Stimulants, that is, drugs that wake you up, like amfetamines such as metamfetamine, cathinones, pemoline, mazindol and cocaine are sometimes called sympathomimetic, as they, as part of their mechanism of action, increase the levels of the catecholamine neurotransmitters responsible for the functioning of the SNS. Although not all stimulants are said to be sympathomimetic, for instance, nicotine is parasympathomimetic as it activates the nicotinic acetylcholine receptors (nAChRs) which are part of the parasympathetic nervous system (PNS). Caffeine, on the other hand, blocks the adenosine receptors and is hence said to be an adenosinergic stimulant.
Amfetamines bind to the proteins responsible releasing dopamine into the synapse, namely VMAT2 and they activate the trace amine associated receptor 1 (TAAR1) as to inhibit the reuptake of the monoamine neurotransmitters. I should mention that stimulant-induced catecholamine release is not solely in the MLP, this is just the site at which they elicit their rewarding and addicting effects, hence catecholamine-type reactions are seen in the entirety of the body. For an explanation of how TAAR1 is involved in the mechanism of action of amfetamines, see the figure to the right.
They are the world’s favourite class of drugs, after all caffeine is a drug that many adults consume on a daily basis. Their therapeutic indices are roughly 100, with the exception of cocaine which has a therapeutic index of roughly 10.
Their chief medicine uses are in treating:
- Amfetamines: attention-deficit/hyperactivity disorder (ADHD, also abbreviated ADD) and narcolepsy.
- Cocaine: to relieve pain in selected situations.
- Caffeine: to relieve fatigue, orthostatic hypotension (drops in blood pressure that occur upon standing up, common as a drug reaction to certain medications and is a common cause of falls in the elderly), improve breathing rate in preterm infants and to relieve pain in migraines.
- Nicotine: usually administered to help smokers quit, although recent evidence supports its use in the treatment of ulcerative colitis, a form of inflammatory bowel disease.
- NCBI Bookshelf provides free book resources on this topic.
- PubMed provides review articles from the past five years (limit to free review articles or to systematic reviews)
- The TRIP database provides clinical publications about evidence-based medicine.
- ↑ Miller, GM (January 2011). "The Emerging Role of Trace Amine Associated Receptor 1 in the Functional Regulation of Monoamine Transporters and Dopaminergic Activity". Journal of Neurochemistry 116 (2): 164–176. doi:10.1111/j.1471-4159.2010.07109.x. PMC 3005101. PMID 21073468.
- ↑ Zucchi, R; Chiellini, G; Scanlan, TS; Grandy, DK (December 2006). "Trace amine-associated receptors and their ligands.". British Journal of Pharmacology 149 (8): 967–78. doi:10.1038/sj.bjp.0706948. PMC 2014643. PMID 17088868.
- ↑ Heal, DJ; Smith, SL; Gosden, J; Nutt, DJ (June 2013). "Amphetamine, past and present--a pharmacological and clinical perspective.". Journal of Psychopharmacology 27 (6): 479–96. doi:10.1177/0269881113482532. PMC 3666194. PMID 23539642.
- ↑ Lewin, AH; Gregory, MM; Brian, G (December 2011). "Trace amine-associated receptor 1 is a stereoselective binding site for compounds in the amphetamine class". Bioorganic & Medicinal Chemistry 19 (23): 7044–7048. doi:10.1016/j.bmc.2011.10.007. PMC 3236098. PMID 22037049.
- ↑ Brayfield, A, ed. (13 December 2013). "Cocaine". Martindale: The Complete Drug Reference. London, UK: Pharmaceutical Press. Retrieved 5 April 2014.
- ↑ Quik, M; Perez, XA; Bordia, T (July 2012). "Nicotine as a potential neuroprotective agent for Parkinson's disease.". Movement Disorders 27 (8): 947–57. PMC 3685410. PMID 22693036. doi:10.1002/mds.25028.