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I'm talking about moments when you watch a film and you bristle, or when you listen to music, etc.
What kind of neurotransmitter flow changes?
One thing is that we can't control the Goosebumps. It is an involuntary function caused by the Sympathetic Nervous System which is the major part of the Automatic Nervous System. The major function of the SNS is fight to flight response along with maintaining homeostasis in which case it internally will be alert maintaining body status from the background.
Before sending any response to target tissue when there is input to SNS it has to secrete neurotransmitters but before this to the sympatho-adrenal response of the body, as the preganglionic sympathetic fibers that end in the adrenal medulla (but also all other sympathetic fibers) secrete acetylcholine, which activates the great secretion of adrenaline (epinephrine) and to a lesser extent noradrenaline (norepinephrine) from it.
So whenever SNS senses (message flow is bidirectional) any stress it responds it in following action mentioned:
At the synapses within the ganglia, preganglionic neurons release acetylcholine, a neurotransmitter that activates nicotinic acetylcholine receptors on postganglionic neurons. In response to this stimulus postganglionic neurons - with two important exceptions - release norepinephrine, which activates adrenergic receptors on the peripheral target tissues. The activation of target tissue receptors causes the effects associated with the sympathetic system.
Once the receptors receive the information then the response flows to the target tissue via neurons with the help of the neurotransmitters. To explain goosebumps technically:
Properly known as piloerection, horripliation or pilomotor reflex, the bumps we get are stimulated by fear and cold and they are essentially just a temporary change in the skin. These stimulants cause a nerve discharge from the sympathetic nervous system (which is an involuntary portion of nerves we have) and the nerve discharges create muscle contractions called arrrectores pilorum that raise the hair follicles in our skin. It is the elevation of the hair that causes the Goosebumps. The name Goosebumps actually comes from the fact that plucked goose feathers resemble the human hair follicles.
Goosebumps also occur when we listen to surprise songs, sad songs or some other kind of thrilling music. Researchers have tried to explain it and they call it "Frisson". Check out this small video which talks about it. It is nice:
Also refer to this website: Goosebumps
Dendrites are projections of a neuron (nerve cell) that receive signals (information) from other neurons. The transfer of information from one neuron to another is achieved through chemical signals and electric impulses, that is, electrochemical signals. The information transfer is usually received at the dendrites through chemical signals, then it travels to the cell body (soma), continues along the neuronal axon as electric impulses, and it is finally transferred onto the next neuron at the synapse, which is the place where the two neurons exchange information through chemical signals. At the synapse meet the end of one neuron and the beginning—the dendrites—of the other.
This figure depicts what a dendrite looks like in a neuron:
Anatomy of Sleep
Several structures within the brain are involved with sleep.
The hypothalamus, a peanut-sized structure deep inside the brain, contains groups of nerve cells that act as control centers affecting sleep and arousal. Within the hypothalamus is the suprachiasmatic nucleus (SCN) &ndash clusters of thousands of cells that receive information about light exposure directly from the eyes and control your behavioral rhythm. Some people with damage to the SCN sleep erratically throughout the day because they are not able to match their circadian rhythms with the light-dark cycle. Most blind people maintain some ability to sense light and are able to modify their sleep/wake cycle.
The brain stem, at the base of the brain, communicates with the hypothalamus to control the transitions between wake and sleep. (The brain stem includes structures called the pons, medulla, and midbrain.) Sleep-promoting cells within the hypothalamus and the brain stem produce a brain chemical called GABA, which acts to reduce the activity of arousal centers in the hypothalamus and the brain stem. The brain stem (especially the pons and medulla) also plays a special role in REM sleep it sends signals to relax muscles essential for body posture and limb movements, so that we don&rsquot act out our dreams.
The thalamus acts as a relay for information from the senses to the cerebral cortex (the covering of the brain that interprets and processes information from short- to long-term memory). During most stages of sleep, the thalamus becomes quiet, letting you tune out the external world. But during REM sleep, the thalamus is active, sending the cortex images, sounds, and other sensations that fill our dreams.
The pineal gland, located within the brain&rsquos two hemispheres, receives signals from the SCN and increases production of the hormone melatonin, which helps put you to sleep once the lights go down. People who have lost their sight and cannot coordinate their natural wake-sleep cycle using natural light can stabilize their sleep patterns by taking small amounts of melatonin at the same time each day. Scientists believe that peaks and valleys of melatonin over time are important for matching the body&rsquos circadian rhythm to the external cycle of light and darkness.
The basal forebrain, near the front and bottom of the brain, also promotes sleep and wakefulness, while part of the midbrain acts as an arousal system. Release of adenosine (a chemical by-product of cellular energy consumption) from cells in the basal forebrain and probably other regions supports your sleep drive. Caffeine counteracts sleepiness by blocking the actions of adenosine.
The amygdala, an almond-shaped structure involved in processing emotions, becomes increasingly active during REM sleep.
The Geography of Thought
Each cerebral hemisphere can be divided into sections, or lobes, each of which specializes in different functions. To understand each lobe and its specialty we will take a tour of the cerebral hemispheres, starting with the two frontal lobes (3), which lie directly behind the forehead. When you plan a schedule, imagine the future, or use reasoned arguments, these two lobes do much of the work. One of the ways the frontal lobes seem to do these things is by acting as short-term storage sites, allowing one idea to be kept in mind while other ideas are considered. In the rearmost portion of each frontal lobe is a motor area (4), which helps control voluntary movement. A nearby place on the left frontal lobe called Broca&rsquos area (5) allows thoughts to be transformed into words.
When you enjoy a good meal&mdashthe taste, aroma, and texture of the food&mdashtwo sections behind the frontal lobes called the parietal lobes (6) are at work. The forward parts of these lobes, just behind the motor areas, are the primary sensory areas (7). These areas receive information about temperature, taste, touch, and movement from the rest of the body. Reading and arithmetic are also functions in the repertoire of each parietal lobe.
As you look at the words and pictures on this page, two areas at the back of the brain are at work. These lobes, called the occipital lobes (8), process images from the eyes and link that information with images stored in memory. Damage to the occipital lobes can cause blindness.
The last lobes on our tour of the cerebral hemispheres are the temporal lobes (9), which lie in front of the visual areas and nest under the parietal and frontal lobes. Whether you appreciate symphonies or rock music, your brain responds through the activity of these lobes. At the top of each temporal lobe is an area responsible for receiving information from the ears. The underside of each temporal lobe plays a crucial role in forming and retrieving memories, including those associated with music. Other parts of this lobe seem to integrate memories and sensations of taste, sound, sight, and touch.
Your Thoughts Activate Your Genes
You are speaking to your genes with every thought you have. The fast-growing field of epigenetics is proving that who you are is the product of the things that happen to you in your life, which change the way your genes operate. Genes are actually switched on or off depending on your life experiences, and your genes and lifestyle form a feedback loop. Your life doesn’t alter the genes you were born with. What changes is your genetic activity, meaning the hundreds of proteins, enzymes, and other chemicals that regulate your cells.
Only about five percent of gene mutations are thought to be the direct cause of health issues. That leaves 95 percent of genes linked to disorders acting as influencers, which can be influenced one way or another, depending on life factors. Of course, many of these are beyond your control, like childhood events, but some are entirely within your control, such as diet, exercise, stress management, and emotional states. The last two factors are directly dependant on your thoughts.
Your Biology Does Not Have to Be Your Destiny
Your biology doesn’t spell your destiny, and you aren’t controlled by your genetic makeup. Instead, your genetic activity is largely determined by your thoughts, attitudes, and perceptions. Epigenetics is proving that your perceptions and thoughts control your biology, which places you in the driver’s seat. By changing your thoughts, you can influence and shape your own genetic readout.
You have a choice in determining what input your genes receive. The more positive the input, the more positive the output of your genes. Epigenetics is allowing lifestyle choices to be directly traced to the genetic level and is proving the mind-body connection irrefutable. At the same time, research into epigenetics is also emphasizing how important positive mental self-care practices are because they directly impact our physical health.
Meditation and mindfulness put you in contact with the source of the mind-body system, giving your thoughts direct access to the beneficial genetic activity which also affects how well your cells function, via the genetic activity inside the cells.
How Does an Erection Occur?
You’ve been getting erections since puberty, but have you ever stopped to think about the reason why? Understanding the physiological process of getting an erection can help you look at ED in a whole new light.
What Makes a Penis Erect? 24
Your penis has two chambers inside it called the corpora cavernosa. These chambers extend from the head of your penis deep into the pelvis. The insides of these chambers are made of spongy tissue and have the ability to gain blood volume and grow in size.
When you’re at work, hitting the gym, or running errands, the arteries supplying blood to your penis are only partially open. This provides the blood flow needed to keep your tissue healthy. (Figure 1)
The magic happens when you become aroused. In response to physical or mental stimulation, your brain sends signals to trigger a hormonal response that allows those same arteries to open completely. (Figure 2)
Open arteries allow more blood to enter the corpora cavernosa. The blood enters faster than it can leave through the veins. The veins get compressed, trapping blood in your penis. This chain reaction lets you achieve and maintain an erection. (Figure 3)
When your brain stops sending signals that indicate sexual arousal, the hormonal response ends. Your arteries go back to their normal state and your penis returns to a flaccid state.
How Erectile Dysfunction Occurs 25
Erectile dysfunction means something is standing in the way of your body’s natural process of getting and sustaining an erection. There are many different causes of this but three of the most common are:
- Your brain isn’t sending the right signals to your penis. Neurological disorders such as multiple sclerosis (MS), Alzheimer’s disease, and Parkinson’s disease can lead to ED by disrupting your brain’s ability to signal sexual arousal to your reproductive system.
- The blood flow to your penis is inadequate. High blood pressure, heart disease, high cholesterol and diabetes can all affect blood flow to the penis, making erections difficult to achieve.
- Your erectile tissue is damaged. This can happen when a man has undergone radiation treatment for prostate or bladder cancer.
Do you have difficulty getting (or maintaining) an erection? Click Here to take our ED Quiz to learn if you may suffer from Erectile Dysfunction.
ED is more common than you might think, affecting approximately 30 million men in the US 6 . If you’re like the vast majority of guys, it’s not something that’s easy to talk about, but you’re definitely not alone in your struggle.
The first step in treating ED is identifying the cause of your difficulty getting or keeping an erection. Once a cause has been identified, you can get the help you need. Review our ED Treatments page to learn more about treatment options such as lifestyle changes, medication or a penile implant.
Shopping, Dopamine, and Anticipation
Let’s say that you’re the CEO of a large retail clothing brand. You have stores throughout the world, and you have a website. People buy shirts, pants, skirts, belts, and so on at your stores and at your site.
If you want people to enjoy the shopping process with your brand and to be excited about buying your products, what should you do?
Let’s say your answer is: “I’m going to make shopping in the stores the best shopping experience possible. We’ll have in-store events, models wearing the clothes in the stores, and exciting sales. We’ll stock the stores with all colors and sizes, so people can be sure that when they come in, we’ll have what they want. I know that we have the online stores too, but if I am going to spend time and energy on one or the other, I'll spend it making the in-store experience the best it can be.”
Excitement and anticipation
Robert Sapolsky is a neuroscientist who studies dopamine in the brain. He trained monkeys to know that when a light comes on that is a signal. The monkeys knew that if they pressed a button 10 times, after the signal (after the light comes on), then on the tenth button press, a food treat would appear.
Sapolsky measured the amount and timing of dopamine release in the monkeys’ brains during the cycle of signal—work (pressing the button)—reward (food treat). The monkeys received the treat as soon as they pressed the bar 10 times. Surprisingly, the dopamine release started as soon as the signal arrived, and ended at the end of the bar pressing.
Many people think that dopamine is released when the brain receives a reward, but dopamine is actually released in anticipation of a reward. It’s the dopamine that keeps the monkey pressing the bar until the treat arrives.
In a second experiment, the monkeys received the food treat only 50 percent of the time after they pressed the bar. What happened to the dopamine in that situation? Twice as much dopamine was released when there was only a 50/50 chance of getting the food treat.
It’s all about unpredictability
In the third and fourth experiments, Sapolsky gave the treat 25 percent of the time or 75 percent of the time. Interestingly, when the treat was given either 25 percent of the time or 75 percent of the time, the dopamine release was the same, and it was halfway between the 100 percent and 50 percent chance of getting a food treat.
Unpredictability increases anticipation
When the monkeys got the treat all the time, a fair amount of dopamine was released during the pressing phase. When getting the treat was unpredictable, the amount of dopamine went up. In the 25 and 75 percent situations, there was actually more predictability. If the monkey got a food treat 25 percent of the time, it meant that they mostly didn’t get one. If they got a food treat 75 percent of the time, it meant that they mostly got one. Getting the food treat 50 percent of the time was the least predictable situation.
What's this got to do with online shopping?
Ok, I realize that most of us are not monkeys. But our brains work a lot like monkeys. We react to anticipation and dopamine the same way. When you place an order for a product online, you don’t get the product right away. You have to wait. And in the waiting is anticipation.
In the report entitled "Digital Dopamine," Razorfish presented results from interviews and surveys of 1,680 shoppers from the US, UK, Brazil, and China in 2014. From the report: "Seventy-six percent of people in the US, 72 percent in the UK, 73 percent in Brazil, and 82 percent in China say they are more excited when their online purchases arrive in the mail than when they buy things in store.”
What really happens in the brain during a hallucination?
A person can experience visual hallucinations for many reasons, including consuming hallucinogenic substances or as a symptom of schizophrenia. But what are the brain mechanisms that explain hallucinations?
Share on Pinterest New research aims to reveal more about how hallucinations manifest in the brain.
The Diagnostic and Statistical Manual of Mental Disorders (DSM-5) defines hallucinations as “perception-like experiences that occur without an external stimulus,” and which “are vivid and clear, with the full force and impact of normal perceptions, [though] not under voluntary control.”
While we understand some of the circumstances that cause hallucinations — often in the context of substance misuse, mental health conditions, or neurological conditions — we are yet to find out the specifics of how these phenomena manifest in the brain.
Recently, a team of researchers from the University of Oregon in Eugene has strived to uncover more information about how hallucinations affect brain activity.
Their new study — conducted in mouse models — has revealed some surprises, which the investigators present in a paper that appears in the journal Cell Reports.
The researchers worked with mice that they injected with a substance called 4-iodo-2,5-dimethoxyphenylisopropylamine (DOI), a hallucinogenic drug that investigators often use in animal research.
Like other hallucinogenics, including LSD, DOI interacts with serotonin 2A receptors, which are involved in the serotonin reuptake process, though they may also play other, less well understood, roles in the brain. Once they gave the mice this drug, the researchers showed them several on-screen images and used various specialized methods to record neural (brain cell) activity in these rodents.
The team found that contrary to what they had expected, the mice experienced reduced signaling between neurons in the visual cortex — the brain region largely responsible for interpreting visual information. The timing of the neurons’ firing patterns also changed.
“You might expect visual hallucinations would result from neurons in the brain firing like crazy, or by mismatched signals,” notes senior author Cris Niell, who is an associate professor at the University of Oregon.
“We were surprised to find that a hallucinogenic drug instead led to a reduction of activity in the visual cortex,” Niell adds. However, he continues, “[i]n the context of visual processing, […] it made sense.”
The researchers also saw that the visual signals sent to the visual cortex were similar to signals sent in the absence of the drug, meaning that the brain still received the same visual information — yet was unable to process it correctly.
“ Understanding what’s happening in the world is a balance of taking in information and your interpretation of that information. If you’re putting less weight on what’s going on around you but then overinterpreting it, that could lead to hallucinations.”
The team admits that studying hallucinations in mouse models is not ideal, since, of course, the animals cannot communicate their experience. However, the researchers note that the same types of drugs that cause hallucinations in humans also cause visible movement and behavioral changes in mice.
This, the investigators explain, reasonably suggests that the same drugs alter brain activity in both animals and people. However, future studies should pay closer attention to the animals’ reactions to visual stimuli in the presence versus the absence of drugs.
“I don’t feel like we’ve necessarily found the smoking gun for the entire underlying cause of hallucinations, but this is likely to be a piece of it,” Niell says.
“The data we’ve collected will provide a foundation for additional studies going forward. In particular, we plan to use genetic manipulation to study particular parts of this circuit in more detail,” the senior researcher adds.
And since previous research has suggested that serotonin 2A receptors — which the researchers also targeted in this study — are involved in schizophrenia, Niell and team would also like to find out whether their present findings may provide new perspectives regarding the treatment of this and other mental health conditions.
When liver disease affects the brain
Valérie McLin, Cristina Cudalbu and Olivier Braissant. Credit: EPFL, Alain Herzog
Scientists have demonstrated how chronic liver diseases cause molecular changes in the brain. They carried out their research using the 9.4 Tesla high-magnetic-field MRI machine at the Center for Biomedical Imaging (CIBM) at EPFL.
The liver plays a vital role as a filter in the human body. But what happens when it malfunctions? A physicist from EPFL, a clinician from the University of Geneva (UNIGE) and the Geneva University Hospitals (HUG) and a biologist from the Vaud University Hospital Centre (CHUV) and the Universities of Lausanne (UNIL) teamed up to perform a detailed analysis of hepatic encephalopathy, a type of brain damage caused by chronic liver disease.
For the first time, the scientists observed how diseased mouse livers can cause molecular disturbances in the animals' brains within two weeks, before any physical symptoms appear. They also discovered the previously unknown role of two particular molecules in the process. Their findings, published in the Journal of Hepatology, suggest that brain scans could help detect liver-related brain damage in humans before their health visibly deteriorates.
The livers of adults suffering from a liver disease like cirrhosis no longer filter out numerous substances. The psychological, motor and neurocognitive disorders that may result, referred to as hepatic encephalopathy, present a wide range of symptoms, including coma. One substance known to play a role in hepatic encephalopathy is ammonium.
"Ammonium is produced when proteins break down," says Valérie McLin, a professor in the Department of Pediatrics, Gynecology and Obstetrics at UNIGE's Faculty of Medicine and HUG. "Some of the ammonium goes to the brain, where it is transformed into glutamine and used to produce neurotransmitters. The rest is filtered by the liver and excreted in urine. When the liver malfunctions, too much ammonium goes to the brain. The resulting rise in glutamine production can trigger cerebral edema and, in some cases, hepatic encephalopathy." That much is known, yet two key questions remained: Are any other molecules involved in hepatic encephalopathy? And how long does it take for a diseased liver to affect the brain?Four weeks after the onset of liver disease (bottom), astrocytic cells (red) in the brains of diseased rats show altered morphology with shortening and reduction in the number of their extensions (scale bar: 25 μm). Credit: Katarzyna Pierzchala et Dario Sessa
Impact much earlier than expected
In order to answer these questions, the researchers observed mice with chronic liver disease for eight weeks. "We monitored the animals individually," says Cristina Cudalbu, a research physicist who manages the 9.4 Tesla MRI machine at the CIBM at EPFL. "Every two weeks, we analyzed them through high-resolution spectroscopy by placing them in a 9.4 Tesla high-magnetic-field MRI machine. This allowed us to track the molecular changes in their brains very precisely from the very onset of the liver disease. And we made some important discoveries!"
The scientists observed molecular changes in the mouse brains within two weeks, before the mice presented any symptoms. "Based on earlier studies, we thought it would take about six weeks for the animal's health to start deteriorating," says Cudalbu.
External signs of the disease, such as jaundice, malnutrition and water in the stomach, appear between the fourth and eighth weeks. "It was at that point that we saw, in addition to the excess ammonium in the brain, a sudden drop in the level of two other molecules: vitamin C, an antioxidant, and creatine, a compound that, among other things, helps produce energy," says Olivier Braissant, a professor in the Clinical Chemistry Department at the CHUV and the Faculty of Biology and Medicine at UNIL. This is the first time that researchers have visibly demonstrated the role these two molecules play in the disease. "They come in later, after the level of ammonium increases in the blood," says Braissant.
Scanning the brain to detect liver disease?
These findings suggest that the neurological signs of chronic liver disease could be detected well before any symptoms appear by analyzing the brain through high-resolution spectroscopy. The researchers are also wondering whether doctors could prevent—or at least limit—liver-related brain damage in patients by prescribing supplements, or probiotics such as Vivomixx, to make up for the drop in creatine and vitamin C. "We're currently conducting similar observations in humans to see whether the brain damage is similar to that in mice," concludes McLin.
Bringing together the right skillset
Drs. Cudalbu, Braissant and McLin work at three different research institutions, and their paths crossed thanks to an entirely different research project being carried out by Cudalbu at the CIBM's EPFL site. "My work consists of developing new, higher-performance spectroscopy methods," she says. While looking specifically at a method using Nitrogen-15, she unintentionally triggered the symptoms of liver disease. "Since the concentration of Nitrogen-15 is too low to detect in healthy mice, I injected them with ammonium chloride. And that worked in terms of spectroscopy—I was able to obtain a better resolution than we typically get with conventional methods. But the problem was the mice now had too much ammonium in their bodies. So I contacted Olivier Braissant, who is a specialist in this area, and Valérie McLin, who was working on clinical cases in humans," says Cudalbu. Her development work could therefore be applied in biomedical research on hepatic encephalopathy.
At EPFL, the CIBM has powerful magnets that can create high-resolution magnetic fields reaching not just 9.4 Tesla but also 14 Tesla—in 2007 the CIBM became the world's first lab to achieve such a high magnetism. The maximum level currently used for clinical medical imaging is 7 Tesla. "The higher the magnetic field, the better the resolution of MRI scans," says Cudalbu. "With these new methods we hope to be able to detect metabolic changes in patients at an early stage and with a high level of precision." The methods being developed at the CIBM will help doctors deliver early diagnoses and provide longitudinal, life-long care. This represents a major step forward for personalized medicine.
What is the reward system and what does it do?
In the 1950s, James Olds and Peter Milner implanted electrodes in the brains of rats and allowed the animals to press a lever to receive a mild burst of electrical stimulation to their brains. Olds and Milner discovered that there were certain areas of the brain that rats would repeatedly press the lever to receive stimulation to. They found a region known as the septal area, which lies just below the front end of the corpus callosum, to be the most sensitive. One of the rats in their experiment pressed a lever 7500 times in 12 hours to receive electrical stimulation here.
Watch this 2-Minute Neuroscience video to learn more about the reward system.
Olds and Milner's experiments were significant because they appeared to verify the existence of brain structures that are devoted to mediating rewarding experiences. For, if the rats were lever-pressing repeatedly to receive stimulation to these areas, it suggested they were enjoying the experience. Subsequent studies attempted to more thoroughly map out these "reward areas," and it was discovered that some of the most sensitive areas are situated along the medial forebrain bundle. The medial forebrain bundle is a large collection of nerve fibers that travels between the VTA and the lateral hypothalamus, making many other connections along the way. Some areas of the medial forebrain bundle were found to be so sensitive that rats would choose receiving stimulation to them over food or sex.
Eventually it was recognized that dopamine neurons are activated during this type of rewarding brain stimulation, and researchers found that they could cause rats to stop lever pressing by administering a dopamine antagonist (a drug that blocks the effects of dopamine). In other words, without the activity of dopamine the rats were less likely to find brain stimulation reinforcing, and so they stopped pressing the lever altogether. Other evidence, such as the discovery that dopamine antagonists seemed to reduce the rewarding qualities of drugs like amphetamines, further supported the importance of dopamine's role in reward.
Based on brain stimulation experiments and the increasingly recognized importance of dopamine in reward, attention began to turn toward major dopamine pathways as playing an important part in mediating rewarding experiences. The medial forebrain bundle connects the dopamine-rich VTA with the nucleus accumbens and is considered part of the mesolimbic dopamine pathway. It eventually became recognized that, when we use an addictive drug or experience something otherwise rewarding, dopamine neurons in the VTA are activated. These neurons project to the nucleus accumbens via the mesolimbic dopamine pathway, and their activation causes dopamine levels in the nucleus accumbens to rise. Furthermore, disrupting this pathway in rodents that had become addicted to pressing a lever for brain stimulation or a drug reward caused them to stop lever-pressing, suggesting these areas are crucially important to the occurrence of addictive behavior.
As the mesolimbic dopamine pathway is activated whenever we use an addictive drug, it has come to be considered the primary pathway of the reward system. However, dopaminergic projections from the VTA travel to the frontal cortex as well they comprise the mesocortical dopamine pathway. These fibers are also thought to be involved in reward and motivation, although their contribution to rewarding experiences is less clear than that of the mesolimbic pathway.
It's important to note that since the earliest research on the reward system our perspective on dopamine's role in reward has changed slightly. At one time dopamine was considered to be the neurotransmitter responsible for causing the experience of pleasure, but it is now thought to be involved with aspects of reward other than the direct experience of enjoyment. While the details are still being worked out, some have suggested dopamine is involved in encoding memories about a reward (e.g. how to get it, where it was obtained) and attributing importance to environmental stimuli that are associated with the reward.
While the reward system is implicated in pleasurable and potentially addictive behaviors, the substrates of pleasure are not confined to the structures mentioned above and dopamine is not the only neurotransmitter involved. The reward system refers to a group of structures that seem to be frequently involved in mediating rewarding experiences, but the actual network dedicated to creating the feelings we associate with these experiences is likely more complex.
References (in addition to linked text above):
Wise RA (1998). Drug-activation of brain reward pathways. Drug and alcohol dependence, 51(1-2): 13-22.
Watch this 2-Minute Neuroscience video to learn more about the ventral tegmental area and this 2-Minute Neuroscience video to learn more about the nucleus accumbens.