HVORFOR ER NOEN MENNESKER MER KREATIVE ENN ANDRE? OG HVORDAN VIRKER EGENTLIG HJERNENE VÅRE? OM VI NÅ ER KREATIVE ELLER IKKE?
It seems that some people are more creative than others simply because their brains have somewhat different biochemistry and seems to be “wired” in a different way, allowing them to combine different areas of the brain at the same time when approaching and addressing a challenge or a problem.
Why it this? Let us try to find out.
Exactly what do we mean when we’re saying that a person is creative? And what is the essence of creativity? How do we recognise these folks?
We found a useful definition of creativity on this page.
Creativity is the act of turning new and imaginative ideas into reality. Creativity is characterised by the ability to perceive the world in new ways, to find hidden patterns, to make connections between seemingly unrelated phenomena, and to generate solutions.
Three additional facts which can give us clues are to study persons with the “illness” bipolar “disorder”. Sam, myself that is, has BP#1, and from the literature we get the following very interesting inputs: Folks with BP#1:
- Remember very well and can use the memories in all sorts of new ways.
- Have higher IQ than “healthy controls” (HC) [Sam: insulting 😊]
- Are generally known to be creative wrt arts, business and many other areas of life
As I am BP#1 myself I will use this competitive advantage to hopefully bring us some clues. And, dear Reader: I am neither manic nor depressed today! And I take my meds. So just take it easy.
In our age … technology … be extra careful …
Creativity begins with a foundation of knowledge, learning a discipline, and mastering a way of thinking. You can learn to be creative by experimenting, exploring, questioning assumptions, using imagination and synthesising information. Learning to be creative is akin to learning a sport. It requires practice to develop the right muscles and a supportive environment in which to flourish.
Studies by Clayton M. Christensen and his researchers uncovered The Innovators’ DNA: Your ability to generate innovative ideas is not merely a function of the mind, but also a function of five key behaviours that optimize your brain for discovery:
- Associating: drawing connections between questions, problems, or ideas from unrelated fields
- Questioning: posing queries that challenge common wisdom
- Observing: scrutinizing the behaviour of customers, suppliers, and competitors to identify new ways of doing things
- Networking: meeting people with different ideas and perspectives
- Experimenting: constructing interactive experiences and provoking unorthodox responses to see what insights emerge
Sir Richard Branson has a mantra that runs through the DNA of Virgin companies. The mantra is A-B-C-D. (Always Be Connecting the Dots). Creativity is a practice, and if you practice using these five discovery skills every day, you will develop your skills in creativity and innovation.
“Creativeness is the ability to see relationships where none exist.”
— Thomas Disch, author, 1974
Creative? Yes, please.
Lots of new knowledge is coming to us these days. See here, for example.
Numerous studies have mapped brain activity across a myriad of creative or artistic tasks from composing poetry to sketching an illustration. While no single “creative” part of the brain has been revealed, what is increasingly understood is that novel thinking generally engages a unique and broad configuration of brain regions that don’t typically work together.
In newly published research an international team of scientists examined 163 subjects under fMRI while participating in a classic divergent thinking test. The results found that three distinct brain networks were key to the most creative thinking. These are known as the default network (related to brainstorming and daydreaming), the executive control network (which activates when a person needs to focus), and the salience network (known for detecting environmental stimuli and switching between executive and default brain networks).
“It’s the synchrony between these systems that seems to be important for creativity,” says Beaty. “People who think more flexibly and come up with more creative ideas are better able to engage these networks that don’t typically work together and bring these systems online.”
Moving forward one of the next questions to be investigated by the researchers is finding out if these brain networks can be modified or improved. Can brain training or certain classes lead to greater brain network connectivity? And if connectivity between these networks can be “grown” would that boost a person’s general creative thinking abilities?
“Creativity is complex, and we’re only scratching the surface here, so there’s much more work that’s needed,” says Beaty.
A new study suggests a person’s creativity can be identified by examining how connected neural activity in the brain is.
Psychology and neuroscience researchers have started to identify thinking processes and brain regions involved with creativity. Recent evidence suggests that creativity involves a complex interplay between spontaneous and controlled thinking – the ability to both spontaneously brainstorm ideas and deliberately evaluate them to determine whether they’ll actually work.
Our findings indicate that the creative brain is “wired” differently and that creative people are better able to engage brain systems that don’t typically work together. Interestingly, the results are consistent with recent fMRI (functional magnetic resonance imaging) studies of professional artists, including jazz musicians improvising melodies, poets writing new lines of poetry and visual artists sketching ideas for a book cover.
Here are two different drawings of the brain areas.
As a bipolar I am always looking for excuses for what I think and do. But looking around the articles and posts which are on creativity, it is hard to avoid comments addressing people with bipolar, or BP#1’ers as we call them.
Asking Google, we got this answer:
Well, I wasn’t asking whether I am a genius or not. Modesty, you know …. But is it a fact and a reality that my brain as a bipolar is wired differently from “normal” people’s brains are? Healthy controls (HC)? The gene which codes for bipolar, I am told, does also code for a relatively high IQ (on group level, that is). And then creativity, it seems.
And here is some proper, it seems, academic research on the topic:
And maybe it is so that a bipolar person has more wires and/or connections between the various subsystems or neuro networks of the brain? Hmm … let us try to find out exactly that.
The human brain consists of neurons or nerve cells which transmit and process the information received from our senses. Many such nerve cells are arranged together in our brain to form a network of nerves. These nerves pass electrical impulses, ie the excitation from one neuron to the other.
Almost like a photon from light hitting an atom? Sam wonders. Obviously, neurology is also physics. Good!
Neurotransmitters are endogenous chemicals acting as signalling molecules that enable neurotransmission. They are a type of chemical messenger which transmits signals across a chemical synapse from one neuron (nerve cell) to another ‘target’ neuron, to a muscle cell, or to a gland cell. Neurotransmitters are released from synaptic vesicles in synapses into the synaptic cleft, where they are received by neurotransmitter receptors on the target cell.
Many neurotransmitters are synthesized from simple and plentiful precursors such as amino acids, which are readily available and only require a small number of biosynthetic steps for conversion. Neurotransmitters are essential to the function of complex neural systems. The exact number of unique neurotransmitters in humans is unknown, but more than 200 have been identified.
We need to spend some time on dopamine because its role in creativity as well as in BP#1, which may bring us creativity clues, is so important, as we shall see.
Dopamine (DA, a contraction of 3,4-dihydroxyphenethylamine) functions both as a hormone and a neurotransmitter and plays several important roles in the brain and body. It is an organic chemical of the catecholamine and phenethylamine families. It is an amine synthesized by removing a carboxyl group from a molecule of its precursor chemical L-DOPA, which is synthesized in the brain and kidneys. Dopamine is also synthesized in plants and most animals.
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 behaviour. The anticipation of most types of rewards increases the level of dopamine in the brain, and many addictive drugs increase dopamine release or block its reuptake into neurons following release. Other brain dopamine pathways are involved in motor control and in controlling the release of various hormones. These pathways and cell groups form a dopamine system which is neuro-modulatory.
In popular culture and media, dopamine is usually seen as the main chemical of pleasure, but the current opinion in pharmacology is that dopamine instead confers motivational salience; in other words, dopamine signals the perceived motivational prominence (i.e., the desirability or aversiveness [avoidance]) of an outcome, which in turn propels the organism’s behaviour toward or away from achieving that outcome.
Outside the central nervous system, dopamine functions primarily as a local paracrine messenger. In blood vessels, it inhibits norepinephrine release and acts as a vasodilator (at normal concentrations); in the kidneys, it increases sodium excretion and urine output; in the pancreas, it reduces insulin production; in the digestive system, it reduces gastrointestinal motility and protects intestinal mucosa; and in the immune system, it reduces the activity of lymphocytes. With the exception of the blood vessels, dopamine in each of these peripheral systems is synthesized locally and exerts its effects near the cells that release it.
Several important diseases of the nervous system are associated with dysfunctions of the dopamine system, and some of the key medications used to treat them work by altering the effects of dopamine. Parkinson’s disease, a degenerative condition causing tremor and motor impairment, is caused by a loss of dopamine-secreting neurons in an area of the midbrain called the substantia nigra. Its metabolic precursor L-DOPA can be manufactured; Levodopa, a pure form of L-DOPA, is the most widely used treatment for Parkinson’s.
There is evidence that schizophrenia involves altered levels of dopamine activity, and most antipsychotic drugs used to treat this are dopamine antagonists which reduce dopamine activity. Similar dopamine antagonist drugs are also some of the most effective anti-nausea agents. Restless legs syndrome and attention deficit hyperactivity disorder (ADHD) are associated with decreased dopamine activity.
Dopaminergic stimulants can be addictive in high doses, but some are used at lower doses to treat ADHD. Dopamine itself is available as a manufactured medication for intravenous injection: although it cannot reach the brain from the bloodstream, its peripheral effects make it useful in the treatment of heart failure or shock, especially in newborn babies.
So what is inside this artistic, beautiful organ? Besides the human eye – a biological masterpiece by God?
Although not trivial, we copy a page in order to get a limited grasp on the subject.
We can look at the brain in 3D here: https://www.visiblebody.com/learn/nervous/brain.
When we rotate it we see the four major regions of the brain: the cerebrum, diencephalon, cerebellum, and brainstem.
|Cerebrum||The cerebrum or telencephalon is a large part of the brain containing the cerebral cortex (of the two cerebral hemispheres), as well as several subcortical structures, including the hippocampus, basal ganglia, and olfactory bulb. In the human brain, the cerebrum is the uppermost region of the central nervous system. The olfactory bulb, responsible for the sense of smell, takes up a large area of the cerebrum in most vertebrates. However, in humans, this part of the brain is much smaller and lies underneath the frontal lobe. The olfactory sensory system is unique since the neurons in the olfactory bulb send their axons directly to the olfactory cortex, rather than to the thalamus first. Damage to the olfactory bulb results in a loss of olfaction (the sense of smell). Language and communication Speech and language are mainly attributed to the parts of the cerebral cortex. Motor portions of language are attributed to Broca’s area within the frontal lobe. Speech comprehension is attributed to Wernicke’s area, at the temporal-parietal lobe junction. These two regions are interconnected by a large white matter tract, the arcuate fasciculus. Damage to the Broca’s area results in expressive aphasia (non-fluent aphasia) while damage to Wernicke’s area results in receptive aphasia (also called fluent aphasia). Explicit or declarative (factual) memory formation is attributed to the hippocampus and associated regions of the medial temporal lobe. This association was originally described after a patient known as HM had both his left and right hippocampus surgically removed to treat chronic temporal lobe epilepsy. After surgery, HM had anterograde amnesia, or the inability to form new memories. Implicit or procedural memory, such as complex motor behaviours, involves the basal ganglia. Short-term or working memory involves association areas of the cortex, especially the dorsolateral prefrontal cortex, as well as the hippocampus.|
|Diencephalon||The diencephalon is the region of the embryonic vertebrate neural tube that gives rise to anterior forebrain structures including the thalamus, hypothalamus, posterior portion of the pituitary gland, and the pineal gland. The diencephalon encloses a cavity called the third ventricle. The thalamus serves as a relay centre for sensory and motor impulses between the spinal cord and medulla oblongata, and the cerebrum. It recognizes sensory impulses of heat, cold, pain, pressure etc. The floor of the third ventricle is called the hypothalamus. It has control centres for control of eye movement and hearing responses.|
|Cerebellum (little brain)||In humans, the cerebellum plays an important role in motor control. It may also be involved in some cognitive functions such as attention and language as well as emotional control such as regulating fear and pleasure responses, but its movement-related functions are the most solidly established. The human cerebellum does not initiate movement, but contributes to coordination, precision, and accurate timing: it receives input from sensory systems of the spinal cord and from other parts of the brain, and integrates these inputs to fine-tune motor activity. Cerebellar damage produces disorders in fine movement, equilibrium, posture, and motor learning in humans|
|Brainstem||The brainstem is a very small component of the brain, making up only around 2.6 percent of its total weight. It has the critical role of regulating cardiac and respiratory function, helping to control heart rate and breathing rate. It also provides the main motor and sensory nerve supply to the face and neck via the cranial nerves.|
Dette samt noen andre helt sentrale spørsmål knyttet til kreativitet skal vi forsøke å komme litt nærmere i lpa denne sektorrapporten som er lagt ut på www.mogstad.tech/sektorrapporter.
IQ er ikke det samme som kreativitet, og vi skal innledningsvis gjøre oss ferdig med det. Når vi en dag er ferdige med dokumentet håper forfatteren (Sam) at vi vet litt mer om hva det er som gjør enkelte mennesker mer kreative enn andre, samt hvilke grupper, hvis noen, dette er.
Og merk deg følgende fra boken «Myten om intelligensen»: Gjør du det bra på en IQ test viser resultatet akkurat det: Nemlig at du er god på å løse IQ tester. Høy IQ er praktisk mht rask tenkning, men er ikke nødvendigvis oppskriften på kloke avgjørelser, empati, relasjons-kompetanse eller et godt liv, generelt sett.
Lykke til – vi håper du får en hyggelig, nyttig og interessant stund med denne rapporten fra Sam, www.mogstad.tech og Mogstad AS.
Maybe we should look into artificial intelligence (AI) and artificial neural networks? Are we onto something when we wonder whether creativity is the ability to learn quickly in new situations? Let’s take a look.
Artificial neural networks like AlphaGo Zero are loosely inspired by the wiring of the neurons in the human brain and need far less human input. Their forte is learning, which they do by analysing huge amounts of input data or rules such as the rules of chess or Go. They have had notable success in recognizing faces and patterns in data and also power driverless cars. The big problem is that scientists don’t know as yet why they work as they do.
But it’s the art, literature and music that the two systems create that really points up the difference between them. Symbolic machines can create highly interesting work, having been fed enormous amounts of material and programmed to do so.
Far more exciting are artificial neural networks, which actually teach themselves and which can therefore be said to be more truly creative.
Symbolic AI produces art which that is recognizable to the human eye as art, but it’s art which that has been pre-programmed. There are no surprises. Harold Cohen’s Aaron AARON algorithm produces rather beautiful paintings using templates which that have been programmed into it. Similarly, Simon Colton at the college of Goldsmith’s College in the University of London programs The Painting Fool to create a likeness of a sitter in a particular style. But neither of these ever leaps beyond its program.
Artificial neural networks are far more experimental and unpredictable. The work springs from the machine itself without any human intervention. Alexander Mordvintsev set the ball rolling with his Deep Dream and its nightmare images spawned from convolutional neural networks (ConvNets) and that seem almost to spring from the machine’s unconscious. Then there’s Ian Goodfellow’s GAN (Generative Adversarial Network) with the machine acting as the judge of its own creations, and Ahmed Elgammal’s CAN (Creative Adversarial Network), which creates styles of art never seen before. All of these generate far more challenging and difficult works—the machine’s idea of art, not ours. Rather than being a tool, the machine participates in the creation.
To put it simply, artificial neural networks are built to learn while symbolic machines are built to reason from a corpus of fed-in, prior knowledge. Looking this up, so to speak. Maybe that is the difference between creative souls and their not-that-creative associates – the creatives learn quickly while the less creative are left to reason, ie use enormous amounts of input data in a rather slow brute force manner?
So where in the brain do we learn? We shall bring some excerpts from the excellent article “How the Brain Learns”. You can find it here: https://trainingindustry.com/articles/content-development/how-the-brain-learns/.
The brain acts as a dense network of fiber pathways consisting of approximately 100 billion (1011) neurons. The brain consists of three principle parts – stem, cerebellum and cerebrum – as shown below. Of the three, the cerebrum is most important in learning, since this is where higher-ordered functions like memory and reasoning occur. Each area of the cerebrum specializes in a function – sight, hearing, speech, touch, short-term memory, long-term memory, language and reasoning abilities are the most important for learning.
So how does learning happen? Through a network of neurons, sensory information is transmitted by synapses (see figure above) along the neural pathway and stored temporarily in short-term memory, a volatile region of the brain that acts like a receiving centre for the flood of sensory information we encounter in our daily lives.
Once processed in short-term memory, our brain’s neural pathways carry these memories to the structural core, where they are compared with existing memories and stored in our long-term memory, the vast repository of everything we have ever experienced in our lives. This process occurs in an instant, but it is not always perfect. In fact, as information races across billions of neurons’ axons, which transmit signals to the next neuron via synapse, some degradation is common. That’s why many of our memories are incomplete or include false portions that we make up to fill holes in the real memory.
Researchers found that when two neurons frequently interact, they form a bond that allows them to transmit more easily and accurately. This leads to more complete memories and easier recall. Conversely, when two neurons rarely interacted, the transmission was often incomplete, leading to either a faulty memory or no memory at all.
This research has important implications for learning, especially regarding how we acquire new knowledge, store it in memory and retrieve it when needed. When learning new things, memory and recall are strengthened by frequency and recency. The more we practice and rehearse something new and the more recently we have practiced, the easier it is for our brain to transmit these experiences efficiently and store them for ready access later. This process is called fluency.
Another recent study found that the structural core of the brain receives sensory information from different regions and then assembles bits of data into a complete picture that becomes a memory of an event. This memory is strengthened by multiple sensory inputs. For example, if we both see and hear something, we are more likely to remember it than if we only hear it.
If we experience an emotional reaction to something – fear, anger, laughter or love – that emotion becomes part of the memory and strengthens it dramatically. In recalling memories, subjects who had experienced an emotional reaction were far more likely to remember the event and with higher accuracy than those who simply witnessed an event without any emotional attachment. That explains why highly emotional events – birth, marriage, divorce and death – become unforgettable.
What does this neuroscience research suggest about learning? We need to ensure that learning engages all the senses and taps the emotional side of the brain, through methods like humour, storytelling, group activities and games. Emphasis on the rational and logical alone does not produce powerful memories.
A third recent discovery confirmed that the brain behaves selectively about how it processes experiences that enter through our five senses. The brain is programmed to pay special attention to any experience that is novel or unusual. It does this by making comparisons between the new information brought through the senses and existing information stored in our brain’s long-term memory. When the brain finds a match, it will quickly eliminate the new memory as redundant.
When new information contradicts what’s already stored in memory, however, our brains go into overdrive, working hard to explain the discrepancy. If the new information proves useful to us, it becomes a permanent memory that can be retrieved later. If this new information does not seem useful or if we do not trust its source, we are likely to forget it or even reject it altogether, preferring to stick with the information we already possess.
Since learning inherently requires acquisition of new information, our brains’ propensity to focus on the novel** and forget the redundant makes it a natural learning ally. In fact, our brains are hard wired to learn, from the moment we are born. Our native curiosity is driven by our brain’s inherent search for the unusual in our environment.
On the other hand, past memories can be an impediment to future learning that contradicts previous information. As we age and gain more experience, we tend to rely too much on our past knowledge. We may miss or even reject novel information that does not agree with previous memories. Recent brain research is unlocking many of the mysteries of learning. Learning professionals should stay abreast of these developments and derive learning methods based upon the way the brain learns naturally.
** Novel means new and not resembling something formerly known or used or not previously identified.
The table below summarizes the three recent research findings and their implications for training.
So – are bipolar people more creative because they learn better because (again) they are so full of feelings and emotions plus they are intense, extreme and “manic” with how they live and go about their lives?
When a learning comes with an intense emotion, it sticks better. Better use all our senses.
We read this page and learn something new about creativity: https://science.howstuffworks.com/life/inside-the-mind/human-brain/5-ways-your-brain-influences-your-emotions3.htm.
The brain is made up of many different parts that all work together to process the information it receives. The main part of the brain responsible for processing emotions, the limbic system, is sometimes called the “emotional brain”.
Part of the limbic system, called the amygdala, assesses the emotional value of stimuli. It’s the main part of the brain associated with fear reactions — including the “fight or flight” response. A person who has a seizure in the temporal lobe (the location of the amygdala) sometimes reports an intense feeling of fear or danger.
The part of the brain stretching from the ventral tegmental area in the middle of the brain to the nucleus accumbens at the front of the brain, for example, has a huge concentration of dopamine receptors that make you feel pleasure. The hypothalamus is in charge of regulating how you respond to emotions.
When excitement or fear causes your heart to beat faster, your blood pressure to rise and your breathing to quicken, it’s the hypothalamus doing its job. The hippocampus turns your short-term memory into long-term memory and also helps you retrieve stored memory. Your memories inform how you respond to the world around you, including what your emotional responses are.
Because different parts of the brain process different emotions in different ways, injury to any part of the brain can potentially change your moods and emotions.
As mentioned earlier, dopamine is a so-called messenger substance or neurotransmitter that conveys signals between neurons. It not only controls mental and emotional responses but also motor reactions. Dopamine is particularly known as being the “happy hormone.” It is responsible for our experiencing happiness.
Even so-called adrenaline rushes, such as those experienced when playing sport, are based on the same pattern. Adrenaline is a close relative of dopamine.
However, serious health problems can arise if too little or too much dopamine is being produced. If too few dopamine molecules are released, Parkinson’s disease can develop, while an excess can lead to mania, hallucinations and schizophrenia. [www.sciencedaily.com]
Aha … so dopamine excess is the reason for Sam’s “manic episodes” (I disagree, of course 😊). But is it too many dopamine molecules, too many Dx receptors (receptor density), or the “quality” of the receptors, call it receptor availability? We are soon to find out,
- Creativity is the ability to learn quickly. That requires good memory, which is stronger with emotions.
- BP#1’ers have an excess of dopamine receptors and/or neurotransmitters. That’s the core of mania.
- BP#1’ers have strong emotions and reward circuitry (dopamine process), probably a genetic thing, and remember as a consequence better: Strong emotions make memories ditto stronger
- BPS#1’ers are intense, probably due to plenty of dopamine = receptor availability.
Dopamine is a type of neurotransmitter. Your body makes it, and your nervous system uses it to send messages between nerve cells. That’s why it’s sometimes called a chemical messenger.
Dopamine plays a role in how we feel pleasure. It’s a big part of our unique human ability to think and plan. It helps us strive, focus, and find things interesting.
Your body spreads it along four major pathways in the brain. Like most other systems in the body, you don’t notice it (or maybe even know about it) until there’s a problem.
However, serious health problems can arise if too little or too much dopamine is being produced and/or processed in the receptors. If too few dopamine molecules are released and/or processed in the receptors, Parkinson’s disease can develop, while an excess can lead to mania, hallucinations and schizophrenia.
Cell to cell communication is critical for the survival of an organism. Cells can communicate through a process called signal transduction pathway. When sending a signal, different molecules, such as hormones, can bind to a receptor on or inside the cell membrane, leading to chemical reactions in the cell ultimately reaching the target. Cells use a second messenger to transmit these messages.
This article will be discussing the different types of receptors, focusing specifically on dopamine receptors, the different types of dopamine receptors, and what function each receptor has. The article will also go into different illnesses and medications that target these receptors.
The dopamine receptors affect many various functions, ranging from hypertension and hormonal regulation to voluntary movement and reward.
There are many different types of signalling receptors in the human body, with the majority being the G-protein coupled receptors (GPCRs). GPCRs have an intracellular C-terminus and an extracellular N-terminus. GPCRs are also known as the seven-pass transmembrane proteins; this is because the receptor consists of seven sequential helices that cross the transmembrane, allowing the receptor to correctly insert into the cell membrane and couple with the G protein. This coupling permits the receptor to modulate signalling cascades. The dopamine receptor is a type of G-protein coupled receptor. Dopamine receptors can also act through G-protein independent mechanisms such as ion channel interactions.
Dopamine is a monoamine catecholamine neurotransmitter and hormone. It binds to the dopamine receptor, and depending on the type of receptor, has many different functions. Dopamine receptors are mostly present in the central nervous system.
The dopamine receptors are located and encoded by different genes. D1 receptor encoding is by the gene, 5q31-q34. The D2 receptor is on chromosome 11, along with the D4 receptor, while the D3 receptor is located on the third chromosome. The D5 receptor is on the fourth chromosome.
Dopamine receptors play an essential role in daily life functions. This hormone and its receptors affect movement, emotions and the reward system in the brain.
Dopamine receptors are expressed in the central nervous system, specifically in the hippocampal dentate gyrus and subventricular zone. Dopamine receptors are also expressed in the periphery, more prominently in kidney and vasculature,
There are five types of dopamine receptors, which include D1, D2, D3, D4, and D5. Each receptor has a different function.
The function of each dopamine receptor:
D1: memory, attention, impulse control, regulation of renal function, locomotion
D2: locomotion, attention, sleep, memory, learning
D3: cognition, impulse control, attention, sleep
D4: cognition, impulse control, attention, sleep
D5: decision making, cognition, attention, renin secretion
The five different dopamine receptors can subdivide into two categories. D1 and D5 receptors group together, and D2, D3, D4 are together in a separate subgrouping.
D1 and D5 receptors couple to G stimulatory sites and activate adenylyl cyclase. The activation of adenylyl cyclase leads to the production of the second messenger cAMP, which leads to the production of protein kinase A (PKA) which leads to further transcription in the nucleus.
D2 through D4 receptors couple to G inhibitory sites, which inhibit adenylyl cyclase and activate K+ channels.
The D1 receptor is the most abundant out of the five in the central nervous system, followed by D2, then D3, D5 and least abundant is D4. D1 receptors help regulate the development of neurons when the dopamine hormone binds to it.
D1 and D5 receptors have high density in the striatum, nucleus accumbens, olfactory bulb, and substantia nigra. These receptors are essential in regulating the reward system, motor activity, memory, and learning [Sam comment and claim: essential for creativity].
D1 and D5 receptors, along with stimulating adenyl cyclase, also activate phospholipase C, which leads to the induction of intracellular calcium release and activation of protein kinase C. Protein kinase C is a calcium-dependent protein kinase. Calcium is also involved in modulating neurotransmitter release by exocytosis. D1 and D5 receptors are also involved in the kidney by inhibiting Na/K ATPase through PKA and PKC pathways. In the kidney, these receptors correlate with an increase in electrolyte excretion and renal vasodilation.
D2, D3, and D4 receptors are expressed mainly in the striatum, as well as the external globus pallidus, core of nucleus accumbens, hippocampus, amygdala, and cerebral cortex. These receptors also affect the postsynaptic receptor-medicated extrapyramidal activity. D2-D4 receptors are important in the signalling for the survival of human dopamine neurons and neuronal development.
Many different diseases involve increased or decreased dopamine leading to different effects. The two primary conditions discussed here along with the pharmacology targeting dopamine receptors are Parkinson disease and schizophrenia.
- A disease caused by decrease amount of dopamine in the substantia nigra (in the nigrostriatal pathway)
- Symptoms include resting tremor, bradykinesia, shuffling gait, postural instability
- Treatment for Parkinson disease includes medications that target to increase dopamine availability
- Bromocriptine is a D2 receptor agonist; other dopamine agonists include pramipexole and ropinirole
- Amantadine increases dopamine availability by increasing the release of dopamine and decreasing reuptake
- Carbidopa and levodopa are commonly used together; in the CNS levodopa is converted into dopamine to increase the amount of dopamine in the CNS and carbidopa inhibits DOPA decarboxylase, which blocks the peripheral conversion of levodopa to dopamine – this decreases the peripheral side effects of dopamine
- Other medications, such as selegiline and tolcapone inhibit the breakdown of dopamine, which increases the availability at the synapse
- Associated with an increase in dopaminergic activity
- Genetic and environmental risk factors affect the dopamine function
- Diagnosis includes greater than 6 months of at least 2 of the following: delusions, disorganized speech, hallucinations, disorganized behaviour, and negative symptoms (anhedonia, flat affect, etc.), and at least one of the symptoms needs to be hallucinations, delusions, or disorganized speech
- Treatment for schizophrenia includes medications that target to decrease dopamine availability, which includes atypical and typical antipsychotics
- Typical antipsychotics are also known as first-generation antipsychotics – these drugs block the D2 receptor
- High potency typical antipsychotics include haloperidol, trifluoperazine, and fluphenazine
- Low potency typical antipsychotics include chlorpromazine and thioridazine.
- The atypical antipsychotics have unique characteristics
- Most are D2 antagonists and they also affect other receptors, such as the serotonin and histamine receptors; aripiprazole is D2 partial agonist
- Atypical antipsychotics bind more loosely to the dopamine D2 receptor than the typical antipsychotics
We asked Google.
Converging findings from pharmacological and imaging studies support the hypothesis that a state of hyper-dopaminergia, specifically elevations in D2/3 receptor availability and a hyperactive reward processing network, underlies mania.
In bipolar depression imaging studies show increased dopamine transporter levels, but changes in other aspects of dopaminergic function are inconsistent.
Puzzlingly, pharmacological evidence shows that both dopamine agonists and antidopaminergics can improve bipolar depressive symptoms and perhaps actions at other receptors may reconcile these findings.
Tentatively, this evidence suggests a model where an elevation in striatal D2/3 receptor availability would lead to increased dopaminergic neurotransmission and mania, whilst increased striatal dopamine transporter (DAT) levels would lead to reduced dopaminergic function and depression.
Thus, it can be speculated that a failure of dopamine receptor and transporter homoeostasis might underlie the pathophysiology of this disorder. [Sam:] Bipolar disorder, that is. Or was it in order?
Interestingly, patients with psychotic mania showed an elevated density of D2/3 receptors as measured by N-[11C]-methylspiperone, when compared with healthy controls (HC) and non-psychotic mania patients, although, as this tracer has significant affinity for 5HT2 receptors as well, this finding requires replication with more selective tracers.
Moreover, no significant difference in the striatal** D2/3 density was noted in non-psychotic mania patients compared to HC. These studies also explored the relationship between manic symptoms (as assessed using Young’s Mania Rating Scale Score) and dopamine synthesis capacity and D2/3 density, finding no significant correlations between these variables in patients with mania. However, in one of these studies D2/3 density was directly correlated with psychosis scores on the present state examination. Taken together, these data suggest that psychotic symptoms in mania may be associated with dopaminergic abnormalities, although the same cannot be inferred in non-psychotic mania patients.
** Striatum: Part of the basal ganglia of the brain. The basal ganglia are interconnected masses of gray matter located in the interior regions of the cerebral hemispheres and in the upper part of the brainstem. The striatum is also called the striate body. It includes the caudate nucleus and the lentiform nucleus.
Our main findings for bipolar mania are that
- There is consistent pharmacological evidence, especially from treatment studies, to support the hypothesis that a state of hyperdopaminergia can lead to mania;
- Imaging studies support this hypothesis, with several studies reporting elevations in D2/3 receptor availability in psychotic mania and fMRI imaging evidence that identifies hyperactivity of the reward circuit in mania. Dopamine synthesis and receptor density appear to remain unchanged, at least in non-psychotic mania patients compared with HC.
While methamphetamine addiction has been associated with both impulsivity and striatal dopamine D2/D3 receptor deficits, human studies have not directly linked the latter two entities. We therefore compared methamphetamine-dependent and healthy control subjects using the Barratt Impulsiveness Scale (version 11, BIS-11) and positron emission tomography with [18F] fallypride to measure striatal dopamine D2/D3 receptor availability.
The methamphetamine-dependent subjects reported recent use of the drug 3.3 g per week, and a history of using methamphetamine, on average, for 12.5 years. They had higher scores than healthy control subjects on all BIS-11 impulsiveness subscales (p < 0.001). Volume-of-interest analysis found lower striatal D2/D3 receptor availability in methamphetamine-dependent than in healthy control subjects (p < 0.01) and a negative relationship between impulsiveness and striatal D2/D3 receptor availability in the caudate nucleus and nucleus accumbens that reached statistical significance in methamphetamine-dependent subjects.
Combining data from both groups, voxelwise analysis indicated that impulsiveness was related to D2/D3 receptor availability in left caudate nucleus and right lateral putamen/claustrum (p < 0.05, determined by threshold-free cluster enhancement). In separate group analyses, correlations involving the head and body of the caudate and the putamen of methamphetamine-dependent subjects and the lateral putamen/claustrum of control subjects were observed at a weaker threshold (p < 0.12 corrected). The findings suggest that low striatal D2/D3 receptor availability may mediate impulsive temperament and thereby influence addiction.
20.Conclusion – Learning and Creativity
Creativity is the ability to learn and act quickly. This requires good memory, which is stronger with emotions. The essence of creativity is to quickly combine stored knowledge with new sensor inputs, conclude, and take action.
Dopamine is an important neurotransmitter within the nervous system and plays several important roles in the brain and body. In popular culture and media, dopamine is usually seen as the main chemical of pleasure, but the current opinion in pharmacology is that dopamine instead confers motivational salience; in other words, dopamine signals the perceived motivational prominence (i.e., the desirability or aversiveness) of an outcome, which in turn propels the organism’s behaviour toward or away from achieving that outcome.
BP#1’ers have an excess of dopamine receptor availability. Receptor density and dopamine synthesis seem to be the same as for healthy controls (HC). This increased receptor availability seems to be the core of mania.
BP#1’ers have strong emotions and reward circuitry (dopamine process), probably a genetic thing, and remember as a consequence better: Strong emotions make memories collaterally stronger.
BP#1’ers are intense, probably due to plenty of dopamine = receptor availability and reward circuitry.
- Strong reward circuitry, motivation and exuberant feelings bring push, speed and lively and precise memories (which are stronger due to the associated feelings).
- High D1 – D5 dopamine receptor density keeps this system running at high intensity.
- Strong motivation and clear, strong memories bring new sensor data in fast combination with stored data and memories, giving associations which again breed ideas and fast learning.
Imaging studies support this hypothesis, with several studies reporting elevations in D2/3 receptor availability in psychotic mania and fMRI imaging evidence that identifies hyperactivity of the reward circuit in mania. Dopamine synthesis and receptor density appear to remain unchanged, at least in non-psychotic mania patients compared with healthy controls (HC). [Sam:] Did you say healthy, Sir? 😊
But new insights are emerging. Se eg here:
MIT biologists have now discovered a possible explanation for how lithium works. In a study of worms, the researchers identified a key protein that is inhibited by lithium, making the worms less active.
While these behavioral effects in worms can’t be translated directly to humans, the results suggest a possible mechanism for lithium’s effects on the brain, which the researchers believe is worth exploring further.
But who want to be less active? 😊
During WW#2 Prime Minister of England MR Winston Churchill (bipolar, by the way) met a female Member of Parliament (MP), and the following was said
- Mr Churchill, you are drunk!
- Yes I am. But you are ugly, Madam. And when I wake up tomorrow, I am sober, but you are still ugly.
Too much dopamine 😊 ?
Take a look at this book and read at least the first 1/3 or so.
Here is a very brief summary.
And again: Thank you very much indeed for reading this sector report from www mogstad.tech.