Why do we Yawn

Why do we yawn and why is yawning contagious?

Just imagine: you’re driving down the highway at 2pm in the heat of the day, and you’re really looking forward to getting to your destination soon. You try to stay awake but drowsiness strikes.

As a result you yawn and then sit up straighter in the driver’s seat, perhaps you’re a little restless and act out in hopes of increasing your arousal.

Is this what people yawn for? Yawning is generally triggered by several things, including fatigue, fever, stress, medications and social and psychological reasons. From one person to another the causes are different.

The question of why we yawn raises a surprising amount of controversy over such a trivial matter. We have no evidence to point us to the exact reason why people yawn.

But there are several theories that explain why people yawn. These include increasing alertness, cooling the brain, and evolutionary theory explains that yawning is to remind others in your group that you are too tired to stay alert, and that someone else should take over.

1. Help us wake up

Yawning comes with increasing drowsiness. This is the hypothesis behind why people yawn. Yawning is also associated with increased activity and stretching movements. Increased body movement may help us stay alert when the pressure of drowsiness increases.

 

Also, certain muscles in the ear ( tensor tympani muscle ) are activated during yawning. This triggers a reset of the range of motion and sensitivity of the eardrum and hearing, which increases our ability to monitor the world around us after we may have lost consciousness before yawning.

Yawning is usually accompanied by stretching movements. from shutterstock.com

In addition, opening the eyeball and flushing the lens of the eye may result in increased visual alertness.

Read: Protect Your Mental Health from Social Media

2. Cools the brain

Another theory as to why we yawn is the thermoregulatory hypothesis which suggests that yawning cools the brain. Yawning draws cold air into the mouth, which then cools the blood to the brain.

Proponents of this theory claim the increase in brain temperature occurs before yawning, with the decrease in temperature occurring after yawning.

But the research that gave rise to this theory only shows that excessive yawning occurs when brain and body temperatures are increasing. The research doesn’t say that yawning has a cooling purpose.

People yawned more frequently when experiments created artificial fevers, which showed a correlation between warm body temperature and yawning. But there’s no evidence to suggest that yawning cools the body—only that a warm body temperature triggers yawning.

3. Guard duty

Yawn-like behavior has been observed in almost all vertebrates. These observations suggest that the yawning reflex is ancient. The behavioral hypothesis based on the theory of evolution refers to humans as social animals. When we are vulnerable to attacks from other species, the function of groups is to protect each other.

Watchkeeping is part of the deal within the group, and yawning and stretching are evidence when an individual’s alertness level is dropping. It is important to change activities to prevent negligence and indicate when to change people just in case.

Neuroscience explanation

The yawning reflex involves many structures in the brain.

A study that looked at the brains of people prone to yawning found activity in the ventromedial prefrontal cortex of the brain. This part of the brain is associated with decision-making activities. Damage to this area is also associated with a loss of empathy.

 

If a certain area around the hypothalamus , which is made up of neurons with oxytocin, is stimulated, in rodents this causes them to yawn. Oxytocin is a hormone associated with social bonding and mental health.

Injecting oxytocin into different regions of the brainstem also causes yawning. These include the hippocampus (associated with learning and memory), the ventral tegmental area (associated with the release of dopamine, the happy hormone) and the amygdala (associated with stress and emotions). Blocking the oxytocin receptors here prevents that effect.

Patients with Parkinson’s disease don’t yawn as often as others, which may be related to their low dopamine levels. Dopamine substitutes have been reported to increase yawning frequency .

Your dog may yawn on a long car trip because your dog is stressed. from shutterstock.com

The same is true of cortisol, a hormone that increases stress. Cortisol is known to trigger people to yawn , while removal of the adrenal glands (which produce the hormone cortisol) prevents people from yawning . This suggests that stress levels may play a role in triggering why people yawn, which could be why your dog may yawn so much on long car trips.

So, it seems that yawning is somehow linked to empathy, stress, and the release of dopamine.

Why is yawning contagious?

Chances are you’ve yawned at least once while reading this article. Yawning is a contagious behavior and seeing someone yawn often causes us to yawn too.

But the only theory offered here suggests that a person’s vulnerability to yawning is correlated with a person’s level of empathy.

It’s interesting to note that people on the autism spectrum are less likely to catch yawns than people with high psychopathic tendencies . And dogs, which are considered to be highly empathetic animals, can get infected when humans yawn .

 

Overall, neuroscientists have developed ideas that explain the various triggers why people yawn, and we have a very detailed picture of the mechanisms underlying yawning behavior. But the purpose of why people yawn remains elusive.

Back in our road trips, yawning may be a physiological cue when levels of self-awareness compete with intense drowsiness. But the important message here is that sleep may be a good choice and encourage drivers to stop and rest, and that should not be ignored.

Protect your Mental Health from Social Media

Six ways to protect your mental health from the dangers of social media

A  psychologist who studies the dangers of online interactions and observes the effects of (wrong) social media use on the lives of my clients , here are six suggestions for reducing the harm social media can do to mental health.

1. Limit the time and place you use social media

Using social media can affect direct communication with others . By turning off social media notifications or turning on airplane mode at a certain time each day, you can better relate to others. For example, not checking social media when eating with family and friends, when playing with children, to talking to a partner. Avoid social media so as not to interrupt work or distract from conversations with colleagues. Special advice, don’t keep your phone or computer in the bedroom, because it will disturb your sleep .

2. Schedule a ‘detox’ period

Several studies have shown that a social media ‘detox’ or a five-day to a week ‘pause’ from Facebook can reduce stress levels and increase life satisfaction . So start scheduling a daily break from social media for a few days.

Reduction doesn’t have to be so extreme that it makes you uncomfortable not being able to access social media, for example using Facebook, Instagram, and Snapchat for 10 minutes a day for three weeks can lead to less loneliness and depression . It may be difficult at first, but you can ask family and friends for support by saying you’re “detoxifying” on social media. Another thing that can be done is to delete your favorite social media apps.

3. Watch what you do and how you feel

Try using your favorite online platforms at different times and durations of the day to see how you feel then and after. You may find that using social media for a short amount of time will help you feel better than spending 45 minutes going through a site’s entire feed in depth.

If you feel like you’re wasting your energy on Facebook every midnight that leads to bad feelings about yourself, don’t go to the page after 10 p.m.

It should be noted that people who passively use social media, just looking at other people’s posts, feel worse than people who actively use social media , posting about themselves and interacting with others online. It’s better to focus on online interactions with people you know offline.

Read: Why Do We Yawn

4. Use social media mindfully: why am I doing this?

If opening Twitter has become the first thing you do in the morning, is it because you want to know the latest news or just a habit as an escape to face a new day? Do you prefer viewing posts on Instagram instead of doing a difficult task at work? Answer this question honestly with yourself. When reaching for the phone (or computer) to check social media, answer this question: why am I doing this now? Decide if this is indeed what you should do.

5. Crop

Over time, many people or organizations you follow on social media. Some of the content is interesting to look at, but there’s a lot that will be boring, annoying, annoying or it could be worse. It’s time to stop following (unfollow) , mute (mute) , or hide your contacts (hide) . They won’t notice if you ‘cut’ social media. As a result, your life will be better.

This is revealed in a recent study of how information about the lives of Facebook friends can affect people more negatively than any other content on Facebook. Meanwhile, content filled with inspirational stories actually creates feelings of gratitude, vitality, and admiration . Cutting out a few “friends” and adding a few motivating or funny sites tends to lessen the negative effects of social media.

6. Social media is not a substitute for real life

It’s good to use Facebook to find out how your cousin has just given birth, but don’t put off a visit after months. Tweeting with colleagues can be interesting and fun, as long as the interaction doesn’t replace direct communication with them.

When used with mindfulness and consideration, social media is a useful addition to your social life. However, only the person sitting across from you can satisfy the basic human need for a sense of connectedness and self-existence.

Neurons & Neurotransmission

We have all experienced the reflex reaction when we accidentally touch something hot. But did you know how fast the nerve impulse that conducts this response is? It is estimated that the speed of a neural impulse can reach up to 120 meters/second or 268 miles/hour! That is much faster than the top speed of any of our cars, unless one of us is lucky enough to own a supercar like the one below. Impressive isn’t it?

 

Records of studying the nervous system dates back to Egyptian manuscripts from 1700 BC. However, major breakthrough discoveries were made in the field of Neuroscience in the late 19th century, and finally in 1906, Golgi and Ramón y Cajal shared the Nobel Prize in Physiology or Medicine in recognition of their work on the structure of the nervous system. A neuron, or a nerve cell, is one of the two main components of the central nervous system (glial cells are the other type).

Unlike other cells in the body, a neuron is a specialized cell (with great powers!) that is capable of conducting electrical and chemical signals in a process known as neurotransmission. A typical neuron is divided into three parts: the soma or cell body, dendrites and axon. While there are as many as 10,000 different types of neurons in the human brain, they can be broadly classified into three types: motor neurons (for conveying motor information), sensory neurons (for transmitting sensory information), and interneurons (which convey information between different types of neurons).

 

 

Synapses are the junctions where neurons pass signals to other neurons, muscle cells, or gland cells. Synaptic signals from other neurons can be received either by the soma, dendrite or axon, whereas signals to other neurons are transmitted only by the axon. The typical synaptic cleft (cell-to-cell distance) can vary between 3.5 nm to 40 nm (compare that to the thickness of your hair which is more than 250 times wider!). Thus the nervous system is wired by numerous neurons interconnected by synapses in a super-complicated neuronal circuit. It is estimated that the human brain alone contains around one hundred billion neurons and one hundred trillion synapses!
There are two main types of synapses, chemical and electrical. Electrical synapse is an electrical connection between neurons through structures known as gap junctions. Gap junctions are intercellular channels that allow ions and small molecules to pass directly from one cell to the other. On the other hand, in a chemical synapse, signals are transmitted via release of neurotransmitters (that are packed in synaptic vesicles in the presynaptic neuron) into the synaptic cleft. Binding of the neurotransmitters to receptors in the postsynaptic membrane causes activation of this cell through the post synaptic density (a protein dense signaling apparatus). Depending on the type of effect the neurotransmitter has on the postsynaptic cell, a chemical synapse can either be excitatory or inhibitory.

The fundamental process that triggers the release of neurotransmitters is the action potential, which is an electrochemical wave that travels along the axon of a neuron when there is a change in the membrane potential. Neurons maintain a steady resting voltage gradient (typically from –70 to –80 millivolts) across their membranes via ion channels and ion pumps.

In response to an external stimulus, when enough voltage-dependent positive ion channels such as sodium or calcium channels are activated, they allow a net inward sodium or calcium current which depolarizes the cell to a threshold potential above the resting potential and this triggers the neuron to fire. Eventually, the sodium/calcium channels inactivate and the potassium/chloride channels are activated which results in an outward current of positively charged potassium ions/inward current of negatively charged chloride ions causing the neuron to repolarize and hyperpolarize and ultimately return to the resting state.

Neuron Fun Fact

Neurons are cells within the nervous system that transfer info to other nerve cells, muscle, or gland cells. Most neurons have a cell body, an axon, and dendrites. The cell body includes the nucleus and cytoplasm. The axon extends from the cell body and often gives rise to many smaller branches before ending at nerve terminals. Dendrites extend from the neuron cell body and receive messages from other neurons. Synapses are the contact points where one neuron communicates with another. The dendrites are covered with synapses formed by the ends of axons from other neurons.

Read : Sensory Neuron

The brain is what it is because of the structural and functional properties of interconnected neurons. The mammalian brain consists of between 100 million and 100 billion neurons, depending on the species. Each mammalian neuron contains a cell body, dendrites, and an axon.

The cell body contains the nucleus and cytoplasm. The axon extends from the cell body and often gives rise to many smaller branches before ending at nerve terminals.

Dendrites extend from the neuron cell body and receive messages from other neurons. Synapses are the contact points where one neuron conveys with another. The dendrites are covered with synapses formed by the ends of axons from other neurons.

 

When neurons receive or send messages, they transmit electrical impulses along their axons, which can range in length from a tiny fraction of an inch (or centimeter) to three feet (about one meter) or more. Many axons are covered with a layered myelin sheath, which accelerates the transmission of electrical signals along the axon. This sheath is made by specialized cells called glia. In the brain, the glia that make the sheath are called oligodendrocytes, and in the peripheral nervous system, they are known as Schwann cells.

The brain consists of at least ten times more glia than neurons. Glia perform many jobs. Researchers have known for a while that glia transport nutrients to neurons, clean up brain debris, digest parts of dead neurons, and help hold neurons in place. Current research is uncovering important new roles for glia in brain function.

Tips for Immunohistochemistry

educationImmunohistochemistry is like cooking. There are many recipes out there, but some of them do not work out well. However, when they do, they are great! You need the right ingredients, a dose of experience, a few tricks from old cooks, and a grain of common sense. Read more to learn about traps to avoid, and important information to report when you publish your findings.

The problem

The validity of scientific results depends to a large extent on the use of appropriate methods providing the required precision and sensitivity, as well as controlled specificity of reagents and procedures. This statement is particularly valid for immunohistochemistry, where sensitivity and specificity of the antibodies, as well as technical procedure are crucial to avoid false-positive and false-negative results.

When using immunohistochemistry, several factors can cause false-negative or false-positive results and all should be verified as much as possible in each experimental set-up used. In particular, primary antibodies can fail to detect their target antigen even if the antigen is present in the tissue for many reasons, including conformation changes induced by fixation/embedding, steric hindrance by interacting proteins/post-translational modifications, low affinity of the antibody for the target, or failure of the antibody to penetrate into the tissue. Conversely, antibodies can bind non-specifically to other targets or tissue components. This observation holds true for both primary and secondary antibodies.

The problem is further confounded by the vast literature describing various procedures – such as the use of distinct “blocking” reagents and antigen-retrieval – to minimize these pitfalls and ensure high-fidelity binding of antibodies. This makes it difficult to choose the adequate method, and testing alternatives can be laborious. However, blindly following an established protocol might prove insufficient. It requires considerable experience, rational thinking and evidence from other methods to determine whether a given staining pattern obtained by immunohistochemistry is likely specific or non-specific. For instance, antibodies directed against a synaptic protein should produce no staining of the cell nucleus (unless this protein plays an additional, previously not described role in this compartment). In such case of wrong labeling, either the antibody or the staining protocol may be unsuitable.

Read: Sensory Neuron

The solutions

Here, we provide a practical guide of what should be tested and what should be reported in order to provide convincing evidence for the validity of immunohistochemical experiments. This includes dealing with the three main steps that can lead to false negative and false positive results:

Detection of the antigen of interest by the primary antibody
Detection of the primary antibody by secondary antibodies
Tissue preparation

1) Primary antibody specificity

The most stringent specificity test is performed in tissue devoid of the antigen of interest (knockout mouse). When not feasible, the best alternative is to show that two antibodies raised against different epitopes of the antigen of interest yield the same staining pattern. A third control includes inactivation of the antibody by incubation with its antigen prior to use for immunohistochemistry. This control does not exclude, however, that several targets sharing a common epitope are detected by this antibody. If doubts remain, additional information about the expression and localization of the antigen of interest should be provided by alternative methods.

As a consequence of the requirement by the Journal of Comparative Neurology to provide detailed characterization of primary antibodies, there is now a large collection of commercially-available antibodies that fulfill these criteria. To avoid unnecessary duplication, the Journal of Comparative Neurology has published an Antibody database listing all these products, which can be considered as being well characterized. Keep in mind, however, that polyclonal antibodies can vary considerably in their affinity and specificity from batch to batch, even when sold under the same catalog number. Every new batch ought to be tested to avoid bad surprises.

2) Secondary antibody specificity

Secondary antibodies are raised against immunoglobulins (typically IgGs) of the species in which primary antibodies were raised. As they are used in fairly high concentration, the likelihood that they bind non-specifically to tissue components (extracellular matrix proteins, blood vessels, etc) is higher than for primary antibodies. Further, they might cross-react with IgGs from other species, which is particularly relevant in multiple-labeling experiments. To minimize cross-reactivity, whenever available, it is best to use highly cross-adsorbed secondary antibodies.

Influence of immunoglobulins in lesioned tissue. Immunoperoxidase staining with secondary antibody binding to IgGs potentiated by tissue lesion. Sections were stained for a marker of microglia in the mouse hippocampus following injection of kainic acid. Left: section from wild-type mouse; Right: section from mouse devoid of IgGs (Zattoni et al., 2011)

To test for specificity, secondary antibodies should be applied in the absence of primary antibodies: all residual staining can be considered as being non-specific. In immunofluorescence experiments, beware of possible autofluorescent molecules that may be contained in tissues, their presence can be detected best in the absence of secondary antibodies. Note, however, that non-specific binding to tissue components depends both on the antibody and the tissue type. Embryonic/neonatal brain tissue has much more non-specific binding than adult tissue, and lesions, which cause damage to the blood-brain-barrier and leakage of serum proteins into brain parenchyma, also increase non-specific binding of secondary antibodies. The same can be said for weak tissue fixation over extended time (e.g., poor perfusion-fixation, fixation by immersion, etc.).

3) Influence of tissue preparation

Relative to antibody specificity, this issue is more versatile and complex and it can result in both, false-positive and false-negative results, even when using highly specific and well-characterized antibodies. As noted above, these effects arise mainly from epitope masking due to fixation-induced conformational changes and failure of the antibody to penetrate the tissue, as well as from non-specific binding of secondary antibodies, which can mask the specific signals. Furthermore, it needs to be emphasized that when antibodies do not recognize or do not have access to their epitope, they will typically bind non-specifically to other tissue components, and therefore produce false-positive results. Finally, it is important to realize that control tests performed with knockout tissue only provide information about false-positive results, but not false-negatives.

There are a number of published examples of pitfalls resulting from the influence of tissue preparation, notably fixation and the need in some cases, to use stringent methods for unmasking epitopes, in particular for postsynaptic proteins (Fritschy et al., 1998; Watanabe et al., 1998; Lorincz & Nusser, 2008).

The following aspects should be considered, when aiming at improving immunohistochemistry procedures because of apparent false-negative or false-positive results produced by an antibody. Typically, a compromise between preservation of the (ultra)-structure and staining sensitivity should be sought.

Reduce (or enhance) tissue fixation: type of fixative, pH, concentration, duration of the fixation (and postfixation), use of additives (e.g. picric acid). These effects are age-dependent (neonatal, but not adult, brain tissue benefits from a longer postfixation) and related to the nature of the antigen (soluble proteins tend to diffuse away in weakly fixed tissue).
When fixation has deleterious effects, consider using weak fixation by brief immersion of tissue slices or tissue sections, as described in detail in (Schneider Gasser et al., 2006).
Antigen-retrieval methods (e.g., heating/boiling tissue in acidic buffer; enzymatic digestion).
Use of detergent or repeated freeze/thaw to enhance penetration of the antibodies into the tissue.
Use of blocking solutions before and during primary antibody incubation. Note that in perfusion-fixed tissue, good results can be obtained without any pre-blocking step (see Fritschy & Mohler, 1995).
Temperature and duration of incubation in primary antibody and secondary antibody solution, as well as duration of the rinsing steps between antibody solutions. Here, an increase in signal-to-noise ratio can be achieved, sometimes with striking reduction of non-specific binding to tissue components.
Standard perfusion-fixation for detection of neurochemical markers. Double immunofluorescence staining for calbindin (green), a cytoplasmic marker of Purkinje cells and vesicular glutamate transporter type 2 (red), a marker of climbing fiber terminals. Staining was performed on perfusion-fixed, free-floating tissue sections (Fritschy et al., 2006).
High sensitivity detection of postsynaptic markers by antigen-retrieval (pepsin treatment). Double-immunofluorescence staining for postsynaptic markers (green; left, PSD-95; right, gephyrin) and presynaptic markers (red; left, vesicular glutamate transporter type 1; right, vesicular GABA transporter) in the hippocampus. Staining was performed using pepsin-mediated antigen retrieval. See Tyagarajan et al., 2011 for details.
Combined detection of soluble cytoplasmic protein (eGFP) and postsynaptic markers in weakly fixed tissue. Triple-immunofluorescence staining showing the presence of GABAergic postsynaptic proteins – GABAA receptor a2 subunit (red) and gephyrin (blue) – in relation to newborn granule cells in the olfactory bulb, selectively expressing eGFP (green) upon transduction with a lentivirus. The combination of eGFP and gephyrin immunofluorescence was achieved by preparing live tissue slices that were briefly fixed by immersion in a paraformaldehyde solution; see Panzanelli et al., 2009 for details.

Submitting to EJN

In the Author guidelines, EJN emphasizes the need to provide enough information in the Materials and Methods section to enable proper evaluation of the results and reproduction of the data. With regards to immunohistochemistry, detailed information about the antibodies used and about control experiments validating their specificity and the sensitivity of the method is mandatory. Authors should indicated which exact antibody was used (catalog and batch number, species of origin, immunogen information) and should provide information on the characterization of the antibody (description -or reference to experiments previously reported- performed to test its specificity, see EJN author guidelines). These requirements are in line with the policy of the Journal of Comparative Neurology, which refuses publication of articles that do not provide detailed characterization of antibodies used for immunohistochemistry. EJN encourages its contributors to consult the antibody database of the Journal of Comparative Neurology when selecting antibodies for experiments and when reporting their use in their manuscripts.

Despite these pitfalls of immunohistochemistry, only a minority of articles submitted to EJN fulfills these explicit requirements of the author guidelines. In 2008, in order to improve this situation, EJN published a technical spotlight emphasizing the necessity to check whether negative findings (failure to detect the antigen of interest in the sample analyzed) might be due to the method – in particular, tissue fixation – used for analysis (Fritschy, 2008).

We hope this article will help you to prepare and analyze your immunohistochemistry experiments. Please feel free to ask questions!

Useful resources:

The antibody database of the Journal of Comparative Neurology

Is my antibody staining specific? (Fritschy and Sarter, 2008)

References:

Fritschy, J.M. (2008) Is my antibody-staining specific? How to deal with pitfalls of immunohistochemistry. Eur. J. Neurosci., 28, 2365-2370.

Fritschy, J.M. & Mohler, H. (1995) GABAA-receptor heterogeneity in the adult rat brain: differential regional and cellular distribution of seven major subunits. J. Comp. Neurol., 359, 154-194.

Fritschy, J.M., Panzanelli, P., Kralic, J.E., Vogt, K.E. & Sassoè-Pognetto, M. (2006) Differential dependence of axo-dendritic and axo-somatic GABAergic synapses on GABAA receptors containing the a1 subunit in Purkinje cells. J. Neurosci., 26, 3245-3255.

Fritschy, J.M., Weinmann, O., Wenzel, A. & Benke, D. (1998) Synapse-specific localization of NMDA- and GABAA-receptor subunits revealed by antigen-retrieval immunohistochemistry. J. Comp. Neurol., 390, 194-210.

Lorincz, A. & Nusser, Z. (2008) Specificity of immunoreactions: the importance of testing specificity in each method. J. Neurosci., 28, 9083-9086.

Panzanelli, P., Bardy, C., Nissant, A., Pallotto, M., Sassoè-Pognetto, M., Lledo, P.M. & Fritschy, J.M. (2009) Early synapse formation in developing interneurons of the adult olfactory bulb. J. Neurosci., 29, 15039-15052.

Schneider Gasser, E.M., Straub, C.J., Panzanelli, P., Weinmann, O., Sassoè-Pognetto, M. & Fritschy, J.M. (2006) Immunofluorescence in brain sections: simultaneous detection of presynaptic and postsynaptic proteins in identified neurons. Nature Protocols, 1, 1887-1897.

Tyagarajan, S.K., Ghosh, H., Yevenes, G.E., Nikonenko, I., Ebeling, C., Schwerdel, C., Sidler, C., Zeilhofer, H.U., Gerrits, B., Muller, D. & Fritschy, J.M. (2011) Regulation of GABAergic synapse formation and plasticity by GSK3beta-dependent phosphorylation of gephyrin. Proc. Natl. Acad. Sci. USA, 108, 379-384.

Watanabe, M., Fukaya, M., Sakimura, K., Manabe, T., Mishina, M. & Inoue, Y. (1998) Selective scarcity of NMDA receptor channel subunits in the stratum lucidum (mossy fibre-recipient layer) of the mouse hippocampal CA3 subfield. Eur. J. Neurosci., 10, 478-487.

Zattoni, M., Mura, M.L., Deprez, F., Schwendener, R., Engelhardt, B., Frei, K. & Fritschy, J.M. (2011) Brain infiltration of leukocytes contributes to the pathophysiology of temporal lobe epilepsy. J. Neurosci., 31, 4037-4050.