Dopaminergic

Summary

Dopaminergic means "related to dopamine" (literally, "working on dopamine"), dopamine being a common neurotransmitter.[1] Dopaminergic substances or actions increase dopamine-related activity in the brain. Dopaminergic brain pathways facilitate dopamine-related activity. For example, certain proteins such as the dopamine transporter (DAT), vesicular monoamine transporter 2 (VMAT2), and dopamine receptors can be classified as dopaminergic, and neurons that synthesize or contain dopamine and synapses with dopamine receptors in them may also be labeled as dopaminergic. Enzymes that regulate the biosynthesis or metabolism of dopamine such as aromatic L-amino acid decarboxylase or DOPA decarboxylase, monoamine oxidase (MAO), and catechol O-methyl transferase (COMT) may be referred to as dopaminergic as well. Also, any endogenous or exogenous chemical substance that acts to affect dopamine receptors or dopamine release through indirect actions (for example, on neurons that synapse onto neurons that release dopamine or express dopamine receptors) can also be said to have dopaminergic effects, two prominent examples being opioids, which enhance dopamine release indirectly in the reward pathways, and some substituted amphetamines, which enhance dopamine release directly by binding to and inhibiting VMAT2.

The chemical structure of the neurotransmitter dopamine

Supplements and drugs edit

The following are examples of dopaminergic substances:

Precursors edit

Receptor agonists edit

Receptor antagonists/receptor blockers edit

Reuptake inhibitors/transporter blockers edit

Releasing agents edit

"Activity enhancers" edit

Monoamine oxidase inhibitors edit

Dopamine synthesis enhancers edit

  • Tyrosine hydroxylase (TH) mRNA upregulators such as bromantane and low dose aspirin.[3][4] Bromantane's upregulation of TH may persist for a time (up to at least one month) after its discontinuation based on data related to its efficacy in treating asthenic disorders in Russia.[5]

Other enzyme inhibitors edit

See also edit

References edit

  1. ^ Melinosky C (27 November 2022). "Parkinson's Disease: Glossary of Terms". WebMD.
  2. ^ Shimazu S, Miklya I (May 2004). "Pharmacological studies with endogenous enhancer substances: beta-phenylethylamine, tryptamine, and their synthetic derivatives". Progress in Neuro-Psychopharmacology & Biological Psychiatry. 28 (3): 421–427. doi:10.1016/j.pnpbp.2003.11.016. PMID 15093948. S2CID 37564231.
  3. ^ Rangasamy SB, Dasarathi S, Pahan P, Jana M, Pahan K (June 2019). "Low-Dose Aspirin Upregulates Tyrosine Hydroxylase and Increases Dopamine Production in Dopaminergic Neurons: Implications for Parkinson's Disease". Journal of Neuroimmune Pharmacology. 14 (2): 173–187. doi:10.1007/s11481-018-9808-3. PMC 6401361. PMID 30187283.
  4. ^ Mikhaylova M, Vakhitova JV, Yamidanov RS, Salimgareeva MK, Seredenin SB, Behnisch T (October 2007). "The effects of ladasten on dopaminergic neurotransmission and hippocampal synaptic plasticity in rats". Neuropharmacology. 53 (5): 601–608. doi:10.1016/j.neuropharm.2007.07.001. PMID 17854844. S2CID 43661752.
  5. ^ Voznesenskaia TG, Fokina NM, Iakhno NN (2010). "[Treatment of asthenic disorders in patients with psychoautonomic syndrome: results of a multicenter study on efficacy and safety of ladasten]". Zhurnal Nevrologii I Psikhiatrii Imeni S.S. Korsakova. 110 (5 Pt 1): 17–26. PMID 21322821.
  6. ^ Krampe H, Stawicki S, Wagner T, Bartels C, Aust C, Rüther E, Poser W, Ehrenreich H (January 2006). "Follow-up of 180 alcoholic patients for up to 7 years after outpatient treatment: impact of alcohol deterrents on outcome". Alcoholism: Clinical and Experimental Research. 30 (1): 86–95. doi:10.1111/j.1530-0277.2006.00013.x. PMID 16433735.