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    Dopamine: The Neurotransmitter With Many Faces
    By Andrea Kuszewski | March 8th 2010 12:23 PM | 5 comments | Print | E-mail | Track Comments
    About Andrea

    Andrea is a Behavior Therapist and Consultant for children on the autism spectrum, residing in the state of FL; her background is in cognitive

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    A new study that was just released on Sunday and published online in Nature Neuroscience has found that Ritalin, a popular medication to treat ADD/HD, helps improve learning not only by improving focus, but also by increasing plasticity of neural connections.

    The player involved in this new discovery is none other than that magical little neurotransmitter, one of my good friends, dopamine. As well as giving insight into to the nature of attention deficit disorders, providing new avenues to pursue for treatment, this study brings to light a few important facts about dopamine.



    First, note that the authors specify particular dopamine receptors that are acted upon by Ritalin, D1 and D2, which result in different changes depending on which receptor is activated.

    From the article:
    "... different dopamine receptor subtypes contribute to distinct aspects of learning performance, such that cue-reward learning depends upon dopamine D1 receptor–dependent mechanisms, and the suppression of task-irrelevant behavior depends upon D2 receptor–dependent mechanisms. Together, these findings indicate a specific synaptic mechanism whereby MPH may enhance associative learning through actions in the lateral amygdala."
    Here is a little more information regarding dopamine. There are (at least) 5 types of known dopamine receptors, D1, D2, D3, D4, and D5. There is some debate as to the existence of further distinct types, but these are the ones currently agreed upon. Each of these receptors has a different function in the brain, and are activated or deactivated in varied circumstances, and under different conditions.

    Dr Patricia Janak, co-senior author of the paper says,

    "We found that a dopamine receptor, known as the D2 receptor, controls
    the ability to stay focused on a task – the well-known benefit of Ritalin. But we also discovered that another dopamine receptor, D1, underlies learning efficiency."

    So what does this mean? For one thing, it shows us that there is more than just one benefit resulting from Ritalin or similar psychostimulants used to treat ADD/HD. It also gives us more insight as the the nature of the deficits in ADD/HD, and how it can be more directly and effectively treated.

    Additionally, it emphasizes the many different types of dopamine receptors and the varying functions of each. Dopamine is often in the headlines as a player in things such as addiction, reward/motivation, novelty-seeking, inattention, learning, sexual behaviors, etc, etc. The point is, dopamine is a multi-functional neurotransmitter, with a multitude of receptors in the brain, with a multitude of functions.

    To say that Person X has a [psychological disorder] because of a "dopamine deficit" or "too much dopamine" is far too vague of a conclusion. You can't look at one function of dopamine under a specific condition and use it as a blanket explanation for all things/syndromes/disorders dopamine-related. Given a person's other genetic traits, a deficit of dopamine may mean vastly different things. For one person, it may mean ADD, for another, an addiction. Dopamine is but one factor that contributes to disorders; a person's other genes determine what role dopamine plays in their behavior.

    The take-home point? Everyone's neurochemistry is different, and not all dopamine receptors are created equal.


    ***The name of the study referenced is, "Methylphenidate facilitates learning-induced amygdala plasticity" and can be found here.

    Comments

    This is indeed a very interesting development, Andrea. I imagine that this discovery regarding D1 and D2 receptors will help to develop more effective treatments, targeting specifically D1 and D2 receptors, for those with ADD/HD. Thanks for apprising us of the new findings. : )
    rychardemanne
    Although this is not my field (what is?) I have been looking at this recently in the context of nicotine addiction. From my understanding, the artificial dopamine high created by nicotine results in a decrease of background dopamine which, in turns, results in more receptors being created to sense this lower background signal. All of which means that the next nicotine hit lights up those rceptors like a christmas tree. All of which means that NRT (why is it called "nicotine replacement therapy" when it should be "alternative nicotine delivery system"?) doesn't work.

    Interesting that rather than having a one-to-one correspondence between neurotransmitter and receptor there is a multiplicity of both leading to many possible permutations. On the one hand, it looks efficient, yet liable to a myriad number of side effects!

    Thanks for the article.

    All things dopamine interest me. I suffer from Restless Legs Syndrome with Periodic Leg Movements in Sleep (RLS/PLMS) and without the medication pramipexole I would long since have gone mad from chronic severe sleep deprivation. This drug is a non-ergotamine dopamine receptor agonist. In this disorder, the dopamine receptors involved are on skeletal muscles; dopamine is essential for the relaxation of these muscle cells (cf. Parkinson's). People with RLS are not more likely to develop Parkinson's disease, but the same medication is helpful in that disease as well. Familial RLS results from a genetic mutation which causes an impairment of the transport mechanism which moves dopamine out of the brain cells which produce it. Low serum ferritin (the plasma storage form of iron) can exacerbate and even be responsible for RLS entirely in the absence of genetic factors. I look forward to the further elucidation of the roles of this neurotransmitter.

    Similar results to ritalin can be obtained by meditation and without the costs and potential negative side effects.

    This is the of the main reasons that self directed behaviour that leads to mental stability is recommended for disorders related to mental instability - or difficulties stabilising and focusing attention like ADHD.

    Research results from a recent study, led by UW-Madison scientist Antoine Lutz, suggest that attention stability is not a fixed capacity, and that it can be improved by directed mental training, such as meditation.

    The new study showed that three months of rigorous training in Vipassana meditation improved people's ability to stabilize attention.

    Lutz and colleagues investigated the moment-to-moment stability of attention by quantifying the trial-to-trial variability of both reaction time in response to attended deviant tones and consistency of brain responses, as measured by electroencephalography (EEG).

    "Attention deficit hyperactivity disorder (ADHD) patients typically show larger intra-individual variability in reaction time than controls during performance of sustained attention tasks. This variability is thought to reflect a more pronounced distractibility and poor attention for ADHD patients than controls. We hypothesized that meditation training would reduce this form of variability." (variability is a key diagnostic of a vata disorder in Ayurveda)

    "The finding that attention is a flexible skill opens up many possibilities," says Lutz. "For example, attention training is worth examining for disorders like attention deficit hyperactivity disorder."

    According to Dr Rick Mendius MD, from Wisebrain.org, in meditation concentration practices sustained high dopamine levels (presumably the D2 type) keep the gates of awareness closed to new and distracting information.

    CJE
    Your conclusion is that everyone's neurochemsitry is different? Christ on a cracker, my cat figured that out faster then you did.

    I think you meant "faster than." But thanks for the otherwise constructive comment.

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