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Increased Dopamine (increased + dopamine)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Increased Dopamine Is Associated With the cGMP and Homocysteine Pathway in Female Migraineurs

HEADACHE, Issue 1 2010
Hans-Jürgen Gruber PhD
(Headache 2010;50:109-116) Background., The group of catecholamines, which include dopamine, adrenaline, and noradrenaline, are neurotransmitters which have been considered to play a role in the pathogenesis of migraine. However, the impact of catecholamines, especially dopamine on migraine as well as the exact mechanisms is not clear to date as previous studies have yielded in part conflicting results. Objective., This study aimed to produce a comprehensive examination of dopamine in migraineurs. Methods., Catecholamines and various parameters of the homocysteine, folate, and iron metabolism as well as cyclic guanosine monophosphate (cGMP) and inflammatory markers were determined in 135 subjects. Results., We found increased dopamine levels in the headache free period in female migraineurs but not in male patients. Increased dopamine is associated with a 3.30-fold higher risk for migraine in women. We found no significant effects of aura symptoms or menstrual cycle phases on dopamine levels. Dopamine is strongly correlated with cGMP and the homocysteine,folate pathway. Conclusion., We show here that female migraineurs exhibit increased dopamine levels in the headache free period which are associated with a higher risk for migraine. [source]

Increased dopamine and its metabolites in SH-SY5Y neuroblastoma cells that express tyrosinase

JOURNAL OF NEUROCHEMISTRY, Issue 2 2003
Takafumi Hasegawa
Abstract Oxidized metabolites of dopamine, known as dopamine quinone derivatives, are thought to play a pivotal role in the degeneration of dopaminergic neurons. Although such quinone derivatives are usually produced via the autoxidation of catecholamines, tyrosinase, which is a key enzyme in melanin biosynthesis via the production of DOPA and subsequent molecules, may potentially accelerate the induction of catecholamine quinone derivatives by its oxidase activity. In the present study, we developed neuronal cell lines in which the expression of human tyrosinase was inducible. Overexpression of tyrosinase in cultured cell lines resulted in (i) increased intracellular dopamine content; (ii) induction of oxidase activity not only for DOPA but also for dopamine; (iii) formation of melanin pigments in cell soma; and (iv) increased intracellular reactive oxygen species. Interestingly, the expressed tyrosinase protein was initially distributed in the entire cytoplasm and then accumulated to form catecholamine-positive granular structures by 3 days after the induction. The granular structures consisted of numerous rounded, dark bodies of melanin pigments and were largely coincident with the distribution of lysosomes. This cellular model that exhibits increased dopamine production will provide a useful tool for detailed analyses of the potentially noxious effects of oxidized catecholamine metabolites. [source]

Region-specific effects of N,N,-dodecane-1,12-diyl-bis-3-picolinium dibromide on nicotine-induced increase in extracellular dopamine in vivo

BRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2008
S Rahman
Background and purpose: Systemic administration of N,N,-dodecane-1,12-diyl-bis-3-picolinium dibromide (bPiDDB), an antagonist of nicotinic acetylcholine receptors (nAChRs) attenuated the nicotine-induced increase in dopamine levels in nucleus accumbens (NAcc). Experimental approach: Using in vivo microdialysis, we investigated the effects of local perfusion of the novel nAChR antagonist bPiDDB into the NAcc or ventral tegmental area (VTA) on increased extracellular dopamine in NAcc, induced by systemic nicotine. We also examined the concentration-dependent effects of bPiDDB on the acetylcholine (ACh)-evoked response of specific recombinant neuronal nAChR subtypes expressed in Xenopus oocytes, using electrophysiological methods. Key results: Nicotine (0.4 mg kg,1, s.c.) increased extracellular dopamine in NAcc, which was attenuated by intra-VTA perfusion of mecamylamine (100 ,M). Intra-VTA perfusion of bPiDDB (1 and 10 ,M) reduced nicotine-induced increases in extracellular dopamine in NAcc. In contrast, intra-NAcc perfusion of bPiDDB (1 or 10 ,M) failed to alter the nicotine-induced increase in dopamine in NAcc. Intra-VTA perfusion of bPiDDB alone did not alter basal dopamine levels, compared to control, nor the increased dopamine in NAcc following amphetamine (0.5 mg kg,1, s.c.). Using Xenopus oocytes, bPiDDB (0.01,100 ,M) inhibited the response to ACh on specific combinations of rat neuronal nAChR subunits, with highest potency at ,3,4,3 and lowest potency at ,6/3,2,3. Conclusions and implications: bPiDDB-Sensitive nAChRs involved in regulating nicotine-induced dopamine release are located in the VTA, rather than in the NAcc. As bPiDDB has properties different from the prototypical nAChR antagonist mecamylamine, further development may lead to novel nAChR antagonists for the treatment of tobacco dependence. British Journal of Pharmacology (2008) 153, 792,804; doi:10.1038/sj.bjp.0707612; published online 3 December 2007 [source]