dopamine activity

I googled science pick-up lines and I was not disappointed
  • You’re so hot, you denature my proteins. 
  • Do you have 11 protons? ‘Cause you’re Sodium fine!  
  • You make my anoxic sediments want to increase their redox potential. 
  • I’m more attracted to you than F is attracted to an electron. 
  • We fit together like the sticky ends of recombinant DNA. 
  • You’re hotter than a bunsen burner set to full power. 
  • If I were a neurotransmitter, I would be dopamine so I could activate your reward pathway. 
  • According to the second law of thermodynamics, you’re supposed to share your hotness with me. 
  • How about me and you go back to my place and form a covalent bond?
  • I wish I were Adenine because then I could get paired with U.
  • If you were C6, and I were H12, all we would need is the air we breathe to be sweeter than sugar.
  • I want to stick to u like glue-cose.
  • You must be the one for me, since my selectively permeable membrane let you through. 
Molecule of the Day: Methylphenidate

Methylphenidate (C14H19NO2), also known as Ritalin, is a white powder that is slightly soluble in water. It is commonly used to treat ADD, ADHD, and narcolepsy.

Methylphenidate inhibits dopamine and norepinephrine transporter proteins, thus preventing dopamine and norepinephrine in the synaptic cleft from being reuptaken into the presynaptic knob. The resultant higher concentration of these substances in the synapse causes the receptors on the postsynaptic knob to be stimulated at a greater frequency, thus achieving greater synaptic transmission. This produces a psychostimulant effect, allowing it to be used in the treatment of ADHD.

In small amounts, methylphenidate has also been shown to enhance memory and control, caused by the activation of dopamine and adrenergic receptors. However, in large doses, it can have the opposite effect.

It has few side effects, which include loss of appetite, nausea, and insomnia. However, like many strong dopamine reuptake inhibitors, it can result in dependence, and is often seen as a gateway drug. 

Methylphenidate is industrially synthesised through a multi-step pathway from 2-bromopyridine and benzyl cyanide.

Requested by @zenbra

Dopamine, Methamphetamines, and You

First things first – What does dopamine do anyway?
1) Dopamine is critical to the way the brain controls our movements. Not enough dopamine – can’t move, or control our movements well. Too much dopamine? Uncontrollable/subconscious movements (like picking, tapping, repetitive moments, jerking, twitching). Remember that the heart is a muscle, too, and too much dopamine will result in increased pulse and blood pressure.

2) Dopamine controls the flow of information from other areas of the brain, especially memory, attention and problem-solving tasks. This becomes important when we talk about amphetamine-induced psychosis that is common in meth abusers.

3) When dopamine is released it provides feelings of enjoyment and reinforcement to motivate us to do, or continue doing, certain activities. Dopamine is released by naturally rewarding experiences such as food and sex. This pre-programmed reward system makes sure that people do eat, do desire to procreate, and basically survive. Without enough dopamine, people feel the opposite of enjoyment and motivation – they feel fatigued and depressed, and experience a lack of drive and motivation.

How do brain chemicals like Dopamine work?
Brain chemicals, including Dopamine, are stored in cells, which you can think of like barrels full of that chemical. When something occurs like a good meal or great sex the brain pours out some dopamine from the dopamine barrels into an open space in the brain called a synapse. It floats around there. Think of the synapse like a street, and dopamine is like little cars driving around aimlessly on the street.

Across the street (not far) from the barrels of dopamine are Dopamine receptors. These receptors have little parking spaces on them that only fit Dopamine (or a substance VERY similar in chemical shape to Dopamine) into them, like a lock and key. As the Dopamine floats around in the synapse, it finds parking spaces at Dopamine receptors, and “plugs in” to the receptors. THIS is the point where we feel good, when the Dopamine is parked in a receptor’s parking space. There are, however, a limited number of receptors with “Dopamine only parking” available, and each receptor has a limited number of parking spaces. So some of the dopamine may not be able to find a place to park.

When all the parking spaces are taken, the remaining dopamine that didn’t find a place to park is normally recycled. There are “reuptake molecules” that do this – think of them like tow trucks. They find the extra dopamine, and tow it back to the barrels of Dopamine so that it can be re-used the next time. After some time has passed, the receptors release the Dopamine that was parked in their parking spaces, and the tow trucks take those Dopamine molecules back to the barrel too.

The brain has a safety-check system that will destroy any excess Dopamine that isn’t in a parking space, and didn’t get picked up by the tow truck. There are special chemicals in our brains that will break down this extra dopamine. Think of this like the toxic waste crew coming in and sweeping up the street.

As a last resort, after repeated long-term over-stimulation, the brain will shut down Dopamine receptors so that nothing can park there ever again. Think of this like the demolition team coming in and permanently barricading off the driveways.

This is your brain on Meth!
So now that we have a basic understanding of how things work normally, I’ll try to explain how things work when meth is ingested.

When someone eats, snorts, injects, or otherwise gets meth into their system, meth stimulates those barrels of Dopamine to pour out Dopamine. Meth continues to tell the cells to pour out dopamine until the body can break down the meth, which is typically 12 hours or so.

So Dopamine is poured out into the synapse (street) and finds parking spaces at dopamine receptors and makes the user feel high.

But meth is a tricky little chemical. It is shaped closely enough to Dopamine that the tow trucks get confused, and pick up meth thinking that it is dopamine. So the tow trucks are busy driving around hijacked by meth molecules leaving the extra Dopamine molecules floating around in the street (synapse). Well… that means the toxic waste crew comes in and destroys that dopamine that did not get recycled. So for the 12 hours or so it takes for the body to break down the meth, it is also spending that time destroying dopamine.

As long as the user keeps ingesting more meth, this process continues until there is not enough dopamine left to feel high from. When the user finally stops using, and the brain breaks down the meth molecules, the recycle trucks try to salvage what dopamine there is left, while the user crashes.

The end result of a “run” or “binge” on meth is a marked decrease in the amount of dopamine left in the brain. This leaves the user feeling exhausted, hungry, depressed, possibly suicidal and definitely unmotivated. They are literally suffering from a brain chemical imbalance. Self-inflicted mental illness.

How can the brain ever be normal again?
Well, luckily, the human body is pretty resilient. We do have the ability to make replacement dopamine. However, the body was not designed to need to do this in large quantities or in quick supplies. So we don’t have a mass-production plant making dopamine. It’s a 3 to 4 step process, too.

The process: Phenylalanine –> Tyrosine –>L-dopa –> Dopamine

Phenylalanine is the first “pre-cursor”. It can be found in the following foods: soybean protein, frozen tofu, dried and salted cod, shellfish, lean meat, organ meat, skin-free chicken, cheese, milk, eggs, many seeds (watermelon, fenugreek, roasted soybean nuts), and chocolate. Equal artificial sweetener also contains Phenylalanine. The body can turn Phenylalanine into Tyrosine.

Tyrosine can also be found in food. This would eliminate the need for the body to synthesize it from Phenylalanine. One step closer to dopamine! Meat, dairy, eggs as well as almonds, avocados and bananas are good sources of Tyrosine.

From there, the body will convert Tyrosine into L-Dopa, and then on to Dopamine (and other neurotransmitters like norepinephrine).

So… to replace dopamine destroyed while high on meth, the recovering user must eat sources of Phenylalanine or Tyrosine.

To aid the body in making Dopamine, the person can use what dopamine they DO have left as often as possible. This tells the body that they need more of it. While you sleep, you use very little dopamine. Exercising, even just a walk around the block will use dopamine (remember, it controls movement). So setting a reasonable sleep schedule, and trying to get some exercise will help speed up recovery from Self-inflicted Dopamine Destruction (aka meth addiction)!

Be patient – remember, we weren’t designed to waste dopamine, we were supposed to be recycling it. The process of replenishing dopamine takes months. Studies show that recovering meth addicts who have abstained from meth use have about 80% of normal dopamine levels after 18 months of abstinence. This WILL be a long battle. It CAN be won.

What about the receptors that were destroyed?
Well, good news again. Even though those receptors can never heal or recover, the brain is able to use existing receptors and find new pathways to accomplish the same results. Some receptors will even get a home equity loan and build on extra parking spaces!

Are there any medicines that can help?
A doctor should always be consulted and included on any medication treatment for a recovering user. Many recovering addicts have found Wellbutrin (Bupropion) to be helpful after a few months of clean time. What Wellbutrin does is block some (not all) of the tow trucks for a little while so that the dopamine the person has left can be more effective. It does not, however, stimulate the barrels to pour out dopamine. The person has to have enough dopamine in their brain before Wellbutrin can help.

anonymous asked:

Namjoonnie why do you keep listening to depressing songs ??

Well it’s actually quite interesting, you see.

Over the past few years, research has been made into why people listen to sad songs when they themselves are in a bad mood, place or situation and what it basically comes down to is that there’s two ways of looking at it, the psychological or the chemical.

The psychological version also splits into two options;
(1) is the notion in which one person’s mood lifts up simply from the knowledge that there are other(s) that have it worst than him.
(2) is the way sad music makes you feel validated, like you’re not wrong for feeling like you do.

The chemical and neuroscience way of looking at it is also a bit split to different opinions; 
It’s a known fact that music activates our dopamine, which is essentially the same neurotransmitter we release during sex, when we eat or when using drugs, so basically what gives you pleasure. 

So then maybe it’s a combination of dopamine and the psychological way our mid works.

It’s also been proven by science and research that most if not all creative individuals suffer from some level of depression and that that in itself fuels the  individual in creating even more. t’s like a sad balance where the negativity helps you reach new potentials.

Dopamine is the ultimate feminist chemical in the female brain. When a woman’s dopamine system is optimally activated – as it is in the anticipation of great sex, an effect heightened by a woman’s knowing what turns her on, letting herself think about it, and letting herself go get it – it strengthens her sense of focus and motivation levels, and energizes her in setting goals.
—  Naomi Wolf, “Vagina”
Researchers Shed Light on How Neurons Exchange Neurotransmitters

For more than a century, neuroscientists have known that nerve cells talk to one another across the small gaps between them, a process known as synaptic transmission (synapses are the connections between neurons). Information is carried from one cell to the other by neurotransmitters such as glutamate, dopamine, and serotonin, which activate receptors on the receiving neuron to convey excitatory or inhibitory messages.

But beyond this basic outline, the details of how this crucial aspect of brain function occurs have remained elusive. Now, new research by scientists at the University of Maryland School of Medicine (UM SOM) has for the first time elucidated details about the architecture of this process. The paper was published in the journal Nature.

Synapses are very complicated molecular machines. They are also tiny: only a few millionths of an inch across. They have to be incredibly small, since we need a lot of them; the brain has around 100 trillion of them, and each is individually and precisely tuned to convey stronger or weaker signals between cells.

To visualize features on this sub-microscopic scale, the researchers turned to an innovative technology known as single-molecule imaging, which can locate and track the movement of individual protein molecules within the confines of a single synapse, even in living cells. Using this approach, the scientists identified an unexpected and precise pattern in the process of neurotransmission. The researchers looked at cultured rat synapses, which in terms of overall structure are very similar to human synapses.

(Image caption: Synapses visualized in live neurons. The overall structure of one cell in a dense network of interconnected neurons is visible from expression of a red and green fluorescent protein that fills that cell entirely)

“We are seeing things that have never been seen before. This is a totally new area of investigation,” said Thomas Blanpied, PhD, Associate Professor in the Department of Physiology, and leader of the group that performed the work. “For many years, we’ve had a list of the many types of molecules that are found at synapses, but that didn’t get us very far in understanding how these molecules fit together, or how the process really works structurally. Now by using single-molecule imaging to map where many of the key proteins are, we have finally been able to reveal the core architectural structure of the synapse.”

In the paper, Blanpied describes an unexpected aspect to this architecture that may explain why synapses are so efficient, but also susceptible to disruption during disease: at each synapse, key proteins are organized very precisely across the gap between cells. “The neurons do a better job than we ever imagined of positioning the release of neurotransmitter molecules near their receptors,” Blanpied says. “The proteins in the two different neurons are aligned with incredible precision, almost forming a column stretching between the two cells.” This proximity optimizes the power of the transmission, and also suggests new ways that this transmission can be modified.

Blanpied’s lab has created a video representation of the process.

Understanding this architecture will help clarify how communication within the brain works, or, in the case of psychiatric or neurological disease, how it fails to work. Blanpied is also focusing on the activity of “adhesion molecules,” which stretch from one cell to the other and may be important pieces of the “nano-column.” He suspects that if adhesion molecules are not placed correctly at the synapse, synapse architecture will be disrupted, and neurotransmitters won’t be able to do their jobs. Blanpied hypothesizes that in at least some disorders, the issue may be that even though the brain has the right amount of neurotransmitter, the synapses don’t transmit these molecules efficiently.

Blanpied says that this improved comprehension of synaptic architecture could lead to a better understanding of brain diseases such as depression, schizophrenia and Alzheimer’s disease, and perhaps suggest new ideas for treatments.

Blanpied and his colleagues will next explore whether the synaptic architecture changes in certain disorders: they will begin by looking at a synapses in a mouse model of the pathology in schizophrenia.

“The complexity of the human brain seems overwhelming. But Dr. Blanpied and his colleagues have taken an important step in helping us understand this system,” said UM SOM Dean E. Albert Reece MD, PhD, MBA, who is also vice president for medical affairs at the University of Maryland and the John Z. and Akiko K. Bowers Distinguished Professor. “This study is impressive scientifically, and it is just the first step of what I am sure will be a long series of important discoveries about the brain and its disorders.”

  • Sheldon : Amy, I think my hypothalamus is secreting serotonin.
  • Amy : Sheldon, if you wanna have sex again just say it, you don't need to use dirty neuroscience talk to seduce me.
  • Sheldon : If I were a neurotransmitter, I would be dopamine so I could activate your reward pathway.
  • Amy : Okay that's hot.