Dopamine, a brief description

Dopamine is a simple organic chemical in the catecholamine family, or a monoamine neurotransmitter which has a number of important physiological roles in the bodies of animals.

In the brain, dopamine functions as a neurotransmitter a chemical released by nerve cells to send signals to other nerve cells. Dopamine is produced in several areas of the brain, including the substantia nigra and the ventral tegmental area.It is a neurohormone that is released by the hypothalamus. Its action is as a hormone that is an inhibitor or prolactin release from the anterior lobe of the pituitary.

Dopamine was first synthesized in 1910 by George Barger and James Ewens at Wellcome Laboratories in London, England. In 1958, Arvid Carlsson and Nils-Åke Hillarp, at the Laboratory for Chemical Pharmacology of the National Heart Institute of Sweden, discovered the function of dopamine as a neurotransmitter. Arvid Carlsson was awarded the 2000 Nobel Prize in Physiology or Medicine for showing that dopamine is not just a precursor of norepinephrine and epinephrine but a neurotransmitter, as well.

Dopamine plays a major role in the brain system that is responsible for reward-driven learning. Every type of reward that has been studied increases the level of dopamine transmission in the brain, and a variety of highly addictive drugs, including stimulants such as cocaine and methamphetamine, act directly on the dopamine system. There is evidence that people with extraverted (reward-seeking) personality types tend to show higher levels of dopamine activity than people with introverted personalities.

Several important diseases of the nervous system are associated with dysfunctions of the dopamine system. Parkinson's disease, an age-related degenerative condition causing tremor and motor impairment, is caused by loss of dopamine-secreting neurons in the substantia nigra. Schizophrenia has been shown to involve elevated levels of dopamine activity in the mesolimbic pathway and decreased levels of dopamine in the prefrontal cortex. Attention deficit hyperactivity disorder (ADHD) and restless legs syndrome (RLS) are also believed to be associated with decreased dopamine activity.
Dopamine is also used as medication. It acts on the sympathetic nervous system. Application of dopamine leads to increased heart rate and blood pressure. When administered through an IV line, dopamine does not cross the blood brain. It acts on the heart by raising its contractility and blood pressure, this is useful in heart failure.
Dopamine cannot cross the blood-brain barrier, so dopamine given as a drug does not directly affect the central nervous system.
Dopamine is needed in some brain diseases as well. This includes diseases such as Parkinson's disease and dopa-responsive dystonia. For these patients levodopa is used. This is a precursor of dopamine. It can cross the blood-brain barrier.
Exercise to increase dopamine levels in the brain naturally. According to specialists regular, vigorous exercise can be just as effective for treating mood issues as medication and therapy. 30 minutes of daily exercise, including aerobic exercise, for overall brain health. Weight training is especially helpful for increasing dopamine. Replace caffeinated soda, coffees and teas drink decaffeinated green tea Restricting your food intake increases dopamine receptors.
Eat lean proteins, beans and vegetables to increase dopamine production in the brain. According to experts, eating lean beef, pork, turkey and chicken facilitate dopamine production. Eating cold water fish, wild game, bison and ostrich helps to produce dopamine. Other foods that increase dopamine are low-fat dairy products, fava beans, edamame, black beans, chick peas, lima beans, lentils, nuts and seeds. Leafy vegetables and green, yellow and red vegetables provide nutrients which indirectly facilitate dopamine production.
While Foods such as sugar, saturated fats, cholesterol, and refined foods interfere with proper brain function and can cause low dopamine.

When dopamine levels are depleted by stress, certain antidepressants, drug use, poor nutrition, and poor sleep. Alcohol, caffeine, and sugar all seem to decrease dopamine activity in the brain.
Low dopamine levels can cause depression, loss of motor control, loss of satisfaction, addictions, cravings, compulsions, low sex drive, poor attention and focus. When dopamine levels are elevated symptoms may manifest in the form of anxiety, paranoia, or hyperactivity.
When a person is depressed, symptoms like a lack of motivation and a reduction in the pleasure he or she experiences in life may be persistent. These symptoms are thought to be caused by lower levels of dopamine. Many doctors prescribe medications that increase dopamine in the brain to help those suffering from major depression. Increasing dopamine is also thought to help with depressive moods in those who have bipolar disorder.
Levels of dopamine in the brain, especially the prefrontal cortex, help in improved working memory. However, this is a delicate balance and as levels increase or decrease to abnormal levels, memory suffers. Dopamine helps in focus and attention. Vision helps a dopamine response in the brain and this in turn helps one to focus and direct their attention. Dopamine may be responsible for determining what stays in the short term memory based on an imagined response to certain information. Reduced dopamine concentrations in the prefrontal cortex are thought to contribute to attention deficit disorder.
Scientists found, had fewer dopamine receptors than normal-weight subjects. Compared with the obese group, the number of dopamine receptors decreased as the subjects' body mass index, an indicator of obesity, increased. That is, the more obese the individual, the lower the number of receptors. It's possible that obese people have fewer dopamine receptors because their brains are trying to compensate for having chronically high dopamine levels, which are triggered by chronic overeating. However, it's also possible that these people have low numbers of dopamine receptors to begin with, making them more vulnerable to addictive behaviors including compulsive food intake.

The researchers note that, based on this study alone, they cannot conclude whether the brain changes they've detected are a consequence or a cause of obesity. They also acknowledge that the regulation of body weight is extremely complex, involving many physiological mechanisms and neurotransmitters. But they do suggest that addressing the dopamine receptor deficiency or finding other ways to regulate dopamine in obese people might help reduce their tendency to overeat.

Unfortunately, many of the drugs that have been shown to alter dopamine levels are highly addictive. But exercise, which has other obvious benefits in weight control, is another way obese subjects might be able to stimulate their dopamine pleasure and satisfaction circuits, the researchers suggest. In animal studies conducted elsewhere, exercise has been found to increase dopamine release and to raise the number of dopamine receptors. This suggests that obese people might be able to boost their dopamine response through exercise instead of eating  just one more reason to exercise if you're trying to lose weight.

The neurobiology of aggression is not well understood, but scientists are aware of a relationship between the neurotransmitter serotonin and certain aggressive behaviors. The objective of this study was to explore whether higher levels of another brain chemical called dopamine, involved in pleasure and reward, increased aggressive response in its subjects. To scientists' surprise, it was not as they first theorized.
"The results of this study were astonishingly opposite of what was previously hypothesized," says Ingo Vernaleken, M.D., lead author of the study and research scientist for the department of psychiatry at RWTH Aachen University in Aachen, Germany.

"Subjects with more functional dopaminergic reward-systems were not more aggressive in competitive situations and could concentrate even more on the game. Subjects with lower dopaminergic capacity were more likely to be distracted by the cheating behavior."
In this study, 18 healthy adults in their twenties were tested for aggression using the psychological behavioral task known as the point subtraction aggression paradigm (PSAP). Participants were asked to play a computer game that required them to press a bar multiple times with the incentive of winning money, but they were also told that an adversary in the next room who is able to cheat may steal some of their winnings. What the paranoid participants did not know was that there was no adversary. The computer program is designed to perform randomized deductions of the subjects' monetary reward to simulate the cheating competitor.The participant had three choices to react: punish the cheater, shield against the adversary by repeatedly pressing a defense button, or continue playing the game in order to maximize their ability to win cash, which indicated resilience.

Results of the study showed a significant impact on aggressive response in areas in the brain where dopamine synthesis was present, especially in the basal ganglia, which among other functions include the motivation center. Minimized aggression was associated with higher dopamine levels in both the midbrain and the striatum, which plays a role in planning and executive function. People with greater capacity for dopamine synthesis were more invested in the monetary reward aspect of the PSAP, instead of acting in defense or with aggression against their perceived adversary, whereas subjects with lower capacities had a higher vulnerability to act either aggressive, defensive or both. A well-functioning reward system causes more resilience against provocation, excluding the behaviors of a competitive personality that is mistaken for aggressive behaviour. The fine balance of dopamine can alter anything from motivation or movement to attention and perhaps aggression. While increase dopamine reduces Impulsivity the slight connection to behaviour might be related to the Dark Triad of personality traits. The dopamine reward system has a complex web of mechanisms not just for motivation but also behavior, which relates to our animal programming. Perhaps in the end when we look to progress in science or extend our families we can thank the rewards triggers of our animal brains... or at least monitor the manifestations for low Dopamine levels.  

The probability of Parkinson's Disease, potential cures and surgery

The Scary thing of Parkinson's disease there is a chance it can be inherited, if the genes in a childs DNA is half of each parent then the odds are logically 50% of risk. Whether we pass on the gene we got from our father or the one from our mother is purely by chance, like flipping a coin heads or tails.

We all have genes that don't work properly. In most cases the other copy of the gene makes up for the one that does not work properly and we are healthy. A problem only arises if we meet someone else who has a non-working copy of the same gene and we have a child who inherits two non-working copies of that gene. This is called recessive inheritance.
Sometimes if one of our genes is not working properly the other copy of the gene cannot make up for it and that causes a condition or an increased risk of developing a condition. Each time we have a child we randomly pass on one copy of each gene. If the child inherits the copy that doesn't work properly, they too may develop the condition. This is called dominant inheritance.
In 1997, we studied a large family that came from a small town in Southern Italy in which PD was inherited from parent to child (dominant inheritance). Researchers found the gene that caused their inherited Parkinson's Disease and it coded for a protein called alpha-synuclein.
A research team from the Taub Institute at CUMC (Columbia University Medical Center) managed to identify the main mechanism that causes the progressive movement disorder in sporadic Parkinson’s disease patients. heritable forms of Parkinson’s disease have shown that a very important role in the onset and development of the disease is played by a protein called alpha-synuclein. Patients that have a higher number of alpha-synuclein gene copies will produce a higher quantity of this protein, thus damaging their neurons. Parkinson’s patients also show an excess of alpha-synuclein aggregates in the brain.
If one studies the brains of people with PD after they die, one can see tiny little accumulations of protein called Lewy Bodies (named after the doctor who first found them). Research has shown that there is a large amount of alpha-synuclein protein in the Lewy Bodies of people who have non-inherited PD as well as in the brains of people who have inherited PD. This immediately told us that alpha-synuclein played an important role in all forms of PD and we are still doing a lot of research to better understand this role.

. The longer forms of the alpha-synuclein gene were found to be specific to human patients, as well as some of the genetic variants that are in close connection to the onset of the disease. The research team also showed that if patients are exposed to environmental toxins that are related to Parkinson’s disease, there is an increase in alpha-synuclein. Currently, seven genes that cause some form of Parkinson's disease have been identified. Mutations (changes) in three known genes called SNCA (PARK1), UCHL1 (PARK 5), and LRRK2 (PARK8) and another mapped gene (PARK3) have been reported in families with dominant inheritance. Mutations in three known genes, PARK2 (PARK2), PARK7 (PARK7), and PINK1 (PARK6) have been found in affected individuals who had siblings with the condition but whose parents did not have Parkinson's disease (recessive inheritance). There is some research to suggest that these genes are also involved in early-onset Parkinson's disease (diagnosed before the age of 30) or in dominantly inherited Parkinson's disease but it is too early yet to be certain.
In most cases inheriting a non-working copy of a single gene will not cause someone to develop Parkinson's disease. many other complicating factors such as additional genes and environmental factors determine who will get the condition, when they get it and how it affects them.

By reprogramming skin cells from Parkinson's disease patients with a known genetic mutation, researchers at the Salk Institute for Biological Studies have identified damage to neural stem cells as a powerful player in the disease. The findings, reported online October 17, 2012 in Nature, may lead to new ways to diagnose and treat the disease. The scientists found that a common mutation to a gene that produce the enzyme LRRK2, which is responsible for both familial and sporadic cases of Parkinson's disease, deforms the membrane surrounding the nucleus of a neural stem cell. Damaging the nuclear architecture leads to destruction of these powerful cells, as well as their decreased ability to spawn functional neurons, such as the ones that respond to dopamine.
This discovery helps explain how Parkinson's disease, which has been traditionally associated with loss of neurons that produce dopamine and subsequent motor impairment, could lead to locomotor dysfunction and other common non-motor manifestations,such as depression and anxiety.

Its possible to use targeted gene-editing technologies to correct the mutation in patient's nuclear stem cells. This genetic correction repaired the disorganization of the nuclear envelope, and improved overall survival and functioning of the neural stem cells. To be able to chemically inhibit damage to the nucleus, producing the same results seen with genetic correction. This opens the door for drug treatment of Parkinson's disease patients who have this genetic mutation, The new finding may also help clinicians better diagnose this form of Parkinson's disease. Due to the striking appearance in patient samples, nuclear deformation parameters could add to the pool of diagnostic features for Parkinson's disease. The new finding may also help clinicians better diagnose this form of Parkinson's disease. Its the first time to our knowledge that human neural stem cells have been shown to be affected during Parkinson's pathology due to aberrant LRRK2.
The study shows that these reprogramming technologies are very useful for modeling disease as well as dysfunction caused by aging.

Alternatively new compounds target and shut a relatively rare membrane protein that allows the destructive calcium to flood into dopamine neurons. Previously published research showed that calcium entry through this protein stresses dopamine neurons, potentially leading to premature aging and death. The earlier research identified the precise protein involved—the Cav1.3 channel.
"These are the first compounds to selectively target this channel,” says D. James Surmeier, chair of physiology at Northwestern University Feinberg School of Medicine. “By shutting down the channel, we should be able to slow the progression of the disease or significantly reduce the risk that anyone would get Parkinson’s disease if they take this drugearly enough.”
As reported in the October 23 Nature Communications, the compounds work in a similar way to the drug isradipine, for which a Phase 2 national clinical trial with Parkinson’s patients—led by Northwestern Medicine neurologist Tanya Simuni—was recently completed. But because isradipine interacts with other channels found in the walls of blood vessels, it can’t be used in a high enough concentration to be highly effective for Parkinson’s disease.
For the next step, the Northwestern team has to improve the pharmacology of the compounds to make them suitable for human use, test them on animals, and move to a Phase 1 clinical trial.
The final technique if drugs don't work, is extradural motor cortex stimulation (EMCS), may provide a less-invasive alternative to electrical deep brain stimulation (DBS) for some patients with the movement disorder Parkinson's disease. The study was led by Dr. Beatrice Cioni of Catholic University, Rome. The researchers evaluated EMCS in nine patients with Parkinson's disease. Over the past decade, DBS using electrodes implanted in specific areas within the brain has become an accepted treatment for Parkinson's disease. In the EMCS technique, a relatively simple surgical procedure is performed to place a strip of four electrodes in an "extradural" location—on top of the tough membrane (dura) lining the brain. The electrodes were placed over a brain area called the motor cortex, which governs voluntary muscle movements. The study was designed to demonstrate the safety of the EMCS approach, and to provide preliminary information on its effectiveness in relieving the various types of movement abnormalities in Parkinson's disease. The electrode placement procedure and subsequent electrical stimulation were safe, with no surgical complications or other adverse events.
In particular, the patients had no changes in intellectual function or behavior and no seizures or other signs of epilepsy. Extradural stimulation led to small but significant and lasting improvements in control of voluntary movement. After one year, motor symptoms improved by an average of 13 percent on a standard Parkinson's disease rating scale, while the patient was off medications. Although DBS is an effective treatment for Parkinson's disease, it's not appropriate for all patients. Some patients have health conditions or old age that would make surgery for electrode placement too risky. Other patients—including four of the nine patients in the new study—are eligible for DBS but don't want to undergo electrode placement surgery.

According to certain web sites, family history of PD in a first degree relative is seen in about 15% of people with PD. There is a 2x risk of developing PD if you have a family history of PD in a first degree relative. Although increased, this risk is still relatively low. The  study also found elevated levels of the alpha-synuclein elongated transcripts in the blood of a group of patients with sporadic Parkinson's, compared with unaffected controls. This would suggest that a test for alpha-synuclein may serve as a biomarker for the disease.
Possible early detection for Parkinson's Disease, would lead to preventative actions. The possible gene reprograming offers a non invasive opportunity of a possible cure. Although another technique is calcium entry of a protein might Cav1.3 channel. Shutting it down might prove a slow progression or a cure. Its is still too early for research to come up with a cure and that avenues of gene manipulation or compound cures can resolve the almost hidden causes to Parkinson's. The last resort would be a surgical approach as deep brail stimulation offers a comfort to those who would risk the dangers for the sake of mobility. Having  pace maker for the brain in my view seems a bit cumbersome as the technology hasn't shrunk the equipment. Instead the current research in a non invasive cure, continues to offer hope. Perhaps in the future it may be a matter of popping a pill to prevent a neurodegenerative disease...

The future of sleep, via brain interfaces

Sleep is a naturally recurring state characterized by reduced or absent consciousness, relatively suspended sensory activity, and inactivity of nearly all voluntary muscles. Sleep is often thought to help conserve energy, but decreases metabolism only about 5–10%. Hibernating animals need to sleep despite the hypometabolism seen in hibernation, and must return from hypothermia to euthermia in order to sleep, making sleeping "energetically expensive."

Sleep remains one of the most poorly understood human biological functions, despite some recent strides in understanding the “social jetlag” of our internal clocks and the relationship between dreaming and depression. A new study finds that sleep may play a role in how we process emotionally-charged memories, which could have important implications in how we understand how post-traumatic stress disorder (PTSD) works in the brain. Though researchers haven't quite reached a consensus on why we sleep, we do know that sleep helps our brains rebound after a long day. Also among its functions are sleep's ability to help consolidate memories, enhance cognitive function, and boost decision-making.

To see how sleep might affect how memories are processed, researchers showed participants 150 emotional images (like an open-mouthed shark) twice, separated by a 12-hour period. Half of the participants were shown the images in the morning, and then again at night. The other half were shown the images at night, and, after a full night's sleep, were presented with the second set of images. The team asked the participants about their subjective responses to the images, and looked at their brain activity with fMRI and EEG. The participants who slept between the two viewings reported a less pronounced reaction to the second set of images. The researchers saw that the reactivity of the amygdala -- a brain region important in emotion and stress -- was reduced during the second viewing in the participants who had slept. Electroencephalograms or EEGs verified that reduced levels of the stress neurochemical norepinephrine were linked to less emotional reactivity the following morning.

While we sleep, research indicates, the brain replays the patterns of activity it experienced during waking hours, allowing us to enter what one psychologist calls a neural virtual reality. A dream about something we’ve just learned seems to be a sign that the new knowledge has been processed effectively. In a 2010 study published in the journal Current Biology, researchers at Harvard Medical School reported that college students who dreamed about a computer maze task they had learned showed a 10-fold improvement in their ability to navigate the maze compared to participants who did not dream about the task.

Robert Stickgold, one of the Harvard researchers, suggests that studying right before bedtime or taking a nap following a study session in the afternoon might increase the odds of dreaming about the material. But some scientists are pushing the notion of enhancing learning through dreaming even further, asking sleepers to mentally practice skills while they slumber. In a pilot study published in The Sport Psychologist journal in 2010, University of Bern psychologist Daniel Erlacher instructed participants to dream about tossing coins into a cup. Those who successfully dreamed about the task showed significant improvement in their real-life coin-tossing abilities. Experiments like Erlacher’s raise the possibility that we could train ourselves to cultivate skills while we slumber.

Researchers working at MIT have successfully manipulated the content of a rat's dream by replaying an audio cue that was associated with the previous day's events, namely running through a maze (what else). The breakthrough furthers our understanding of how memory gets consolidated during sleep — but it also holds potential for the prospect of "dream engineering."
Looking ahead, the researchers believe that this simple example of dream engineering could open up the possibility of more extensive control of memory processing during sleep — and even the notion that selected memories could be either enhanced, blocked, or modified. The researchers are also aiming to develop new approaches to learning and behavioral therapy through similar kinds of cognitive manipulation.
The military has an interest in neural devices for several functions, as well as a interface for vehicles they hope to find a way to reduce post traumatic stress by way of a neural device. Advances in technology has improved to the point that a particular neuron which retains the memory of a person can trigger a sound or a electrical device. Only a matter of time until we can map the brain for images and thus trigger a stream of images in which we may be able to de-code dreams. It may be possible to tray to use a MRI and computer to correlate single thought and image to a data bank and retrieve images when ever the MRI pick up brain patterns.
For a conscious person to register a picture of a animal and to think back the same animal so that the computer can look through its data banks and present a picture on a screen, would be the next step in technology. The trouble is would every person have a same brain pattern for the same image of the same animal?. Also can these brain patterns be extracted from dreams? so that we can find the stream of images during sleep?
Humans are more drawn into a graphical representation of the data then just brain waves. It is still in the early stages where we can fly AR drones with our minds and control robots slowly. As we study sleep for its benefits and create devices for quality in sleep. There will be a broad range of ideas and technology that will connect neural-interfaces with brain states. These might include inception of ideas and learning through sleep to mind hacking and even hypnotic control.

Shrinking Brain?, try having sex or Blueberries

Neurology seems to pop up every now and again to mention if there is a break though in discovery or if something is good or in this case bad for us. If you believe in the analogy that the brains whole structure is based on a highly complex computer that needs fine adjustments to reach optimum performance. In this case people should actually surround them selves with positive feeling and reinforce with a healthy lifestyle.


Yale scientist have discovered that major depression or chronic stress can cause the loss of brain volume, which is a form of cognitive impairment. A single genetic switch that triggers loss of brain connections in humans and animal models. The switch known as a transcription factor represses the expression of several genes that are necessary for the formation of synaptic connections between brain cells, which in turn could contribute to loss of brain mass in the prefrontal cortex. The area responsible for executive function, which relates to abilities to differentiate among conflicting thoughts, determine good and bad, better and best, same and different, future consequences of current activities, working toward a defined goal, prediction of outcomes, expectation.

The research team analyzed tissue of depressed and non-depressed patients donated from a brain bank and looked for different patterns of gene activation. The brains of patients who had been depressed exhibited lower levels of expression in genes that are required for the function and structure of brain synapses. Lead author and postdoctoral researcher H.J. Kang discovered that at least five of these genes could be regulated by a single transcription factor called GATA1. When the transcription factor was activated, rodents exhibited depressive-like symptoms, suggesting GATA1 plays a role not only in the loss of connections between neurons but also in symptoms of depression. Maybe one day genetic variations in GATA1 may one day help identify people at high risk for major depression or sensitivity to stress.
Your brain is bound to shrink as you age — it’s unavoidable. But there are certain lifestyle factors that hasten the process, according to a new study by researchers at University of California, Davis.

The four factors that were associated with faster declines in brain volume were:

•   High blood pressure 
•   Diabetes 
•   Cigarette smoking 
•   Being overweight or obese

The researchers found that all four risk factors were associated with faster declines in brain size: people with high blood pressure in midlife more quickly developed a condition called white matter change, in which areas of blood vessels in the brain are damaged, compared with those who had normal blood pressure. People with diabetes had faster shrinkage in a brain region called the hippocampus, which is involved with memory. Smokers had more rapid overall brain shrinkage than nonsmokers, and also showed faster white matter changes. On cognitive tests, these participants showed declines in executive function, or the ability to make decisions, plan, organize, and pay attention to and remember details. People who were overweight or obese in middle age, for example, were more likely to be among the top quartile of those with the fastest rates of decrease in brain volume and the most rapid declines in executive function.

Neurogenesis is a way to generate new neurons and it is possible to generate neurons throughout out your entire adult life.
These new cells can take over the function of damaged cells and provide protection against dementia and Alzheimer’s. They will help you learn faster and retain more of what you learn. You can boost or inhibit this process by various habits and techniques.

Exercise – In addition to the other well known and documented benefits of exercise, we can now add neurogenesis! The best thing you can do to grow and improve your brain is aerobic exercise.

Eat Blueberries – The ingredient that seems to trigger neurogenesis is anthocyanin. It can also be found in blackberries, black currant, bilberries, and black raspberries. Eat dark berries for your brain! One cup per day of blueberries is enough for the neurogenic effect.
Not only does learning improve as a result of neurogenesis, scientist now believe that learning itself stimulates neurogenesis.
Avoid Caffeine – I know, I know! I love caffeine too, but its long term impact on your brain is bad. Avoid Stress – Stress inhibits neurogenesis so do whatever it takes to reduce it. Restrict Your Calories – Calorie restriction is a universally agreed upon method for life-extension. Well, it turns out it is an effective brain extender as well. Take Ibuprofen – There is evidence that Ibuprofen reduces your risk of Alzheimer’s and can stimulate neurogenesis. Take small amounts because too much is not good for you.

To adopt a healthy and positive lifestyle is the  best way forward to reduce brain shrinkage or brain atrophy. Excessive alcohol and vitamin deficiency certainly are factors which are important for maintaining higher brain function. Also emotion is a factor and on some level modern living may be a harmful factor in brain development. One of the more interesting contributers of Neurogenesis is sex
professor Elizabeth Gould, also found that when male rats were allowed to mate with female rats multiple times over the course of the experiment ("chronic" sexual experience) as opposed to just once ("acute" sexual experience), the level of stress-response chemicals went down, but neurogenesis continued. In other words, repeated sexual experience in rats led to beneficial neurogenesis without the harmful chemical stress response. This might scale up in humans but hopefully if stress or modern life is getting you down, then maybe its time to try one some methods for neurogenesis to balance those brain cells.