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How do receptors lose their sensitivity?

How do receptors lose their sensitivity?


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Recently, I learned that one of the causes of Type II diabetes is that insulin receptors on cell surfaces lose their sensitivity due to long-term high exposure to insulin (which occurs as a result of high blood sugar).

How do receptors (like that for insulin) become more resistant to ligands? Is the receptor itself getting damaged? If so, how, and why don't other frequently activated proteins/receptors (like GPCR's) also get damaged? If not, then how does the cell become more "resistant" to insulin?


How do receptors lose their sensitivity? - Biology

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

Learning Objectives

Differentiate among the types of stimuli to which receptors respond

Key Takeaways

Key Points

  • Chemoreceptors detect the presence of chemicals.
  • Thermoreceptors detect changes in temperature.
  • Mechanoreceptors detect mechanical forces.
  • Photoreceptors detect light during vision.
  • More specific examples of sensory receptors are baroreceptors, propioceptors, hygroreceptors, and osmoreceptors.
  • Sensory receptors perform countless functions in our bodies mediating vision, hearing, taste, touch, and more.

Key Terms

  • photoreceptor: A specialized neuron able to detect and react to light.
  • mechanoreceptor: Any receptor that provides an organism with information about mechanical changes in its environment such as movement, tension, and pressure.
  • baroreceptor: A nerve ending that is sensitive to changes in blood pressure.

Sensory receptors can be classified by the type of stimulus that generates a response in the receptor. Broadly, sensory receptors respond to one of four primary stimuli:

  1. Chemicals (chemoreceptors)
  2. Temperature (thermoreceptors)
  3. Pressure (mechanoreceptors)
  4. Light (photoreceptors)

A schematic of the classes of sensory receptors: Sensory receptor cells differ in terms of morphology, location, and stimulus.

All sensory receptors rely on one of these four capacities to detect changes in the environment, but may be tuned to detect specific characteristics of each to perform a specific sensory function. In some cases, the mechanism of action for a receptor is not clear. For example, hygroreceptors that respond to changes in humidity and osmoreceptors that respond to the osmolarity of fluids may do so via a mechanosensory mechanism or may detect a chemical characteristic of the environment.

Sensory receptors perform countless functions in our bodies. During vision, rod and cone photoreceptors respond to light intensity and color. During hearing, mechanoreceptors in hair cells of the inner ear detect vibrations conducted from the eardrum. During taste, sensory neurons in our taste buds detect chemical qualities of our foods including sweetness, bitterness, sourness, saltiness, and umami (savory taste). During smell, olfactory receptors recognize molecular features of wafting odors. During touch, mechanoreceptors in the skin and other tissues respond to variations in pressure.

Classification of Sensory Receptors

Adequate Stimulus

Adequate stimulus can be used to classify sensory receptors. A sensory receptor’s adequate stimulus is the stimulus modality for which it possesses the adequate sensory transduction apparatus.

Sensory receptors with corresponding stimuli to which they respond.
Receptor Stimulus
Apmullae of Lorenzini (primarily function as electroreceptors) Electric fields, salinity, and temperature
Baroreceptors Pressure in blood vessels
Chemo receptors Chemical stimuli
Electromagnetic radiation receptors Electromagnetic radiation
Electroreceptors Electrofields
Hydroreceptors Humidity
Infrared receptors Infrared radiation
Magnetoreceptors Magnetic fields
Mechanoreceptors Mechanical stress or strain
Nociceptors Damage or threat of damage to body tissues (leads to pain perception)
Osmoreceptors Osmolarity of fluids
Photoreceptors Visible light
Proprioceptors Sense of position
Thermoreceptors Temperature
Ultraviolet receptors Ultraviolet radiation

Location

Sensory receptors can be classified by location:

  • Cutaneous receptors are sensory receptors found in the dermis or epidermis.
  • Muscle spindles contain mechanoreceptors that detect stretch in muscles.

Morphology

Somatic sensory receptors near the surface of the skin can usually be divided into two groups based on morphology:

  1. Free nerve endings characterize the nociceptors and thermoreceptors.
  2. Encapsulated receptors consist of the remaining types of cutaneous receptors. Encapsulation exists for specialized functioning.

Rate of Adaptation

A tonic receptor is a sensory receptor that adapts slowly to a stimulus, while a phasic receptor is a sensory receptor that adapts rapidly to a stimulus.


Changes in receptor response by disease states

Disease states may alter the number of available receptors, which can alter the sensitivity and response of a given cell or tissue. Disease states may therefore alter the actual function or activity of those receptors either through loss or gain of function.

Example • Loss of Receptors

Myasthenia Gravis is an autoimmune disorder in which antibodies destroy nicotinic acetylcholine receptors [nAChR] located in skeletal muscle. nAChRs help communicate signals resulting in muscle contraction. Thus, Myasthenia Gravis causes muscle weakness, droopy eyes and even difficulty in swallowing.

Myasthenia Gravis is treated with immunosuppressants to decrease the production of antibodies that destroy nAChRs as well as with acetylcholine esterase inhibitors [AChEIs] that prevent the breakdown of acetylcholine, a nAChR agonist, to increase its level in the synapse.

Example • Loss of Function • Androgen Receptors [AR]

Androgen receptors have variants caused by genetic mutations. These variants have varied levels of function, ranging from partial to complete loss of function. Individuals who have complete AR insensitivity exhibit Complete Androgen Insensitivity Syndrome [CAIS], and those who have partial AR insensitivity suffer from Partial Androgen Insensitivity Syndrome [PAIS]. Both syndromes cause a loss of receptor function.

Treatment for these syndromes includes hormone therapy testosterone and/or dihydrotestosterone [DHT]. One great advantage of DHT over testosterone is that cannot be aromatized to estrogen, eliminating possible side effects associated with estrogen exposure.

Example • Gain-of-Function •A number of endocrine diseases are caused by gain-of-function mutations of GPCRs.

Type 2 Diabetes Mellitus [DM2] • DM2 can be associated with a gain-of-function mutation, resulting in increased expression of the a2A-adrenergic receptor a GPCR that prevents or suppresses the secretion of insulin. As you can imagine, a patient with this gain-of-function mutation will have elevated blood glucose, potentially leading to type II diabetes mellitus.

Familial Hypocalcemia Hypocalciuria • This disease involves a gain-of-function mutation of the calcium-sensing receptor [ CaSR ] a GPCR that allows the body to monitor and regulate the amount of calcium in the blood. This gain-of-function leads to increased sensitivity to calcium. Because CaSR maintains calcium homeostasis, its exaggerated response to calcium tells the body to excrete more calcium. This leads to decreased calcium levels in the blood (hypocalcemia) by suppressing the secretion of parathyroid hormone and increased renal excretion of calcium (hypercalciuria).


How Neurons Lose Their Connections

MIT neuroscientists discovered that the protein CPG2 connects the cytoskeleton (represented by the scaffold of the bridge) and the endocytic machinery (represented by the cars) during the reabsorption of glutamate receptors. Each "car" on the &ldquobridge" carries a vesicle containing glutamate receptors. Image credit: Mark Steele Strengthening and weakening the connections between neurons, known as synapses, is vital to the brain&rsquos development and everyday function. One way that neurons weaken their synapses is by swallowing up receptors on their surfaces that normally respond to glutamate, one of the brain&rsquos excitatory chemicals.

In a new study, MIT neuroscientists have detailed how this receptor reabsorption takes place, allowing neurons to get rid of unwanted connections and to dampen their sensitivity in cases of overexcitation.

&ldquoPulling in and putting out receptors is a dynamic process, and it&rsquos highly regulated by a neuron&rsquos environment,&rdquo says Elly Nedivi, a professor of brain and cognitive sciences and member of MIT&rsquos Picower Institute for Learning and Memory. &ldquoOur understanding of how receptors are pulled in and how regulatory pathways impact that has been quite poor.&rdquo

Nedivi and colleagues found that a protein known as CPG2 is key to this regulation, which is notable because mutations in the human version of CPG2 have been previously linked to bipolar disorder. &ldquoThis sets the stage for testing various human mutations and their impact at the cellular level,&rdquo says Nedivi, who is the senior author of a Jan. 14 Current Biology paper describing the findings.

The paper&rsquos lead author is former Picower Institute postdoc Sven Loebrich. Other authors are technical assistant Marc Benoit, recent MIT graduate Jaclyn Konopka, former postdoc Joanne Gibson, and Jeffrey Cottrell, the director of translational research at the Stanley Center for Psychiatric Research at the Broad Institute.

Forming a bridge

Neurons communicate at synapses via neurotransmitters such as glutamate, which flow from the presynaptic to the postsynaptic neuron. This communication allows the brain to coordinate activity and store information such as new memories.

Previous studies have shown that postsynaptic cells can actively pull in some of their receptors in a phenomenon known as long-term depression (LTD). This important process allows cells to weaken and eventually eliminate poor connections, as well as to recalibrate their set point for further excitation. It can also protect them from overexcitation by making them less sensitive to an ongoing stimulus.

Pulling in receptors requires the cytoskeleton, which provides the physical power, and a specialized complex of proteins known as the endocytic machinery. This machinery performs endocytosis&mdashthe process of pulling in a section of the cell membrane in the form of a vesicle, along with anything attached to its surface. At the synapse, this process is used to internalize receptors.

Until now, it was unknown how the cytoskeleton and the endocytic machinery were linked. In the new study, Nedivi&rsquos team found that the CPG2 protein forms a bridge between the cytoskeleton and the endocytic machinery.

&ldquoCPG2 acts like a tether for the endocytic machinery, which the cytoskeleton can use to pull in the vesicles,&rdquo Nedivi says. &ldquoThe glutamate receptors that are in the membrane will get pinched off and internalized.&rdquo

They also found that CPG2 binds to the endocytic machinery through a protein called EndoB2. This CPG2-EndoB2 interaction occurs only during receptor internalization provoked by synaptic stimulation and is distinct from the constant recycling of glutamate receptors that also occurs in cells. Nedivi&rsquos lab has previously shown that this process, which does not change the cells&rsquo overall sensitivity to glutamate, is also governed by CPG2.

&ldquoThis study is intriguing because it shows that by engaging different complexes, CPG2 can regulate different types of endocytosis,&rdquo says Linda Van Aelst, a professor at Cold Spring Harbor Laboratory who was not involved in the research.

When synapses are too active, it appears that an enzyme called protein kinase A (PKA) binds to CPG2 and causes it to launch activity-dependent receptor absorption. CPG2 may also be controlled by other factors that regulate PKA, including hormone levels, Nedivi says.

Link to bipolar disorder

In 2011, a large consortium including researchers from the Broad Institute discovered that a gene called SYNE1 is number two on the hit list of genes linked to susceptibility for bipolar disorder. They were excited to find that this gene encoded CPG2, a regulator of glutamate receptors, given prior evidence implicating these receptors in bipolar disorder.

In a study published in December, Nedivi and colleagues, including Loebrich and co-lead author Mette Rathje, identified and isolated the human messenger RNA that encodes CPG2. They showed that when rat CPG2 was knocked out, its function could be restored by the human version of the protein, suggesting both versions have the same cellular function.

Rathje, a Picower Institute postdoc in Nedivi&rsquos lab, is now studying mutations in human CPG2 that have been linked to bipolar disorder. She is testing their effect on synaptic function in rats, in hopes of revealing how those mutations might disrupt synapses and influence the development of the disorder.

Nedivi suspects that CPG2 is one player in a constellation of genes that influence susceptibility to bipolar disorder.

&ldquoMy prediction would be that in the general population there&rsquos a range of CPG2 function, in terms of efficacy,&rdquo Nedivi says. &ldquoWithin that range, it will depend what the rest of the genetic and environmental constellation is, to determine whether it gets to the point of causing a disease state.&rdquo

The research was funded by the Picower Institute Innovation Fund and the Gail Steel Fund for Bipolar Research.


The 3 Sets of Genes That Make You Highly Sensitive

Although high sensitivity is genetic, there’s not just a single gene that causes it. In fact, scientists have increasingly found that personality traits are based on a whole collection of genes, not just one or two. That’s true of traits as different as introversion and intelligence.

With high sensitivity, there are at least three separate sets of genes that play a role — and different highly sensitive people may have some or all of them. Interestingly, every single one of these genes affects your brain or nervous system.

Below, we’ll look at each of the three sets of genes, including the one that’s the best candidate for being the official “sensitive” gene. But remember: your genes alone are only part of who you are, and every HSP has grown up with different experiences. Your mileage may vary.

1. The ‘Sensitive’ Gene (Serotonin Transporter)

Serotonin is a chemical in the body that does, well, a lot of things. But one of the most important? It stabilizes your mood.

Serotonin transporter, on the other hand, is a chemical that helps move serotonin out of the brain. So it’s the on/off switch for all that mood-balancing serotonin.

And guess what? Highly sensitive people have a special variation of the serotonin transporter gene that behaves a little differently. If you have this gene variant, you have lower serotonin levels, and chances are good you’ll be a highly sensitive person. (The gene is officially called 5-HTTLPR, so we’re going to stick with “the sensitive gene.”)

This gene variant was originally believed to cause depression, but that’s not exactly right. In fact, it doesn’t cause any mood disorder at all on its own, but it does make you sensitive to your surroundings — and more likely to learn lessons from them. That matters a lot in childhood development. If you combine this gene with an unhealthy childhood environment, you do have a higher risk of depression and other disorders throughout life. But, combine it with a safe, supportive environment, and you get better-than-normal outcomes as an adult. Basically, it boosts the effects of both good and bad upbringings.

So what does this mean if you’re a highly sensitive person? Well, you should know that your childhood experiences will have an outsized impact on your wellbeing as an adult. That doesn’t mean you can’t address and get past the effects of a rough childhood, but it does mean it will affect you more than it might affect others.

2. The Dopamine Genes

While the first gene matters, it’s not the only one. Researchers have also found a connection between sensitivity and a set of 10 different gene variants related to dopamine. Dopamine is the brain’s “reward” chemical.

Strictly speaking, we don’t yet know how these dopamine genes relate to sensitivity, but we have some hints. For starters, it makes sense that someone with a sensitive system would need to feel less “rewarded” by external stimuli — otherwise you’d be constantly drawn to the same loud, busy environments that exhaust you. (And the evidence bears that out: the gene variants with the biggest effect on sensitivity all have to do with dopamine receptors, which affect how sensitive you are to dopamine in the first place.)

It would also make sense for sensitive people to feel more rewarded by positive social or emotional cues, which they are more tuned into than others in the first place.

As a highly sensitive person, have you ever been baffled why your friends want to go somewhere loud and crazy — or why they’d enjoy a fast-paced, aggressive game? If so, it’s probably because you don’t get the same “dopamine hit” from these loud external stimuli. And that may be some or all of these gene variants at work.

3. The ‘Emotional Vividness’ Gene

Everyone tends to experience life more vividly during emotionally charged moments. But this emotional “vividness” is stronger for some people than it is for others. And it’s no surprise that high sensitivity has been linked to the gene variant that controls it.

This gene, which I’ll call the “emotional vividness” gene, is related to norepinephrine. Norepinephrine is a neurotransmitter that also helps with the body’s stress response. And there’s one variant — which may be common in HSPs — that turns up the dial on emotional vividness. If you have it, you will perceive the emotional aspects of the world more vividly. You’ll also have much more activity in the parts of the brain that create internal emotional responses to your experiences.

Most highly sensitive people are keenly aware that they have stronger emotional reactions than the people around them, and often notice emotional undercurrents where others pick up nothing. If you’re highly sensitive, this is not your imagination — you may actually have a brighter palette of emotional “colors,” so to speak, because of this gene variant. And it directly drives the level of empathy and awareness you have for others’ feelings.


How the brain reacts to loss of vision

If mice lose their vision immediately after birth due to a genetic defect, this has a considerable impact, both on the organisation of the cerebral cortex and on memory ability. This is the conclusion drawn by researchers at Ruhr-Universität Bochum in a study published online in the journal Cerebral Cortex on 7 December 2018. They demonstrated that, in the months after blindness emerged, the density of neurotransmitter receptors that regulate excitation balance and are required for memory encoding was altered in all areas of the cortex that process sensory information. Furthermore, the hippocampus, a brain region that plays a crucial role in memory processes, was profoundly affected.

Mirko Feldmann, Daniela Beckmann, Professor Ulf Eysel and Professor Denise Manahan-Vaughan from the Department of Neurophysiology conducted the study.

Other senses sharpen after loss of vision

Following the loss of vision, other senses become gradually more sensitive: tactile and hearing acuity and one's sense of smell all improve, enabling a blind individual to use these senses to navigate accurately through the environment, despite a lack of visual input. But this process takes time and practice. The associated changes in the brain are facilitated by synaptic plasticity, a process that enables experience-dependent adaptation, learning and memory. One clue as to whether reorganizational adaptation is taking place in the brain is obtained by analysing the density and distribution of neurotransmitters that are crucial for synaptic plasticity.

Adaptation requires major effort from the brain

The researchers from Bochum studied what happens in the brain after loss of vision in mice. They examined the density of neurotransmitter receptors after the emergence of blindness and compared the results with the brains of healthy mice. In addition, they tested how well the blind mice performed in spatial recognition tests, in order to examine the animals' memory.

Before any changes had developed in the sensory cortices, the researchers observed that loss of vision was first followed by changes in the density of neurotransmitter receptors and impairments of synaptic plasticity in the hippocampus. In subsequent months, hippocampal plasticity became more impaired and spatial memory was affected. During this time the density of neurotransmitter receptors also changed in the visual cortex, as well as in other cortical areas that process other sensory information.

"After blindness occurs, the brain tries to compensate for the loss by ramping up its sensitivity to the missing visual signals," explains Denise Manahan-Vaughan, who led the study. When this fails to work, the other sensory modalities begin to adapt and increase their acuities. "Our study shows that this process of reorganisation is supported by extensive changes in the expression and function of key neurotransmitter receptors in the brain. This is a major undertaking, during which time the hippocampus' ability to store spatial experiences is hampered," says Manahan-Vaughan.


Content: Alcohol Interacts with Receptors in the Brain to Produce its Effects

By inhibiting the firing of electrical impulses in neurons, alcohol can impair judgment, coordination, alertness, memory, and visual perception, among other things. Exactly, how does alcohol achieve all of these unrelated effects?

Alcohol affects the function of specific proteins or receptors embedded in the membranes of neurons. Alcohol can interact with a variety of neurotransmitter receptors, but at non-fatal concentrations of alcohol in the brain, alcohol interacts primarily with receptors for the amino acid neurotransmitters γ-aminobutyric acid (or GABA) and glutamate (the same amino acid found in “Chinese food” seasoning—MSG or mono-sodium glutamate). When alcohol binds to GABA and glutamate receptors, it causes many of the intoxicating symptoms that develop when one drinks too much.

How does this happen? To answer this, it’s helpful understand how these neurotransmitter receptors function in a neuron. A closer look at these neurotransmitter receptors reveals that they consist of several smaller proteins (called subunits) arranged to form a pore or channel in the middle. Normally the channel is closed. But when the neurotransmitter binds to the receptors, the channels will open briefly, allowing small cations such as sodium (Na+) or calcium (Ca2+) or anions such as chloride (Cl-) to pass into or out of the cell, along the concentration gradient. The type of ion that moves through the channel depends on the whether it’s a GABA or a glutamate receptor.

As ions move through the receptor channels, an electrical current is spread over the cell membrane. When positive ions (current) enter the cell, neurons fire electrical impulses. When negative charges (current) enter the cell, neuron firing is suppressed.

Figure 2.5 When GABA binds to its receptor, the ion channel opens and chloride ions (Cl-) flow into the cell with the concentration gradient. In the presence of ethanol, the channel remains open longer so more Cl- goes into the cell. Thus, the neuron can’t fire an electrical impulse.

Learn more about basic neuron structure and function and view a 3D animation

Alcohol works in a “double-duty” fashion. It can bind to GABA receptors, where it increases the amount of chloride ions (negative charges) entering the neuron. Also, alcohol can bind to glutamate receptors, where it decreases the amount of sodium and calcium (positive charges) entering the neuron. In both cases, the result is that the environment inside the cell becomes more “negative” and this suppresses the electrical activity (i.e., the firing rate) of the neuron. Thus, the neuron can’t communicate with its neighbors.

The suppression of neural communication causes most of the symptoms of intoxication. The particular symptom of intoxication will depend on where in the brain the suppression of neuron activity occurs. As the blood alcohol concentration increases, new symptoms of intoxication emerge (Figure 2.1).

Interestingly, repeated use of alcohol can decrease the receptor sensitivity to alcohol, making it more difficult for a person to become intoxicated.


Pain Receptors and Their Stimulation

Pain Receptors Are Free Nerve Endings. The pain receptors in the skin and other tissues are all free nerve endings. They are widespread in the superficial layers of the skin as well as in certain internal tissues, such as the periosteum, the arterial walls, the joint surfaces, and the falx and tentorium in the cranial vault. Most other deep tissues are only sparsely supplied with pain endings nevertheless, any widespread tissue damage can summate to cause the slow-chronic-aching type of pain in most of these areas.

Three Types of Stimuli Excite Pain Receptors—Mechanical, Thermal, and Chemical. Pain can be elicited by multiple types of stimuli. They are classified as mechanical, thermal, and chemical pain stimuli. In general, fast pain is elicited by the mechanical and thermal types of stimuli, whereas slow pain can be elicited by all three types.

Some of the chemicals that excite the chemical type of pain are bradykinin, serotonin, histamine, potassium ions, acids, acetylcholine, and proteolytic enzymes. In addition, prostaglandins and substance P enhance the sensitivity of pain endings but do not directly excite them. The chemical substances are especially important in stimulating the slow, suffering type of pain that occurs after tissue injury.

Nonadapting Nature of Pain Receptors. In contrast to most other sensory receptors of the body, pain receptors adapt very little and sometimes not at all. In fact, under some conditions, excitation of pain fibers becomes progressively greater, especially so for slow-aching-nauseous pain, as the pain stimulus continues. This increase in sensitivity of the pain receptors is called hyperalgesia. One can readily understand the importance of this failure of pain receptors to adapt, because it allows the pain to keep the person apprised of a tissue-damaging stimulus as long as it persists.


Neurotransmitter Receptors

The Glycine Receptor is Closely Related to the GABAA Receptor

Glycine receptors are the major inhibitory receptors in the spinal cord and the brain stem. Glycine receptors are similar to GABA A receptors in that both are ion channels selectively permeable to the anion Cl - . As one would anticipate, they both lie on the same main branch of the evolutionary tree of ionotropic receptors ( Fig. 8.2 ) Interestingly, only three amino acid replacements in the TM1-TM2 loop and the TM2 segment can change the selectivity of the glycine receptor from anionic to cationic, pointing again to the critical nature of residues in the TM2 segment in determining a receptor's ion selectivity. The overall structure of the glycine receptor is indicative of this similarity in properties. The native complex is approximately 250 kDa and is composed of two main subunits: α (48 kDa) and β (58 kDa). The receptor appears to be pentameric, most likely composed of three α and two β subunits. The glycine receptor has an open channel conductance of approximately 35–50 pS, similar to that of the GABAA receptor. The rat poison strychnine is a potent antagonist of the glycine receptor.

Four distinct α subunits and one β subunit of the glycine receptor have been cloned and are highly related ( Fig. 8.2 ). Each exhibits the typical predicted four TMs and is approximately 50% identical to the others at the amino acid level. Expression of a single α subunit in oocytes is sufficient to produce functional glycine receptors, indicating that the α subunit is the pore-forming unit of the native receptor. β subunits play exclusively modulatory roles, affecting, for example, sensitivity to the inhibitory actions of picrotoxin. They are widespread in the brain but not always found in neurons expressing α subunits, suggesting β subunits may serve other functions independent of their association with glycine receptors.


Evolution, women, touch, and social bonds

The reason why women have a higher touch sensitivity that facilitates social bonding in them could be because they’ve evolved as natural caregivers and nurturers.

Human babies, unlike other mammals, require extended periods of nurturing and caring. The higher touch sensitivity in women would ensure that human babies receive all the extra care and nurturing they require while women simultaneously feel good providing it.

Physical contact with infants is critical for their physical and psychological development. It not only reduces the stress levels of both the mother and the infant but a study conducted on premature infants also showed that the benefits they received from ample touching by their mothers extended up to the first 10 years of their lives. 6

Therefore, the importance that women give to touching in relationships is likely an extension of their predisposition to provide adequate skin-skin contact to their babies.

References

  1. Moir, A. P., & Jessel, D. (1997). Brain sex. Random House (UK). American Society of Plastic Surgeons. (2005, October 25). Study Reveals Reason Women Are More Sensitive To Pain Than Men. ScienceDaily. Retrieved July 22, 2017 from www.sciencedaily.com/releases/2005/10/051025073319.htm
  2. Society for Neuroscience. (2009, December 28). Women tend to have better sense of touch due to smaller finger size. ScienceDaily. Retrieved July 22, 2017 from www.sciencedaily.com/releases/2009/12/091215173017.htm
  3. Bartley, E. J., & Fillingim, R. B. (2013). Sex differences in pain: a brief review of clinical and experimental findings. British journal of anaesthesia, 111(1), 52-58.
  4. Pease, A., & Pease, B. (2016). Why Men Don’t Listen & Women Can’t Read Maps: How to spot the differences in the way men & women think. Hachette UK.
  5. Feldman, R., Rosenthal, Z., & Eidelman, A. I. (2014). Maternal-preterm skin-to-skin contact enhances child physiologic organization and cognitive control across the first 10 years of life. Biological psychiatry, 75(1), 56-64.

Hi, I’m Hanan Parvez (MBA, MA Psychology), founder and author of PsychMechanics. I’ve published one book and authored 300+ articles and on this blog (started in 2014) that have garnered over 4 million views. PsychMechanics has been featured in Forbes, Business Insider, Reader’s Digest, and Entrepreneur. Feel free to contact me if you have a query.


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