User:Lauren Beaton/Sandbox: Difference between revisions
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So far in Dopamine article: | So far in Dopamine article: | ||
===Psychiatric disorders=== | ===Psychiatric disorders=== | ||
Latest revision as of 03:15, 22 November 2023
The account of this former contributor was not re-activated after the server upgrade of March 2022.
So far in Dopamine article:
Psychiatric disorders
Attention deficit hyperactivity disorder
ADHD may result from reduced inhibitory dopamine transmission in the midbrain. This may be due to an increase in dopamine plasma membrane transport protein density which may remove dopamine from the synapse too quickly.[1][2]
Drug abuse
The rewarding effects of amphetamines and cocaine are due to dopamine activity. Cocaine increases monoamine levels by binding to serotonin (5-HT), norepinephrine (NE), and dopamine (DA) catecholamine plasma membrane transport proteins. This blockade prevents the reuptake of neurotransmitters, thus increasing the amount available at the synapse to bind to the post synaptic cell. In contrast to amphetamine, a similar psychomotor stimulant, cocaine is a dopamine uptake inhibitor and does not stimulate DA release.[3] Cocaine's rewarding effects come primarily from increased activity in the mesolimbic dopamine pathway.[4]
Novelty Seeking Personality Trait
Novelty seeing personality trait may be related to polymorphisms in the dopamine receptor D4 that affects dopamine activity in the tuberoinfundibular dopaminergic system.[5]
Schizophrenia
The dopamine hypothesis proposes that schizophrenia is in part due to excessive dopaminergic activity.[6]
The third version of the dopamine hypothesis was indroduced in May 2009 by Howes & Kapur [7]. This is important because ...
- ↑ Volkow, Nora D.; Gene-Jack Wang, Scott H. Kollins, Tim L. Wigal, Jeffrey H. Newcorn, Frank Telang, Joanna S. Fowler, Wei Zhu, Jean Logan, Yeming Ma, Kith Pradhan, Christopher Wong, James M. Swanson (2009-09-09). "Evaluating Dopamine Reward Pathway in ADHD: Clinical Implications". JAMA 302 (10): 1084-1091. DOI:10.1001/jama.2009.1308. Retrieved on 2009-09-09. Research Blogging.
- ↑ Dougherty DD, Bonab AA, Spencer TJ, Rauch SL, Madras BK, Fischman AJ (1999 Dec 18-25). "Dopamine transporter density in patients with attention deficit hyperactivity disorder.". Lancet 354 (9196): 2132-3. DOI:10.1016/S0140-6736(99)04030-1. PMID 10609822. Research Blogging.
- ↑ Gold LH, Geyer MA, Koob GF (1989). "Neurochemical mechanisms involved in behavioral effects of amphetamines and related designer drugs". NIDA Res. Monogr. 94: 101–26. PMID 2514360. [e]
- ↑ Kuhar MJ, Ritz MC, Boja JW (1991). "The dopamine hypothesis of the reinforcing properties of cocaine". Trends Neurosci. 14 (7): 299–302. PMID 1719677.
- ↑ Online Mendelian Inheritance in Man, OMIM®. Johns Hopkins University, Baltimore, MD. MIM Number: 601696 . World Wide Web URL: http://omim.org/.
- ↑ Katzung, Bertram G. (2001). Basic & clinical pharmacology. New York: Lange Medical Books/McGraw-Hill, 479. ISBN 0-8385-0598-8.
- ↑ Howes, O.D. & S. Kapur (2009), "The Dopamine Hypothesis of Schizophrenia: Version III – The Final Common Pathway", Schizophrenia Bulletin 35 (3): 549-562, DOI:10.1093/schbul/sbp006
Citation 1: Howes, O.D. & S. Kapur (2009), "The Dopamine Hypothesis of Schizophrenia: Version III – The Final Common Pathway", Schizophrenia Bulletin 35 (3): 549-562, DOI:10.1093/schbul/sbp006
Citation 2: Cousins, D.A.; K Butts & Young (2009), "The role of dopamine in bipolar disorder", Bipolar Disorders 11 (8): 787-806, DOI:10.1111/j.1399-5618.2009.00760.x
>> fix my references