001) Acute pain induces insulin resistance in humans. Anesthesiology 95: 3, 578.

Griebeler ML et al (2014) Pharmacologic interventions for painful diabetic neuropathy: an umbrella systematic review and comparative effectiveness network meta-analysis. Annals of Internal Medicine 161: 9, 639-649.

Hannibal KE (2014) Chronic stress, cortisol dysfunction, and pain: a psychoneuroendocrine rationale for stress management in pain rehabilitation. Physical Therapy 94: 12, 1816-1826.

Lahoria R et al (2017) Clinical-pathologic correlations in voltage-gated Kv1 potassium channel complex-subtyped autoimmune painful polyneuropathy. Muscle and Nerve 55: 4, 520-525.

McMahon SB et al (2015) Crosstalk between the nociceptive and immune systems in host defence and disease. Nature Reviews Neuroscience 16: 389-402.

Melzack R, Wall PD (1965) Pain mechanisms: a new theory. Science 150: 971-979.

Sansone P et al (2015) Epidemiology and incidence of acute and chronic post-surgical pain. Annali Italiani di Chirurgia 86: 4, 285-292.

Shin JY et al (2016) Congenital insensitivity to pain and anhidrosis. Archives of Plastic Surgery 43: 1, 95-97.

Singh P et al (2016) Nausea: a review of pathophysiology and therapeutics. Therapeutic Advances in Gastroenterology 9: 1, 98-112.

Sluka KA, Walsh D (2003) Transcutaneous electrical nerve stimulation: basic science mechanisms and clinical effectiveness. Journal of Pain 4: 3, 109-121.

Sullivan D et al (2016) Exploring opioid-sparing multimodal analgesia options in trauma: a nursing perspective. Journal of Trauma Nursing 23: 6, 361-375.

Uceyler N et al (2009) Mode of action of cytokines on nociceptive neurons. Experimental Brain Research 196: 1, 67-78.

Uman LS et al (2013) Psychological interventions for needle-related procedural pain and distress in children and adolescents. Cochrane Database of Systematic Reviews 10: CD005179.

Wei J et al (2014) Meta-analysis of mental stress-induced myocardial ischemia and subsequent cardiac events in patients with coronary artery disease. American Journal of Cardiology 114: 2, 187-192.

Wiech K, Tracey I (2009) The influence of negative emotions on pain: behavioral effects and neural mechanisms. Neuroimage 47: 3, 987-994.

Wood TJ et al (2016) Preoperative predictors of pain catastrophizing, anxiety, and depression in patients undergoing total joint arthroplasty. Journal of Arthroplasty 31: 12, 2750-2756.

Woolf C, Salter MW (2000) Neuronal plasticityincreasing the gain in pain. Science 288: 5472, 1765-1769.

Zheng S et al (2016) Monoclonal antibodies for the treatment of osteoarthritis. Expert Opinion on Biological Therapy 16: 12, 1529-1540.

Zhuo M (2017) Descending facilitation. Molecular Pain 13: 1744806917699212.

Sense of Touch

Your sense of touch, unlike your other senses is not restricted to any particular part of your body. The sense of touch originates at the bottom-most layer of your skin called the dermis.

Your dermis has millions of tiny nerve endings which relay information about the objects, textures and temperatures that come into contact with your body. It relays this information to your brain in the form of small electrical impulses sent via the spinal cord that tells you whether something is hot, cold, rough, smooth or sticky.

There are mainly four common receptors sending information to your brain:

1. Heat
2. Cold
3. Pain
4. Pleasure

Each of these nerve endings are responsible for telling your brain when it is exposed to a particular type of stimulus. Certain parts of your body like the fingertips, lips and face have more nerve endings than the rest of the body, which is why they are more sensitive to touch.

Some parts of body contain more of one type of receptor than the rest. Like your tongue, which has more taste receptors and fewer heat and cold receptors.

Head on to Biology for Kids for more such interesting biology videos and interactive articles.

Location may be key to effectively controlling pain

In real estate, location is key. It now seems the same concept holds true when it comes to stopping pain. New research published in Nature Communications indicates that the location of receptors that transmit pain signals is important in how big or small a pain signal will be -- and therefore how effectively drugs can block those signals.

Blocking pain receptors in the nucleus of spinal nerve cells could more effectively control pain than interfering with the same type of receptors located on cell surfaces. The scientists also found that when spinal nerve cells encounter a painful stimulus, some of the receptors will migrate from the cell surface into the nucleus.

A team of researchers led by McGill University's Director of Anesthesia Research Terence Coderre and Karen O'Malley at Washington University in St. Louis, found that rats treated with investigational drugs to block the activity of the receptors in the nucleus soon began behaving in ways that led them to believe the animals had gotten relief from neuropathic pain. According to Prof. Coderre, "drugs that penetrate the spinal nerve cells to block receptors at the nucleus were effective at relieving pain, while those that don't penetrate the nerve cells were not. Rats with nerve injuries had less spontaneous pain and less pain hypersensitivity after blocking receptors at the nucleus, while the pain sensitivity of normal rats was not affected."

Location is key

Scientists have been studying glutamate receptors in the pain pathway for decades. What's new, Coderre explained, is that these most recent experiments -- in cell cultures and rats -- demonstrate that the location of the receptor in the cell has a major effect on the cell's ability to transmit pain signals.

The researchers focused mainly on nerve cells in the spinal cord, an important area for transmitting pain signals coming from all parts of the body.

"We'll now focus our research at determining what events cause the glutamate receptors to migrate to the nucleus, and how to produce drugs that more specifically block glutamate receptors only at the nucleus," added Coderre.

Emotional and Physical Pain Activate Similar Brain Regions

When people feel emotional pain, the same areas of the brain get activated as when people feel physical pain: the anterior insula and the anterior cingulate cortex. In one study, these regions were activated when people experienced an experimental social rejection from peers. In another more real-life study, the same regions were activated when people who had recently broken up with romantic partners viewed pictures of the former partner.

So, if physical and emotional pain have similar neural signatures, why not take Tylenol (acetaminophen) for grief, loss, or despair?

In one study, people who had experienced a recent social rejection were randomly assigned to take acetaminophen vs. a placebo daily for three weeks. The people in the acetaminophen condition reported fewer hurt feelings during that period. When their brains were scanned at the end of the treatment period, the acetaminophen takers had less activation in the anterior insula and the anterior cingulate cortex.

This study was not done in order to promote acetaminophen and other analgesics as psychoactive drugs. Rather, the idea was to emphasize that over the course of evolution, our bodies decided to take the economic route and use a single neural system to detect and feel pain, regardless of whether it is emotional or physical. While it may be a good idea to take a pain reliever in the acute phase of feeling physical and emotional pain, no one is proposing this a long-term cure for dealing with hurt feelings and grief.

Pain, of course, is always both a physical and an emotional experience. If I stub my toe, in addition to the physical pain, I am likely to be also angry or disappointed with myself or with someone else who is convenient to blame (Why did you leave that box in the hallway where I couldn’t see it until I hurt myself? Now look what you’ve done!).

Speaking of blaming, I begin to feel annoyed when people who do these studies (and also those who apply them clinically) don’t go far enough into the body. Emotional pain doesn’t just hurt psychologically it hurts in my body.

These days, it seems, the discovery of a link between a brain region and a psychological experience gives the experience an aura of authenticity, as if to say, "Now we know it’s real." Also, people sometimes say, upon reading or hearing that depression, anxiety, and many other psychological ailments have specific neural signatures, “It’s not just in my head.” Well, I agree, but the brain happens to be located in the head. (Maybe saying it’s not just my imagination is more accurate?)

Showing only brain activation for a particular experience—without acknowledging a corresponding activation in the peripheral nervous system and a corresponding felt sense in the body—doesn’t do much to convince me that the experience is somewhere else than in my head.

Here’s the part that most psychologizing tends to leave out: The brain is massively interconnected with the rest of the body. There are direct neural connections via the brain stem and spinal cord. The circulatory and lymphatic systems also carry neurotransmitters (hormones and immune cells) that find receptor sites in the brain which feedback and modulate the links between brain and body. In this way, every cell in the body—every cell—is linked into the nervous system and as such, can be sensed and felt, whether or not we allow ourselves to be aware of this psychobiological fact (I feel better now, having said this in writing).

With a physical pain, there is an obvious link between the psychological experience of pain and an awareness of a physical location in the body. The pain seems to come from an elbow, or a toe, or a hip.

Weirdly, we can feel the physical pain in that location even though most, but not all, of the processing is going on in the brain. The neural, blood, and immune pathways between brain and body are tagged with body location information, beginning in the spinal cord and with successively more specific tagging up through the brain stem and thalamus, each adding another layer of redundancy and complexity, until the experience becomes conscious and further identified as “mine” in the insula, parietal, and motor cortices.

The marvel of the nervous system is that even though body sense awareness is largely a creation of cortical complexity, we feel in 3-D: the pain is “in” my knee, that object is “out there” in space, etc. No one actually knows exactly how acetaminophen increases the pain threshold: It may act specifically in the anterior insula and anterior cingulate, or throughout this whole body network.

So, with this kind of logic, we can come back to the neural similarities between emotional and physical pain. If the similarity is not just in the brain but in the body, it’s perfectly reasonable to ask: Where does an emotional pain hurt? If there really is an economy of pain networks that includes both physical and emotional pain, and if physical pain has a body location, then this simple syllogism leads to the conclusion that emotional pain must have a physical location in the body.

In what way might emotions be embodied? All emotions have a motor component. Even if we try to hide our feelings, there will be micro-momentary muscular activation. The anterior cingulate is located right next to the premotor area, which begins the process of forming an emotional expression in the body. The premotor area connects to the motor cortex above it, and then back to the specific muscles of expression.

Emotional pain may be located in the body in those places where an expression was meant to happen but failed to materialize. If I felt like screaming at the person who left the object in the hall, the object that stubbed my toe, but I didn’t actually scream, and in fact, I didn’t take my anger out on the person, I might still have residual muscle tension in my neck, throat, and jaw (holding back my angry scream). That neglectful person, for me, is experienced as a pain in the neck or a pain in the butt (the suppressed urge to kick?) or that I’m fed up (a feeling in my chest and gut that I’m going to burst?). Deeper insults go deeper into the body. Rage and hatred are the ultimate gut feelings, down in the bowels (I’m so mad I could puke You make me sick to my stomach).

The studies cited at the beginning of this post were about social rejection. Where is that felt in the body? A broken heart? Downhearted? Is love and its loss more than metaphorically connected to the heart and chest? Yes, says research from behavioral medicine and health psychology. The sense of safety that comes from being in the company of loved ones is partly created by vagal-parasympathetic activation which promotes an easy and relaxed integration of breathing and heart rate, both of which are located in the chest.

Feelings of insecurity get the heart and the breath out of synch and activate the sympathetic nervous system as if we were dealing with a threat (elevated heart rate and blood pressure), and can create a sense of unease in the chest, and even pain. People who have been hurt by others often have retracted chests and downcast postures, which are muscular ways of protecting the heart and closing off the self from fully engaging with others for fear of being hurt again. And people in insecure relationships are more likely to have cardiovascular (and other health) problems than those who are more secure.

With physical pain, we’d be in big trouble if we could not locate it in our body via the direct inner experience of feeling it. How would we (our brain) know how to deal with the pain (how to move, how to sit, or how to lie down without further injury) in the absence of a location and a direct body sense? Sometimes pain relievers make the important work of the body—to find and heal the injury—more bearable but we need to allow body sense to play a role in feeling into what our body needs.

For emotional pain, an analgesic will help us temporarily but it won’t take away the unresolved feelings that never got seen or expressed or really felt. In order to get over grief, resolve anger, and even embrace happiness, we have to really feel those things in the body. We are quick to access the body locations of pleasurable feelings (food, drink, sex, warmth, touch) so why not also let ourselves go to the places of emotional pain? Yes, it hurts for a while, but then—miraculously—there can be relief and the emergence of a new perspective on ourselves and others.

Body Parts List

Are you searching for a list of human body parts? Then, you have clicked on the right page. This article presents a list of human organs and provides the related information too. Scroll down and take a look at the list and some interesting facts about the human body.

Are you searching for a list of human body parts? Then, you have clicked on the right page. This article presents a list of human organs and provides the related information too. Scroll down and take a look at the list and some interesting facts about the human body.

We are familiar with the exterior body parts like ear, eye, nose, hands, and legs but we might not be knowing about all the internal human organs.

Before reading the body parts list, take a look at different human body systems so that it will be easier to understand how the body functions as a self-sustaining single unit.

Major Human Body Systems

  • Circulatory System: Pumps and channels blood to and from the body and lungs, plays an important role in the transportation of nutrients, gases, hormones and wastes through the body. It consists of heart, blood and blood vessels.
  • Digestive System: Digests and processes the ingested food. It is involved in the breakdown and absorption of nutrients and it promotes growth and maintenance. It consists of salivary glands, esophagus, stomach, liver, gallbladder, pancreas, intestines, rectum, and anus.
  • Endocannabinoid System: Consists of neuromodulatory lipids and receptors which help in a variety of physiological processes including appetite, pain-sensation, mood, motor learning, synaptic plasticity, and memory.
  • Endocrine System: Communicates within the body using hormones made by endocrine glands like the hypothalamus, pituitary gland, pineal gland, thyroid, parathyroid and adrenal glands. Hormones control the physiological processes in the body and psychological behavior of the person.
  • Integumentary System: Consists of skin, hair, and nails.
  • Immune System: Fights off diseases, consists of leukocytes, tonsils, adenoids, thymus, and spleen.
  • Lymphatic System: Transfers lymph between tissues and the bloodstream, consists of the lymph and lymph nodes and vessels that transport it.
  • Musculoskeletal System: Helps move the body with muscles and tendons. Movement of the muscles promotes movement of fluids, food or blood (for example, in the stomach, intestines, and heart). It consists of both skeletal and smooth muscles.
  • Nervous System: Gathering, processing and transferring information to and from the body with the brain, spinal cord, and the nerves.
  • Reproductive System: Female reproductive system consists of ovaries, fallopian tubes, uterus, vagina, mammary glands, and the male reproductive system consists of testes, vas deferens, seminal vesicles, prostate, and penis.
  • Respiratory System: Breathing system that helps absorb oxygen from the air and expel carbon dioxide from the body. It consists of the nose, pharynx, larynx, trachea, bronchi, lungs, and diaphragm.
  • Skeletal System: Gives shape to the body and holds the body. It protects the delicate organs. It consists of bones, cartilage, ligaments, and tendons.
  • Urinary System: Maintains fluid balance, electrolyte balance and administers excretion of urine. It helps get rid of the cellular wastes, toxins, excess water or nutrients from the circulatory system. It consists of kidneys, ureters, bladder, and urethra.
  • Vestibular System: It helps maintain the balance of the body and the sense of spatial orientation.

Human Body

Would you like to write for us? Well, we're looking for good writers who want to spread the word. Get in touch with us and we'll talk.

Let us now divide the body into different regions so that it will be easier to make a body parts list.

Regional Parts

  • Head and Neck: The upper region of the body includes everything above the neck, for instance, hair, scalp, eyes, ears, nose, mouth, tongue, teeth, etc.
  • Upper Limb: This region includes the shoulder, arm, hand, wrist, forearm, elbow and fingers.
  • Thorax: This is the region of the chest from the thoracic inlet to the thoracic diaphragm.
  • Middle Region: This includes human abdomen to the pelvic brim or to the pelvic inlet.
  • Back Region: The region includes the spine and its components, the vertebrae, sacrum, coccyx, and intervertebral discs.
  • Pelvic Region: This region includes the pelvis which consists of everything from the pelvic inlet to the pelvic diaphragm. The perineum is the region that consists of the sex organs and the anus.
  • Lower Limb Region: This includes everything below the inguinal ligament, including the hip, the thigh, the knee, the leg, the ankle and the foot.

Internal Parts

For the sake of convenience, you may divide body organs into ‘Organs on the left side of the body’ and ‘Organs on the right side of the human body’. Here is a list of the main internal organs of the human body.

  • Adrenals
  • Appendix
  • Bladder
  • Brain
  • Esophagus
  • Eyes
  • Gallbladder
  • Heart
  • Intestines
  • Kidney
  • Liver
  • Lung
  • Ovaries
  • Pancreas
  • Parathyroids
  • Pituitary
  • Prostate
  • Spleen
  • Stomach
  • Testicles
  • Thymus
  • Thyroid
  • Uterus
  • Veins

It is just impossible to mention all the organs, here. Almost every organ is made up of various parts which can also be named separately as organs. For example, the brain consists of Amygdala, Brainstem, Cerebellum, Cerebral cortex, Limbic system, Medulla, Midbrain, and Pons. There are specific names for the nerves, muscles, bones, tendons etc. which are present at the given specific locations. For instance, Achilles tendon, Bachmann’s bundle, Ducts of Bellini, Darwin’s tubercle, etc.

External Parts

  • Head
  • Forehead
  • Jaw
  • Cheek
  • Chin
  • Eye
  • Ear
  • Nose
  • Mouth
  • Teeth
  • Tongue
  • Throat
  • Neck
  • Adam’s apple
  • Shoulders
  • Arm
  • Elbow
  • Wrist
  • Hand
  • Fingers
  • Thumb
  • Spine
  • Chest
  • Thorax
  • Breast
  • Abdomen
  • Groin
  • Hip
  • Buttocks
  • Navel
  • Penis
  • Scrotum
  • Clitoris
  • Vulva
  • Leg
  • Thigh
  • Knee
  • Calf
  • Heel
  • Ankle
  • Foot
  • Toes

Anatomical charts and models of bodily systems help study human physiology. The human body, a scientific marvel has always been an interesting topic for various researches related to body mechanisms like aging, fighting diseases, the effect of stress on health, etc.

Lipid Epoxides Target Pain and Inflammatory Pathways in Neurons

When modified using a process known as epoxidation, two naturally occurring lipids are converted into potent agents that target multiple cannabinoid receptors in neurons, interrupting pathways that promote pain and inflammation, researchers report. These modified compounds, called epo-NA5HT and epo-NADA, have much more powerful effects than the molecules from which they are derived, which also regulate pain and inflammation.

Reported in the journal Nature Communications, the study opens a new avenue of research in the effort to find alternatives to potentially addictive opioid pain killers, researchers say.

The work is part of a long-term effort to understand the potentially therapeutic byproducts of lipid metabolism, a largely neglected area of research, said University of Illinois Urbana-Champaign comparative biosciences professor Aditi Das, who led the study. While many people appreciate the role of dietary lipids such as omega-3 and omega-6 fatty acids in promoting health, the body converts these fat-based nutrients into other forms, some of which also play a role in the healthy function of cells, tissues and organ systems.

“Our bodies use a lot of genes for lipid metabolism, and people don’t know what these lipids do,” said Das, also an affiliate of the Beckman Institute for Advanced Science and Technology and of the Cancer Center at Illinois. “When we consume things like polyunsaturated fatty acids, within a few hours they are transformed into lipid metabolites in the body.”

Scientists tend to think of these molecules as metabolic byproducts, “but the body is using them for signaling processes,” Das said. “I want to know the identity of those metabolites and figure out what they are doing.”

She and her colleagues focused on the endocannabinoid system, as cannabinoid receptors on cells throughout the body play a role in regulating pain. When activated, cannabinoid receptors 1 and 2 tend to reduce pain and inflammation, while a third receptor, TRPV1, promotes the sensation of pain and contributes to inflammation. These receptors work together to modulate the body’s responses to injury or disease.

Previous research identified two lipid molecules, known as NA5HT and NADA, that naturally suppress pain and inflammation. Image is in the public domain

“Understanding pain regulation in the body is important because we know we have an opioid crisis,” Das said. “We’re looking for lipid-based alternatives to opioids that can interact with the cannabinoid receptors and in the future be used to design therapeutics to reduce pain.”

Previous research identified two lipid molecules, known as NA5HT and NADA, that naturally suppress pain and inflammation. Das and her colleagues discovered that brain cells possess the molecular machinery to epoxidize NA5HT and NADA, converting them to epo-NA5HT and epo-NADA. Further experiments revealed that these two epoxidated lipids are many times more potent than the precursor molecules in their interactions with the cannabinoid receptors.

“For example, we found that epo-NA5HT is a 30-fold stronger antagonist of TRPVI than NA5HT and displays a significantly stronger inhibition of TRPV1-mediated responses in neurons,” Das said. It inhibits pathways associated with pain and inflammation, and promotes anti-inflammatory pathways.

The team was unable to determine whether neurons naturally epoxidate NA5HT and NADA in the brain, but the findings hold promise for the future development of lipid compounds that can combat pain and inflammation without the dangerous side effects associated with opioids, Das said.

The Das research group collaborated with Hongzhen Hu, a pain and itch researcher and professor of anesthesiology at Washington University in St. Louis, and with U. of I. biochemistry professor Emad Tajkhorshid, who helped simulate how the lipids are metabolized by enzymes known as cytochrome P450s.

Endorphins: Natural Pain and Stress Fighters

Endorphins are among the brain chemicals known as neurotransmitters, which function to transmit electrical signals within the nervous system. At least 20 types of endorphins have been demonstrated in humans. Endorphins can be found in the pituitary gland, in other parts of the brain, or distributed throughout the nervous system.

Stress and pain are the two most common factors leading to the release of endorphins. Endorphins interact with the opiate receptors in the brain to reduce our perception of pain and act similarly to drugs such as morphine and codeine. In contrast to the opiate drugs, however, activation of the opiate receptors by the body's endorphins does not lead to addiction or dependence.

In addition to decreased feelings of pain, secretion of endorphins leads to feelings of euphoria, modulation of appetite, release of sex hormones, and enhancement of the immune response. With high endorphin levels, we feel less pain and fewer negative effects of stress. Endorphins have been suggested as modulators of the so-called "runner's high" that athletes achieve with prolonged exercise. While the role of endorphins and other compounds as potential triggers of this euphoric response has been debated extensively by doctors and scientists, it is at least known that the body does produce endorphins in response to prolonged, continuous exercise.

Endorphin release varies among individuals. This means that two people who exercise at the same level or suffer the same degree of pain will not necessarily produce similar levels of endorphins. Certain foods, such as chocolate or chili peppers, can also lead to enhanced secretion of endorphins. In the case of chili peppers, the spicier the pepper, the more endorphins are secreted. The release of endorphins upon ingestion of chocolate likely explains the comforting feelings that many people associate with this food and the craving for chocolate in times of stress.

Even if you don't participate in strenuous athletics, you can also try various activities to increase your body's endorphin levels. Studies of acupuncture and massage therapy have shown that both of these techniques can stimulate endorphin secretion. Sex is also a potent trigger for endorphin release. Finally, the practice of meditation can increase the amount of endorphins released in your body.

3. Merkel Cells

Merkel cells are also 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.

Merkel cells are found in the skin often close to hairs. They mediate excellent two-point discrimination 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.)