Monday, July 2, 2012

Dopamine





What exactly is it and what does it do?



History

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

Functions in the brain


Dopamine has many functions in the brain, including important roles in behavior and cognitionvoluntary movementmotivationpunishment andreward, inhibition of prolactin production (involved in lactation and sexual gratification), sleepmoodattentionworking memory, and learning. Dopaminergic neurons  are present chiefly in the ventral tegmental area (VTA) of themidbrain, the substantia nigra pars compacta, and the arcuate nucleus of the hypothalamus.



WOW!  Did you appreciate the list of brain functions that are influenced by dopamine?

behavior, cognition, voluntary movement, motivation, punishment & reward, lactation, sexual gratification, sleep, mood, attention, working memory and learning.

FOR PETE'S SAKE...WHAT ELSE IS LEFT?  Now you know why I need a cure.

For those of you who are interested in a bit more info on this topic just read on...or feel free to skip past this section.

Anatomy

Dopaminergic neurons form a neurotransmitter system which originates in substantia nigra pars compacta, ventral tegmental area (VTA), and hypothalamus. These project axons to large areas of the brain through four major pathways:
  • This innervation explains many of the effects of activating this dopamine system. For instance, the mesolimbic pathway connects the VTA and nucleus accumbens; both are central to the brain reward system.

Movement

Via the dopamine receptors, D1-5, dopamine reduces the influence of the indirect pathway, and increases the actions of the direct pathway within the basal ganglia. Insufficient dopamine biosynthesis in the dopaminergic neurons can cause Parkinson's disease, in which a person loses the ability to execute smooth, controlled movements.

Cognition and frontal cortex

In the frontal lobes, dopamine controls the flow of information from other areas of the brain. Dopamine disorders in this region of the brain can cause a decline in neurocognitive functions, especially memory, attention, and problem-solving. Reduced dopamine concentrations in the prefrontal cortex are thought to contribute to attention deficit disorder. It has been found that D1 receptors as well as D4 receptors are responsible for the cognitive-enhancing effects of dopamine. On the converse, however, anti-psychotic medications act as dopamine antagonists and are used in the treatment of positive symptoms in schizophrenia, although the older, so-called "typical" antipsychotics most commonly act on D2 receptors, while the atypical drugs also act on D1, D3 and D4 receptors.

Motivation and pleasure

Reinforcement

Dopamine is commonly associated with the pleasure system of the brain, providing feelings of enjoyment and reinforcement to motivate a person proactively to perform certain activities. Dopamine is released (particularly in areas such as the nucleus accumbens and prefrontal cortex) by naturally rewarding experiences such as food, sex, drugs, and neutral stimuli that become associated with them. Recent studies indicate that aggression may also stimulate the release of dopamine in this way. This theory is often discussed in terms of drugs such as cocaine, nicotine, and amphetamines, which directly or indirectly lead to an increase of dopamine in the mesolimbic reward pathway of the brain, and in relation to neurobiological theories of chemical addiction (not to be confused with psychological dependence), arguing that this dopamine pathway is pathologically altered in addicted persons.



Dopamine can be supplied as a medication that acts on the sympathetic nervous system, producing effects such as increased heart rate and blood pressure. However, because dopamine cannot cross the blood-brain barrier, dopamine given as a drug does not directly affect the central nervous system. To increase the amount of dopamine in the brains of patients with diseases such as Parkinson's diseaseand dopa-responsive dystonia, L-DOPA, which is the precursor of dopamine, can be given because it can cross the blood-brain barrier.


Levodopa is a dopamine precursor used in various forms to treat Parkinson's disease and dopa-responsive dystonia. It is typically co-administered with an inhibitor of peripheral decarboxylation (DDC, dopa decarboxylase), such as carbidopa or benserazide. Inhibitors of alternative metabolic route for dopamine by catechol-O-methyl transferase are also used. These include entacapone and tolcapone.


And then there is the next best thing to L-Dopa:


dopamine agonist is a compound that activates dopamine receptors in the absence of dopamine. Dopamine agonists activate signaling pathways through the dopamine receptor and trimeric G-proteins, ultimately leading to changes in gene transcription.


So, we have L-Dopa aka Sinemet and a whole host of dopamine agonists .... neither of which change my disease or cure me.  We take them to treat symptoms while we wait for better alternatives. 

Exercise, like cycling,  is just one of the Non-pharmaceutical ways to reduce symptoms.  If you would like to know about other such activities, visit my new web page 


And of course, personally I am not beyond voodoo or hocus pocus which is why I am sporting a silver dopamine molecule around my neck in the top photo...I will think of it as my good luck charm. 

I must admit that I have no scientific basis for "good luck charms" but at the end of the day, I say to myself

Why not?


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    1 comment:

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