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Thread: Dopamine: Dopamine Pathways; Agonists and Antagonists

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    Default Dopamine: Dopamine Pathways; Agonists and Antagonists

    Dopamine


    Dopamine is a neurotransmitter which activates the dopaminergic pathways of the brain.

    Mesolimbic : Reward pathway - connects the midbrain to the nucleus accumbens; involved in motivation, preoccupation, initiative, drive ex. rewarding effects of euphoric drugs;
    Mesocortical; Connects dopamine producing cells in the midbrain to the frontal lobes.
    Nigrostriatal ; Parkinson syndrome; movement, reward related cognition
    Tuberoinfundibular: Prolactin release is tonically inhibited by dopamine
    Last edited by Petros Agapetos; 11-27-2018 at 03:45 AM.

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    Veteran Member Petros Agapetos's Avatar
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    What is dopamine?

    The Dopamine Activated Pathways of the Brain



    Dopamine is a neurotransmitter, which transmits neuronal messages from one neuron to the other; on the four dopaminergic pathways of the brain. Dopamine is used by the brain to activate its dopaminergic pathways: the Mesolimbic, Mesocortical, Nigrostriatal, and Tuberoinfundibular pathways.

    Dopamine helps with reinforcement — motivating an animal to do something again and again. Reward and reinforcement help us learn where to find important things such as food or water, so that we can go back for more. Dopamine affects mood. Things that are rewarding tend to make us feel good. Lowering dopamine can make animals lose pleasure in activities like eating and drinking. This joyless state is called anhedonia.

    Because of its roles in reward and reinforcement, dopamine also helps animals focus on things. Anything that’s rewarding, after all, is usually well worth our attention.

    But dopamine has a more sinister side. Drugs such as cocaine, nicotine and heroin cause huge boosts in dopamine. The “high” people feel when they use drugs comes partly from that dopamine spike. And that prompts people to seek out those drugs again and again — even though they are harmful. Indeed, the brain “reward” associated with that high can lead to drug abuse and eventually to addiction.

    The dopamine pathways and norepinephrine pathways which project to the prefrontal cortex and striatum are directly responsible for modulating executive function (cognitive control of behavior), motivation, reward perception, and motor function; these pathways are known to play a central role in the pathophysiology of ADHD.

    The release of dopamine from the mesolimbic pathway into the nucleus accumbens regulates incentive salience (i.e., motivation and desire for rewarding stimuli) and facilitates reinforcement and reward-related motor function learning; it may also play a role in the subjective perception of pleasure. The dysregulation of the mesolimbic pathway and its output neurons in the nucleus accumbens plays a significant role in the development and maintenance of an addiction.

    Last edited by Petros Agapetos; 11-27-2018 at 03:54 AM.

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    Default The Mesolimbic Pathway

    The mesolimbic pathway regulates incentive salience, motivation, reinforcement learning, and fear, among other cognitive processes. The mesolimbic pathway is involved in motivation cognition.

    Depletion of dopamine in this pathway, or lesions at its site of origin, decrease the extent to which an animal is willing to go to obtain a reward (e.g., the number of lever presses for nicotine or time searching for food).

    Dopaminergic drugs are also able to increase the extent an animal is willing to go to get a reward, and the firing rate of neurons in the mesolimbic pathway increases during anticipation of reward. Mesolimbic dopamine release was once thought to be the primary mediator of pleasure, but is now believed to have only a minor role in pleasure perception.

    Clinical significance
    The mesolimbic pathway and a specific set of the pathway's output neurons (i.e., D1-type medium spiny neurons within the nucleus accumbens) play a central role in the neurobiology of addiction. It is also implicated in schizophrenia and depression. Addiction, schizophrenia, and depression all involve distinct structural changes within the mesolimbic pathway.

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    Agonists of dopamine receptor activate the receptor.

    The following are dopamine receptor agonists:

    Dopamine
    Pramipexole
    Ropinirole
    Bromocriptine


    Antagonists of the dopamine receptor block the receptor and (do not activate it, intrinsic activity = 0%)

    The following are dopamine receptor antagonists:

    Risperidone
    Haloperidol
    Chlorpromazine


    Partial Agonists of the dopamine receptor partially activate the receptor (with intrinsic activity between 0% and 100%) compared to a full agonist (which activates the receptor with 100% intrinsic activity)

    The following are dopamine receptor partial agonists:
    Aripriprazole
    Brexiprazole
    Cariprazine


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    Default Dopamineric Drugs - Psychostimulants

    Cocaine is a dopamine reuptake inhhibitor, which increases dopaminergic transmission rapidly , creating phasic events (dopmamine surges).

    Methamphetamine is a trace amine associated receptor agonists; TAAR 1 agonist, which releases dopamine, norepinephrine, and serotonin.

    Welbutrin is a dopamine and norepinephrine reuptake inhibiting antidepressant.

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    Location of D2 Receptors in the Human Brain
    The different sub-types of D2 receptor possess broad and varied anatomical distribution patterns in the brain and periphery. D2 are highly expressed in the caudate, putamen (basal ganglia), nucleus accumbens, ventral tegmental area and the substantia nigra and in lower concentrations in the septal region, amygdala, hippocampus, thalamus, cerebellum and cerebral cortex. Specifically in the cerebellum the highest concentrations are in lobules IX and X.

    D3 receptors have a more limited pattern of distribution and favor limbic expression such as the nucleus accumbens. Lower levels are detectable in the substantia nigra, ventral tegmental area, septal region, thalamus, cerebellum and cerebral cortex.

    D4 has the lowest level of expression in the brain. It is found in moderate levels in the hippocampus, substantia nigra, nucleus accumbens, ventral tegmenta area, amygdala and frontal cerebral cortex.

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    Pathophysiology
    Dopamine receptors are target of action for drugs used to treat schizophrenia and Parkinson’s disease in addition to other disorders such as substance abuse, depression, Tourette’s syndrome and attention deficit hyperactivity disorder (ADHD).

    Schizophrenia
    Schizophrenia is a disabling psychiatric disorder characterized by a myriad of positive, negative and cognitive symptoms that can be attributable to an imbalance between dopaminergic pathways that signal D2 and D1 receptors.

    According to the classical theory, the positive symptoms of schizophrenia are attributable to hyperactivity of dopamine at D2 receptors in the mesolimbic pathway. This occurs in different stages including changes in dopamine synthesis, dopamine release, as well as the dopamine D2 receptors. Advances in neurochemical imaging studies have demonstrated that the presynaptic striatial dopamine availability is increased. Following this it has been observed that in schizophrenia the release of dopamine from the striatial synapse is also increased, leading to an increase in the baseline occupancy of D2 receptors by dopamine.

    At the receptor level, an increase in striatial D2 and D3 receptor density in schizophrenic patients has been described. Alongside this, a higher sensitivity of existing postsynaptic dopamine D2 receptors and an increase in the proportion of dopamine D2 receptors that are in a high affinity state has been recorded.

    Hypothetically, the negative and cognitive symptoms associated with schizophrenia are attributable to hypo stimulation of D1 receptors.

    Parkinson’s disease
    Parkinson’s disease (PD) is an extrapyramidal motor disorder characterized by dopaminergic neuronal degeneration in the substantia nigra. Most of the dopaminergic projections are found in the striatum, degeneration of the cells tends to follow a pattern with the highest degree of dopaminergic depletion being seen in the dorso-lateral putamen. There is very little change in the dopaminergic neurons in the mesolimbic and mesocortical systems.

    It has been shown that D2 dopamine receptor density is altered in the basal ganglia in patients with PD. This is a complex change that is thought to be dependent upon the stage of the disease.

    When neurons die, the D2 receptors located on the nigrostriatial terminals are lost. However, further along the disease, the concentration of the D2 receptors in the striatal region increases, possibly due to an up regulation of postsynaptic D2 receptors. In addition, the coupling of D2 receptors to Gαi may be enhanced and the remaining D2 receptors are super sensitized.

    The loss of D2 receptors means a reduction in inhibitory control over corticostriatal transmission and enhanced glutamatergic activity.

    List of D2 agonists and antagonists
    This list serves as an example of drugs in clinical use that have the ability to bind to D2 receptors.

    Agonists:
    Bromocriptine
    Cabergoline
    Pramipexole
    Ropirinole
    Apomorphine

    Partial agonist
    Aripiprazole
    Brexpiprazole
    Cariprazine

    Antagonists
    Metoclopramide
    Antipsychotics
    First-generation antipsychotics
    Second-generation antipsychotics

    Source
    : https://psychopharmacologyinstitute..../d2-receptors/

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    d1 = receptor responsible for pleasure and euphoria
    d2 = wanting things, libido, and overactivation is the main culprit responsible for amphetamine psychosis
    d3 = movement, so involved in parkinsons and RLS
    d4 = I've read problems with the d4 receptors may be the one that has most to do with ADHD.

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