In Parkinsons Disease (PD) dopaminergic neurons of the substantia nigra degenerate leading to a dopamine deficiency. Dopamine (that is used in the acute treatment of cardiac failure) cannot be used directly for PD because does not pass the the blod-brain barrier. This is the reason why we use levodopa that passes the barrier and is then converted in dopamine directly in the nigrostriatal neurons.

I hope that this answer will help you.

Hi Rhiannon,

If you want to know more about it just check this paper:

http://www.sciencedirect.com/science/article/pii/S0896627311008890

It may help you to understand the circuit itself.

Hope it helps.

I'm not sure if you are curious beyond Parkinson's (I liked Jean-Marc's answer for that), but dopamine (and specific dopamine receptor agonists/antagonists) can be used to treat a variety of disorders.

Dopamine agonists (D1 and D5 receptors) have been used in treatment of spinal cord injury along with serotonergic agonists to induce stepping in spinalized mice: http://www.ncbi.nlm.nih.gov/pubmed/18480366

Dopamine agonists have also been used in the treatment of pain and restless legs syndrome:

http://www.ncbi.nlm.nih.gov/pubmed/21715702

http://www.ncbi.nlm.nih.gov/pubmed/20832967

Dopamine has cardiovascular effects, but I am not sure on its use clinically:

http://www.ncbi.nlm.nih.gov/pubmed/?term=Cardiovascular+and+renal+actions+of+dopamine%3A+potential+clinical+applications

Similarly, dopamine can be effective experimentally on diabetes, but again, I am not sure of its clinical use:

http://www.ncbi.nlm.nih.gov/pubmed/?term=Biochemical+mechanisms+responsible+for+the+attenuation+of+diabetic+and+obese+conditions+in+ob%2Fob+mice+treated+with+dopaminergic+agonists

There are lots of possible ways for dopamine to be used as a therapeutic agent and these are just a few of which I am aware. However, because of its far reaching effects physiologically and its neuromodulatory effects, it likely impacts many more disease states. Also, because it can have alternative and often antagonistic effects via the D1-like and D2-like receptors, its use as a treatment via specific receptor agonists/antagonists is enhanced by being able to modulate dopamine's effect either way.

I don't think this has been said in the previous answers, but some individuals suffering of depression benefit from molecules than inhibit metabolization of monoamines, including dopamine. While serotonin depletion has been considered a serious candidate for understanding the causes of depression, dopamine depletion may contribute as well. Medication such as Bupropion increase dopaminergic and serotoninergic transmission. Conversely, Schizophrenia is characterized by eccessive dopaminergic production and antipsychotic drugs typically act by lowering dopaminergic levels.

Parkinson's disease (PD) is a progressive extrapyramidal motor disorder. Pathologically, this disease is characterized by the selective dopaminergic (DAergic) neuronal degeneration in the substantia nigra. These classic symptoms include bradykinesia, akinesia, rigidity, tremor at rest, and postural instability. Since the disease progresses slowly, these motor symptoms may initially appear sporadically and develop consistency over several years. While the symptoms of Parkinson's disease are generally believed to consist only of motor abnormalities, nonmotor symptoms are also common in these patients, especially as the disease progresses. These nonmotor symptoms include depression, cognitive dysfunction, and psychosis. Correcting the DA deficiency in PD with levodopa (L-dopa) significantly attenuates the motor symptoms; however, its effectiveness often declines, and L-dopa-related adverse effects emerge after long-term treatment. Nowadays, DA receptor agonists are useful medication even regarded as first choice to delay the starting of L-dopa therapy.Dopamine receptors can be divided into two separate classes known as D1-like receptors and D2-like receptors. The D1-like receptors include D1 and D5 receptors, whereas the D2-like receptors include D2, D3, and D4 receptors. All of them function as G protein-coupled receptors, meaning that they exert their effects via a complex second messenger system. The ultimate effect of D1-like receptors (D1 and D5) can be excitation (via opening of sodium channels) or inhibition (via opening of potassium channels); the ultimate effect of D2-like receptors (D2, D3, and D4) is usually inhibition of the target neuron. Consequently, it is incorrect to describe dopamine itself as either excitatory or inhibitory. Its effect on a target neuron depends on which types of receptors are present on the membrane of that neuron and on the internal responses of that neuron to cyclic AMP. There are two distinct classes of dopamine agonists, known as ergoline and non-ergoline agonists. The ergoline agonists used in the United States include bromocriptine, cabergoline, and pergolide; the non-ergoline agonists are pramipexole and ropinirole. Ergoline agonists were the first to be developed and exhibit predominant D2-like receptor agonism; however, both pergolide and bromocriptine exhibit some D1-like receptor agonism. The non-ergoline agonists are newer agents that are selective for the D2-like receptors with exceptionally high affinity for D3 receptors.