Serotonin Neurons Contribute to Fail Safe Mechanism that Ensures Recovery From Interrupted Breathing

Source: Harvard.

Scientists trying to identify the roots of sudden infant death syndrome (SIDS), the leading cause of death in U.S. infants between 1 month and 1 year old, have increasingly turned their attention to the neurotransmitter serotonin and the brain cells that produce it.

Studies have linked serotonin-producing neurons to the regulation of breathing, which may go awry in SIDS. In addition, tissue samples from SIDS infants often show abnormalities specifically in those neurons.

Now, a new study in mice suggests that abnormalities in serotonin-producing neurons do not simply accompany a subset of SIDS cases but could actually contribute to those premature deaths.

The findings, published Oct. 23 in eLife, show that an acute loss of normal activity in the serotonin-producing nerve cells blunts the body’s ability to recover from interrupted breathing. The results provide evidence that young animals need properly functioning serotonin neurons to maintain normal cardiorespiratory function.

“If we can determine whether serotonin-producing neurons play an active and necessary role in regulating breathing, heart rate and the recovery response to apneas in young mouse pups, it could provide a plausible biological explanation for at least some SIDS cases,” said Susan Dymecki, professor of genetics at Harvard Medical School and senior author of the study.

“This possible explanation might provide some hope, even if minutely, for the profound grief experienced by families who have lost a child to SIDS, and may one day help researchers prevent SIDS altogether,” she said.

Normally, the brain coordinates the heart and lungs to provide a continuous flow of oxygen into the body and carbon dioxide out.

In conditions such as sleep apnea, when breathing temporarily stops, oxygen levels in cells can fall too low and carbon dioxide levels can rise too high. To restore healthy levels, the brain triggers a series of gasps and raises the heart rate, a process called autoresuscitation.

But heart rate monitor readings in some SIDS infants support the hypothesis that this fail-safe mechanism doesn’t always kick in, and that its failure can lead to SIDS.

Dymecki and colleagues set out to explore the role of serotonin-producing neurons in regulating autoresuscitation in week-old mice, which the researchers estimate are within the corresponding age window that conveys highest risk of SIDS in humans.

The researchers genetically modified the mice so their serotonin neurons would quickly and temporarily be inhibited in response to an injected chemical. Other neurons remained unaffected.

Setting up this inducible neuron perturbation technique in mouse pups and coupling it with the ability to measure respiratory and heart function was the key, said Dymecki.

“Although initially technically challenging, this novel approach allowed for precise brain cell manipulation and real-time measurement of cardiac and respiratory activity,” said Ryan Dosumu-Johnson, a graduate student in the Dymecki lab and first author of the paper.

The researchers then induced apneas in the mice.

serotonin neurons

Those with inhibited serotonin-producing neurons had weaker breathing recovery and more instances of sudden death in the face of apneas than mice with a normally functioning serotonin production system.

“These results indicate a vital role for serotonin neurons at an early age after birth,” said Dymecki.

To the researchers’ surprise, the heart rates in mice with inhibited serotonin neurons recovered normally, at least initially, even though their breathing was impaired.

“This uncoupling of the breathing and heart-rate recovery responses was unexpected,” said Dymecki. “It suggests that these two vital physiological responses–heart rate and breathing–could be more separable at the level of brain cells and circuits than previously anticipated, despite their interwoven physiology.”

Although further studies will be needed to uncover whether the same principles hold true in humans, the current findings support the theory that defects in the functioning of serotonin neurons can render infants more vulnerable to dying from apneas and other cardiorespiratory challenges, the authors said.

If replicated in human studies, the new findings could eventually help improve screening tools to identify infants at higher SIDS risk and suggest new strategies for drug development, said Dymecki.


Additional authors of the paper were postdoctoral researcher YoonJeung Chang of HMS and Andrea Corcoran and Eugene Nattie of the Geisel School of Medicine at Dartmouth.

Funding: This study was funded by National Institutes of Health grant HD036379 as well as a Howard Hughes Medical Institute Gilliam Fellowship for Advanced Study, National Institute of General Medical Sciences award T32GM07753 and the Neuroscience Scholars Program of the Society for Neuroscience.

Source: Ekaterina Pesheva – Harvard
Publisher: Organized by
Image Source: image is credited to Dymecki lab/Harvard Medical School.
Original Research: Open access research for “Acute perturbation of Pet1-neuron activity in neonatal mice impairs cardiorespiratory homeostatic recovery” by Ryan T Dosumu-Johnson, Andrea E Cocoran, YoonJeung Chang, Eugene Nattie, and Susan M Dymecki in eLife. Published October 23 2018.

Harvard”Serotonin Neurons Contribute to Fail Safe Mechanism that Ensures Recovery From Interrupted Breathing.” NeuroscienceNews. NeuroscienceNews, 25 October 2018.


Acute perturbation of Pet1-neuron activity in neonatal mice impairs cardiorespiratory homeostatic recovery

Cardiorespiratory recovery from apneas requires dynamic responses of brainstem circuitry. One implicated component is the raphe system of Pet1-expressing (largely serotonergic) neurons, however their precise requirement neonatally for homeostasis is unclear, yet central toward understanding newborn cardiorespiratory control and dysfunction. Here we show that acute in vivo perturbation of Pet1-neuron activity, via triggering cell-autonomously the synthetic inhibitory receptor hM4Di, resulted in altered baseline cardiorespiratory properties and diminished apnea survival. Respiratory more than heart rate recovery was impaired, uncoupling their normal linear relationship. Disordered gasp recovery from the initial apnea distinguished mice that would go on to die during subsequent apneas. Further, the risk likelihood of apnea-related mortality associated with suppression of Pet1 neurons was higher for animals with baseline elevated ventilatory equivalents for oxygen. These findings establish that Pet1 neurons play an active role in neonatal cardiorespiratory homeostasis and provide mechanistic plausibility for the serotonergic abnormalities associated with SIDS.

Balance your Serotonin, Dopamine and Endorphins with Happy foods

dopa ser.JPGPain and itch are influenced by two chemicals , Serotonin and Dopamine. Eat the following whole foods to balance Serotonin, Dopamine and Endorphins and do get a hug too.  Hugging can increase the production of dopamine in your brain.  Endorphins are endogenous opioid neuropeptides and peptide hormones in humans and other animals. They are produced by the central nervous system and the pituitary gland.  Scratching an itch causes minor pain, which prompts the brain to release serotonin. But serotonin also reacts with receptors on neurons that carry itch signals to the brain, making itching worse.  It has been observed that the release of the neurotransmitter dopamine stimulates this brain center to feel pleasure in “peak experiences,” such as from solving a difficult problem.

Raw pumpkin seeds
Raw spinach
Sesame seeds
Raw almonds
Raw dried dates
Sunflower seeds
Pumpkin leaves
Turnip greens

All of the above are geared toward a vegan diet and they all offer the perfect balance to help enhance your mood through the natural production of serotonin.

Non-vegans may add:

Cottage cheese

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Physical inactivity, dopamine, lactate , glucose and aging

aging exerAfter 96 years of age, he has crying spells in the afternoon or early evening hours when our brain hormones are slowing down to ready for sleep.  With less exercise and more time sitting down watching TV and eating every 2 hours, he forgets to remember things as his brain and muscles are not working as it should when he was young.  Whenever I see him, I give him a hug and trains other caregivers to hug him more. He perks up and can do more walking.

Hugging can increase the production of dopamine in your brain, and this can be seen in PET scans of the brain. Dopamine levels are low in people with conditions like Parkinsonism and mood disorders like Depression.

So if you see someone depressed, give him a hug, and bring a little joy to their life.
Dopamine levels are low to those with Alzheimer and Parkinson’s diseases.
Dopamine containing neurons control  voluntary movements. The association with a physiologically reduced glutamate release from frontal and prefrontal cortices, hippocampi and amygdala would induce further decrease of Dopamine release, inducing hypo-activity, gait disturbances and decline of executive functions.

The earlier the impairment of Dopamine system occurs, the fastest the cognitive decline goes.

Hormones and nuerotransmitters dopamine, norepinephrine and epinephrine are responsible for our emotions and affects our memory and muscles causing Alzheimer and Parkinson’s disease.
In the brain, dopamine functions as a neurotransmitter—a chemical released by neurons (nerve cells) to send signals to other nerve cells. The brain includes several distinct dopamine pathways, one of which plays a major role in the motivational component of reward-motivated behavior.
Epinephrine, also called adrenaline, hormone that is secreted mainly by the medulla of the adrenal glands and that functions primarily to increase cardiac output and to raise glucose levels in the blood.
Norepinephrine, also called noradrenaline, substance that is released predominantly from the ends of sympathetic nerve fibers and that acts to increase the force of skeletal muscle contraction and the rate and force of contraction of the heart.

Supplements and Nutrition

Eat happy foods: eggs, colorful whole foods and yams and whole foods/dietary supplements rich in the following nutrients:
Folate, Vitamin B complex, SAM-E,omega 3, digestive enzymes, probiotic, Vitamin C, copper, iron from greens, NAC
Suggested exercises should include walking, dancing , stretching, yoga, meditation, and other body movement.
Remember all the above information assumes that you have a healthy liver. Take care of the laboratory organ of your body, the liver which processes all chemicals, drugs, alcohol and nutrition in your body.
During sleep, your brain is helping the liver detox your body. The lymphatic system which travels opposite your circulatory system is responsible for cleaning your blood.

Lactate and brain

Lactate is considered an important metabolite in the human body, but there has been considerable debate about its roles in brain function. Research in recent years has suggested that lactate from astrocytes may be crucial for supporting axonal function, especially during times of high metabolic demands or hypoglycemia. The astrocyte-neuron lactate transfer shuttle system serves a protective function to ensure a supply of substrates for brain metabolism, and oligodendrocytes appear to also influence availability of lactate. There is increasing evidence for lactate acting as a signaling molecule in the brain to link metabolism, substrate availability, blood flow and neuronal activity.
The brain produces its own lactate from the metabolism of glycogen and tends to export lactate at rest []. Lactate is brought into the brain across the BBB to be used as fuel when plasma lactate is high or plasma glucose is low [].

Aphrodisiac foods

Cook together. Soft music, soft lights, aroma of cinnamon and garlic are all conducive for a seductive lunch or dinner.

Wine, beer or healthy smoothie are important. Do know that happy foods are chocolate, eggs, yams and beer.

Aphrodisiac Foods

  • Oysters
  • Watermelon
  • Cocoa or Chocolate
  • Asparagus
  • Avocados
  • Maca
  • Pumpkin Seeds. pumpkin seeds
  • Celery

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What sugar does to your brain – Dr Axe

What sugar does to your brain - Dr. AxeDextrose. Fructose. Lactose. Maltose. Glucose. A sugar by any other name is still sugar. In fact, there are more than 50 different names for it. But is sugar bad for you? Essentially, there are two types of sugar; there is “good” sugar that occurs naturally in fruits and vegetables and “bad” added sugar that’s added to sweeten sodas, candy, baked goods, and so on.

The “good” sugar is actually needed within the body, particularly within the brain. Following a meal, food is broken down; specifically glycogen, carbohydrates, proteins, fats and triglycerides, which are broken down into glucose. Glucose is so crucial to cell function that glucose deprivation can lead to loss of consciousness and eventual cell death. Therefore, after a meal, the body has a system in place in which excess glucose is stored as a reserve.

All cells need the energy to function; the large mass of neuron cells that make up the brain needs energy, largely in the form of glucose, to function. Did you know that the brain uses approximately 20 percent of an individual’s daily energy intake? (1)

Not only is sugar essential for your basic brain functions, but it tastes delicious too! Once you eat something with sugar in it, your taste receptors are activated, sending signals to your brain that set off an entire cascade of stimulation. In particular, the dopaminergic pathway is activated and triggers your “YUM!” signal. This pathway starts in a cluster of cells at the base of your brainstem called the ventral tegmental area (VTA) and extends through the lateral hypothalamus to the nucleus accumbens in the forebrain. Behaviors that stimulate the release of the neurotransmitter, dopamine, within this pathway have been shown to be highly motivational.

What sugar does to your brain - Dr. AxeGlucose is crucial to cell function and survival and it stimulates the reward pathway in your brain which makes everything feel like unicorns and rainbows. Life is good. Except that too much of something, is usually the opposite of good. But how many grams of sugar should you ingest per day? The American Heart Association suggests that individuals ingest a maximum daily intake of 6 teaspoons of sugar for women and 9 teaspoons for men. On average, people ingest 22 teaspoons of added sugar, which is on top of the naturally occurring sugar in our diet. (23)

So as our reward pathway keeps getting stimulated, the dopamine receptors become desensitized and require more dopamine to get the same pleasant feeling.

Therefore, there needs to be more consumption of, in this case, the sugary food or beverage, to elicit the same response. This increase in consumption has been shown to result in obesity, including childhood obesity. An increased diet in saturated fats and sugar (also known as a high-energy diet) can have fundamental changes within the brain that in conjunction with the increased neurotransmitter release (dopamine) can have detrimental effects. Such effects include…

Learning and Memory

Studies show that a diet high in sugar and saturated fats can promote oxidative stress, leading to cell damage. In 2010 Scott Kanoski, an associate professor of biological sciences at Perdue University, demonstrated that a three-day diet of increased sugar and saturated fats resulted in impaired hippocampal function (learning and memory), causing the rats to have difficulty finding food within a maze. (4)

Other studies also illustrate that the hippocampus, in particular, is sensitive to a high-energy diet. (5)

Your brain on sugar - Dr. AxeAddiction

Sugar addiction is real. The pathway activated for addiction is the same as the reward pathway. Persistent increases in the release of the neurotransmitter, dopamine, leads to desensitization and requires more consumption for the reward. It changes gene expression and creates a consumption→ Dopamine release→ reward→ pleasure→ motivate cycle that is increasingly difficult to break. (6)

Depression & Anxiety

Attempts in trying to break the addictive cycle can lead to mood swings and irritability. Eliminating all additive sugar from your diet can lead to some of the same symptoms of drug withdrawal. Sugar withdrawal symptoms include headaches, anxiety, cravings and even chills.

Cognitive Deficits

Prolonged diets with high sugar may lead to changes in gene expression. That affects everything from neurotransmitters to receptors and the basic function of the cell. In particular, studies suggest the brain-derived neurotrophic factor (BDNF) is impacted. This is active in the hippocampus, cortex and forebrain and is vital to learning and memory, as well as supporting existing neurons while promoting the formation of new synapses. This is reduced in high sugar diets. (7)

Therefore, it’s unsurprising that a correlation between low BDNF levels and Alzheimer’s, depression and dementia has been discovered. New and continuing research in the field of neuroscience continues to provide valuable information on the effect that excessive sugar has on the brain. Further information gained from such research could also lead to changes in the way that specific cognitive disorders are treated. (8)

Dopamine may have given humans our social edge over other apes


Male chimpanzees signal their aggression when they display their big canines, in contrast with humans, who show small canines when they smile.

Sergey Uryadnikov/

Dopamine may have given humans our social edge over other apes

Humans are the ultimate social animals, with the ability to bond with mates, communicate through language, and make small talk with strangers on a packed bus. (Put chimpanzees in the same situation and most wouldn’t make it off the bus alive.) A new study suggests that the evolution of our unique social intelligence may have initially begun as a simple matter of brain chemistry.

Neuroanatomists have been trying for decades to find major differences between the brains of humans and other primates, aside from the obvious brain size. The human brain must have reorganized its chemistry and wiring as early human ancestors began to walk upright, use tools, and develop more complex social networks 6 million to 2 million years ago—well before the brain began to enlarge 1.8 million years ago, according to a hypothesis proposed in the 1960s by physical anthropologist Ralph Holloway of Columbia University. But neurotransmitters aren’t preserved in ancient skulls, so how to spot those changes?

One way is to search for key differences in neurochemistry between humans and other primates living today. Mary Ann Raghanti, a biological anthropologist at Kent State University in Ohio, and colleagues got tissue samples from brain banks and zoos of 38 individuals from six species who had died of natural causes: humans, tufted capuchins, pig-tailed macaques, olive baboons, gorillas, and chimpanzees. They sliced sections of basal ganglia—clusters of nerve cells and fibers in a region at the base of the brain known as the striatum, which is a sort of clearinghouse that relays signals from different parts of the brain for movement, learning, and social behavior. They stained these slices with chemicals that react to different types of neurotransmitters, including dopamine, serotonin, and neuropeptide Y—which are associated with sensitivity to social cues and cooperative behavior. Then, they analyzed the slices to measure different levels of neurotransmitters that had been released when the primates were alive.

Compared with other primates, both humans and great apes had elevated levels of serotonin and neuropeptide Y, in the basal ganglia. However, in line with another recent study on gene expression, humans had dramatically more dopamine in their striatum than apes, they report today in the Proceedings of the National Academy of Sciences. Humans also had less acetylcholine, a neurochemical linked to dominant and territorial behavior, than gorillas or chimpanzees. The combination “is a key difference that sets apart humans from all other species,” Raghanti says.

Those differences in neurochemistry may have set in motion other evolutionary changes, such as the development of monogamy and language in humans, theorizes Kent State paleoanthropologist Owen Lovejoy, a co-author. He proposes a new “neurochemical hypothesis for the origin of hominids,” in which females mated more with males who were outgoing, but not too aggressive. And males who cooperated well with other males may have been more successful hunters and scavengers. As human ancestors got better at cooperating, they shared the know-how for making tools and eventually developed language—all in a feedback loop fueled by surging levels of dopamine. “Cooperation is addictive,” Raghanti says.

Lovejoy thinks these neurochemical changes were already in place more than 4.4 million years ago, when Ardipithecus ramidus, an early member of the human family, lived in Ethiopia. Compared with chimpanzees, which display large canines when they bare their teeth in aggressive displays, A. ramidus males had reduced canines. That meant that when they smiled—like male humans today—they were likely signaling cooperation, Lovejoy says.

However, it’s a big leap to prove that higher levels of dopamine changed the evolution of human social behavior. The neurochemistry of the brain is so complex, and dopamine is involved in so many functions that it’s hard to know precisely why natural selection favored higher dopamine levels—or even whether it was a side effect of some other adaptation, says evolutionary geneticist Wolfgang Enard at Ludwig Maximilian University of Munich in Germany. But he says this painstaking research to quantify differences in neurochemistry among primates is important, especially as researchers study differences in gene expression in the brain. Raghanti agrees and is now writing a grant to study the brain tissue of bonobos.