1-too much dopamine was first associated with SCHIZOPHRENIA when Arvid Carlssen found that antipsychotic medication blocked dopamine receptors

2-psychostimulants may help persons with ADHD by increasing perfusion of prefrontal cortex (PFC)

Arvid Carlsson had nothing to do with that particular finding. See:

Madras, B. K. (2013). History of the discovery of the antipsychotic dopamine D2 receptor: a basis for the dopamine hypothesis of schizophrenia. Journal of the History of the Neurosciences, 22(1), 62-78.

Lewis has done a pretty concise job of a lay person's explanation.

Both the symptoms of psychosis and the symptoms of ADHD appear to be closely linked to dysregualtion of the neurotransmitter dopamine.

The acute, positive symptoms of schizophrenia (euphoria, hallucination, delusions, psychosis) relate to excessively elevated levels of dopamine in some pathways in the brain, and all modern anti-psychotics work by blocking the receptors for dopamine. However the chronic, negative symptoms of schizophrenia (social withdrawal, low libido, anhedonia, dysthemia, problems with concentration and memory, depression), may relate to  chronically depressed levels of dopamine in other brain regions, and there is evidence that in some individuals anti-psychotics can actually make these symptoms worse. .

The symptoms of ADHD appear to relate to chronically depressed levels of dopamine ("hypodopaminergic traits"). This is why dexamphetamine and methylphenidate appear to alleviate some of these symtpoms, as both of these medications elevate dopamine levels.

This is an excellent (and very readable) review of the dopamine theory of psychosis.

Journal of Psychopharmacology, 1999 Dec;13(4):358-71

Dopamine as the wind of the psychotic fire: new evidence from brain imaging studies.

Laruelle M, + Abi-Dargham.

PMID: 10667612

I thoroughly recommend reading the full text. Sorry, I can only find a link to the abstract;

http://www.ncbi.nlm.nih.gov/pubmed/10667612

.

re: Hypodopaminergic traits and ADHD, I would suggest reading;

Neuropsychiatr Dis Treat. 2008 Oct; 4(5): 893–918.

Attention-deficit-hyperactivity disorder and reward deficiency syndrome

Blum et al.

PMCID: PMC2626918

The full text is available here;

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2626918/

.

Regards,

Paul.

Thank you/merci beaucoup to Professor Seaman for correcting my misinformation re: Arvid Carlsson; I will read 

Madras, B. K. (2013). History of the discovery of the antipsychotic dopamine D2 receptor: a basis for the dopamine hypothesis of schizophrenia. Journal of the History of the Neurosciences, 22(1), 62-78.

I am still impressed by Carlsson's writings in which he speculates that the motor side effects might be due to block D2 receptors in the striatum and hyperprolactinemia to block of D2 receptors o=in the tuberinfundibular region; but getting the history re: the dopamine hypothesis of schizophrenia coreectly is important -- never cared if I was "politically correctt" or not but due wish to be historically accurate.

J Hist Neurosci. 2013;22(1):62-78. doi: 10.1080/0964704X.2012.678199.

History of the discovery of the antipsychotic dopamine D2 receptor: a basis for the dopamine hypothesis of schizophrenia.

Madras BK1.

Author information

1Department of Psychiatry, Harvard Medical School, New England Primate Research Center, Southborough, MA 01772-9102, USA. [email protected]

Abstract

The 1975 publication of Seeman et al. (Proc Nat Acad Sci, USA), reporting the discovery of the antipsychotic receptor in the brain, is a classic example of translational medicine research. In searching for a pathophysiological mechanism of psychosis, the team sought to identify sites that bound the antipsychotic drug haloperidol. Their criterion was that haloperidol bound to the site at one to two nanomoles per liter, corresponding to haloperidol concentrations found in spinal fluid or plasma water in treated patients. They requested de novo synthesis of tritiated haloperidol, and it readily detected specific haloperidol binding sites in brain striatum. With dopamine binding the haloperidol-labeled sites with higher potency than other neurotransmitters, the sites were named antipsychotic/dopamine receptors (now designated dopamine D2 receptors). Most significantly, they found that all antipsychotics bound these sites at concentrations and with a rank order of potencies that were directly related to the mean daily antipsychotic dose taken by patients with schizophrenia. Their findings enabled screening for new antipsychotics, initiated D2 receptor measurements in brain of living patients, and determination of minimum occupancy (65%) of D2 receptors for antipsychotic benefit. The collective work is generally viewed as providing a fundamental basis for the dopamine hypothesis of schizophrenia.

Thank you Dr. Paul Dessauer and Dr. Jeff GuIna for your enlightening answers on the Dopaminergic Theory in layman's terms.  Both of you have inspired me to recreate a strong conceptual framework and redesign a better methodology for a scientific proposal of a budget friendly adjunct therapy for kids with adhd. 

Due to lack of finances more parents in the Philippines have decreased or discontinued the expensive therapies for kids with adhd.  Thus it is quite common in big city jails to find increasing cases of delinquent young adults with adhd.

Your help in this study would someday mprove the lives of persons with adhd in the school I would be assigned to.

Maraming salamat po (Thank you very much) !

Best Regards, 

Trishan / Crystal

G'day Crystal,

I'm glad that was useful.

But, be careful; I'm not a Doctor!

:)

You can just call me Paul.

Regards,

Paul.