Serenic

See also: Anger § Medication therapy

Serenic

Drug class
Class identifiers
Synonyms| Anti-aggressive drug; Anti-aggressive agent; Anti-aggressive medication; Antiaggressive drug; Antiaggressive agent; Antiaggressive medication
Use| To reduce aggression and anger
Legal status
In Wikidata

A serenic, or anti-aggressive drug, is a type of drug which reduces the capacity for aggression.[1]

## Examples

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### Serotonergic agents

[edit]

The recreational drug MDMA ("ecstasy") and a variety of related drugs have been described as empathogen-entactogens, or simply as entactogens.[2] These agents possess serenic and empathy-increasing properties in addition to their euphoriant effects, and have been associated with increased sociability, friendliness, and feelings of closeness to others as well as emotional empathy and prosocial behavior.[3][4] The entactogenic effects of these drugs are thought to be related to their ability to temporarily increase the levels of certain brain chemicals, including serotonin,[5] dopamine, and, particularly, oxytocin.[3][6][7]

Certain other serotonergic drugs, such as 5-HT1A receptor agonists, also increase oxytocin levels and may possess serenic properties as well.[8] The phenylpiperazine mixed 5-HT1A and 5-HT1B receptor agonists eltoprazine, fluprazine, and batoprazine have been described based on animal research as serenics.[9] The selective 5-HT1A biased full agonist F-15,599 (NLX-101) has shown antiaggressive effects in rodents as well.[10]

The serotonin 5-HT2C receptor agonist lorcaserin has been found to reduce impulsive aggression in people with intermittent explosive disorder (IED).[11][12][13][14] Serotonin 5-HT2C receptor agonists have also been found to produce antiaggressive effects in rodents.[11]

The serotonergic psychedelics DOB and DOI, which act as serotonin 5-HT2 receptor agonists, show antiaggressive effects in rodents.[11][15][16][17] However, DOI has also been found to have pro-aggressive effects, and serotonin 5-HT2A receptor antagonists have been found to reduce aggression in animals.[11] Additionally, atypical antipsychotics, which act in part as serotonin 5-HT2A receptor antagonists, have antiaggressive effects in humans.[11]

The selective serotonin reuptake inhibitors (SSRIs) sertraline, fluvoxamine, and fluoxetine inhibited aggression in rodents, whereas the SSRIs citalopram and paroxetine were ineffective.[18][19]

### Hormonal and related agents

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Agonists and antagonists of the receptors for the endogenous hormones oxytocin and vasopressin, respectively, have been shown to decrease aggressive behavior in scientific research, implicating them in the normal regulation of pathways involving aggressive behavior in the brain.[20][21] Certain neurosteroids, such as allopregnanolone, also appear to play a role in the regulation of aggression, including, notably, sexually-dimorphic aggressive behavior.[22] The sex hormones testosterone and estradiol regulate aggression as well.[23][24][25]

### Antidopaminergic agents

[edit]

Antipsychotics, which are dopamine D2 receptor antagonists, are well-known as reducing aggression in humans and have been clinically employed for this purpose.[26] Molindone is under development for the treatment of impulsive aggression in children and adolescents with attention deficit hyperactivity disorder (ADHD).[27][28]

### Cholinergic agents

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Nicotinic acetylcholine receptors within the CNS, specifically α7 homopentameric receptors, are implicated in the regulation of aggression. The serenic effect of nicotine is well documented both in laboratory animals and humans, and, conversely, nicotinic receptor antagonists and nicotine withdrawal are associated with irritability and aggression.[29][30][31] Additionally, nicotinic receptors are required for rabies virus entry into a neuron, and the dysfunction of these neurons is implicated in the rabies-associated aggression.[32]

## See also

[edit]

* List of investigational aggression drugs

## References

[edit]

1. ^ Olivier B, Mos J (10 July 1986). Chan DK (ed.). "Serenics and aggression". Stress & Health. 2 (3). Arlington, Virginia, United States of America: Wiley: 197–209\. doi:10.1002/smi.2460020305. ISSN 1532-2998.197-209&rft.date=1986-07-10&rft_id=info:doi/10.1002/smi.2460020305&rft.issn=1532-2998&rft.aulast=Olivier&rft.aufirst=B&rft.au=Mos,+J&rft_id=https://onlinelibrary.wiley.com/doi/10.1002/smi.2460020305&rfr_id=info:sid/en.wikipedia.org:Serenic" class="Z3988">
2. ^ Bedi G, Hyman D, de Wit H (December 2010). Krystal JH (ed.). "Is ecstasy an "empathogen"? Effects of ±3,4-methylenedioxymethamphetamine on prosocial feelings and identification of emotional states in others". Biological Psychiatry. 68 (12). Brentwood, Tennessee, United States of America: Society of Biological Psychiatry: 1134–1140\. doi:10.1016/j.biopsych.2010.08.003. LCCN 78009779. OCLC 424038458. PMC 2997873. PMID 20947066.1134-1140&rft.date=2010-12&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2997873#id-name=PMC&rft_id=info:doi/10.1016/j.biopsych.2010.08.003&rft_id=info:oclcnum/424038458&rft_id=info:lccn/78009779&rft_id=info:pmid/20947066&rft.aulast=Bedi&rft.aufirst=G&rft.au=Hyman,+D&rft.au=de+Wit,+H&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2997873&rfr_id=info:sid/en.wikipedia.org:Serenic" class="Z3988">
3. ^ a b Hysek CM, Schmid Y, Simmler LD, Domes G, Heinrichs M, Eisenegger C, et al. (November 2014). Lieberman MD (ed.). "MDMA enhances emotional empathy and prosocial behavior". Social Cognitive and Affective Neuroscience. 9 (11). Oxford University Press: 1645–1652\. doi:10.1093/scan/nst161. PMC 4221206. PMID 24097374.1645-1652&rft.date=2014-11&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4221206#id-name=PMC&rft_id=info:pmid/24097374&rft_id=info:doi/10.1093/scan/nst161&rft.aulast=Hysek&rft.aufirst=CM&rft.au=Schmid,+Y&rft.au=Simmler,+LD&rft.au=Domes,+G&rft.au=Heinrichs,+M&rft.au=Eisenegger,+C&rft.au=Preller,+KH&rft.au=Quednow,+BB&rft.au=Liechti,+ME&rft_id=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4221206&rfr_id=info:sid/en.wikipedia.org:Serenic" class="Z3988">
4. ^ Cami J, Farré M, Mas M, Roset PN, Poudevida S, Mas A, et al. (August 2000). "Human pharmacology of 3,4-methylenedioxymethamphetamine ("ecstasy"): psychomotor performance and subjective effects". Journal of Clinical Psychopharmacology. 20 (4): 455–466\. doi:10.1097/00004714-200008000-00010. PMID 10917407.455-466&rft.date=2000-08&rft_id=info:doi/10.1097/00004714-200008000-00010&rft_id=info:pmid/10917407&rft.aulast=Cami&rft.aufirst=J&rft.au=Farré,+M&rft.au=Mas,+M&rft.au=Roset,+PN&rft.au=Poudevida,+S&rft.au=Mas,+A&rft.au=San,+L&rft.au=de+la+Torre,+R&rfr_id=info:sid/en.wikipedia.org:Serenic" class="Z3988">
5. ^ Piper BJ, Fraiman JB, Owens CB, Ali SF, Meyer JS (April 2008). Carlezon WA, George TP, Neumaier JF (eds.). "Dissociation of the neurochemical and behavioral toxicology of MDMA ('Ecstasy') by citalopram". Neuropsychopharmacology. 33 (5). Brentwood, Tennessee, United States of America: American College of Neuropsychopharmacology (ACNP): 1192–1205\. doi:10.1038/sj.npp.1301491. PMID 17609680.1192-1205&rft.date=2008-04&rft_id=info:doi/10.1038/sj.npp.1301491&rft_id=info:pmid/17609680&rft.aulast=Piper&rft.aufirst=BJ&rft.au=Fraiman,+JB&rft.au=Owens,+CB&rft.au=Ali,+SF&rft.au=Meyer,+JS&rft_id=https://doi.org/10.1038%2Fsj.npp.1301491&rfr_id=info:sid/en.wikipedia.org:Serenic" class="Z3988">
6. ^ Dumont GJ, Sweep FC, van der Steen R, Hermsen R, Donders AR, Touw DJ, et al. (2009). Eslinger P, Boggio PS, Young L, Zahn R (eds.). "Increased oxytocin concentrations and prosocial feelings in humans after ecstasy (3,4-methylenedioxymethamphetamine) administration". Social Neuroscience. 4 (4). London, United Kingdom of Great Britain: Society for Social Neuroscience/Taylor & Francis: 359–366\. doi:10.1080/17470910802649470. LCCN 2006244001. OCLC 69984013. PMID 19562632. S2CID 12310995.359-366&rft.date=2009&rft_id=https://api.semanticscholar.org/CorpusID:12310995#id-name=S2CID&rft_id=info:doi/10.1080/17470910802649470&rft_id=info:oclcnum/69984013&rft_id=info:pmid/19562632&rft_id=info:lccn/2006244001&rft.aulast=Dumont&rft.aufirst=GJ&rft.au=Sweep,+FC&rft.au=van+der+Steen,+R&rft.au=Hermsen,+R&rft.au=Donders,+AR&rft.au=Touw,+DJ&rft.au=van+Gerven,+JM&rft.au=Buitelaar,+JK&rft.au=Verkes,+RJ&rfr_id=info:sid/en.wikipedia.org:Serenic" class="Z3988">
7. ^ Broadbear JH, Kabel D, Tracy L, Mak P (April 2014). Koob JF, Schulteis G, Kantak KM, Arends M, Buisman-Pijlman FT, Broadbear JH, Zoltán S (eds.). "Oxytocinergic regulation of endogenous as well as drug-induced mood". Pharmacology, Biochemistry, and Behavior. 119 (1). Amsterdam, Netherlands: Elsevier: 61–71\. doi:10.1016/j.pbb.2013.07.002. LCCN 73644949. OCLC 1787728. PMID 23872370. S2CID 19772247.61-71&rft.date=2014-04&rft_id=https://api.semanticscholar.org/CorpusID:19772247#id-name=S2CID&rft_id=info:doi/10.1016/j.pbb.2013.07.002&rft_id=info:oclcnum/1787728&rft_id=info:pmid/23872370&rft_id=info:lccn/73644949&rft.aulast=Broadbear&rft.aufirst=JH&rft.au=Kabel,+D&rft.au=Tracy,+L&rft.au=Mak,+P&rfr_id=info:sid/en.wikipedia.org:Serenic" class="Z3988">
8. ^ de Boer SF, Koolhaas JM (December 2005). Redegeld FA, Verri WA, Burk J (eds.). "5-HT1A and 5-HT1B receptor agonists and aggression: a pharmacological challenge of the serotonin deficiency hypothesis". European Journal of Pharmacology. 526 (1–3). Amsterdam, Netherlands: Elsevier: 125–139\. doi:10.1016/j.ejphar.2005.09.065. LCCN sf97001017. OCLC 01568459. PMID 16310183.1–3&rft.pages=125-139&rft.date=2005-12&rft_id=info:oclcnum/01568459&rft_id=info:pmid/16310183&rft_id=info:lccn/sf97001017&rft_id=info:doi/10.1016/j.ejphar.2005.09.065&rft.aulast=de+Boer&rft.aufirst=SF&rft.au=Koolhaas,+JM&rfr_id=info:sid/en.wikipedia.org:Serenic" class="Z3988">
9. ^ Olivier B (December 2004). "Serotonin and aggression". Annals of the New York Academy of Sciences. 1036 (1). New York City, New York, United States of America: New York Academy of Sciences: 382–392\. Bibcode:2004NYASA1036..382O. doi:10.1196/annals.1330.022. LCCN 12037287. OCLC 01306678. PMID 15817750. S2CID 45595253.382-392&rft.date=2004-12&rft_id=https://api.semanticscholar.org/CorpusID:45595253#id-name=S2CID&rft_id=info:bibcode/2004NYASA1036..382O&rft_id=info:oclcnum/01306678&rft_id=info:pmid/15817750&rft_id=info:doi/10.1196/annals.1330.022&rft_id=info:lccn/12037287&rft.aulast=Olivier&rft.aufirst=B&rfr_id=info:sid/en.wikipedia.org:Serenic" class="Z3988">
10. ^ Sałaciak K, Pytka K (November 2021). "Biased agonism in drug discovery: Is there a future for biased 5-HT1A receptor agonists in the treatment of neuropsychiatric diseases?". Pharmacol Ther. 227: 107872. doi:10.1016/j.pharmthera.2021.107872. PMID 33905796.
11. ^ a b c d e Popova NK, Tsybko AS, Naumenko VS (August 2022). "The Implication of 5-HT Receptor Family Members in Aggression, Depression and Suicide: Similarity and Difference". Int J Mol Sci. 23 (15): 8814. doi:10.3390/ijms23158814. PMC 9369404. PMID 35955946. "There are some pharmacological data indicating a link between aggressive behavior and 5-HT2A receptor activity. In animals, 5-HT2A agonists, such as DOI, reduced aggressive behavior in flies, amphibians, mice and rats [34]. However, accumulated data also revealed a pro-aggressive effect of the 5-HT2A agonist DOI [119,120], whereas 5-HT2A antagonists effectively suppressed aggressive behavior [119,121,122]. In humans, a number of atypical antipsychotics, which act as antagonists of 5-HT2A receptors, had antiaggressive effects in clinical trials reviewed by Comai and co-authors [123]. [...] There are a few currently available data in support of the antiaggressive role of 5-HT2C receptors: (1) the activation of 5-HT2C receptors enhanced the display of defeat submissive and defensive behavior in golden hamsters [172]. (2) 5-HT2C receptor agonist/alpha 2 receptor antagonist S32212 suppressed aggressive behavior in mice [173]. (3) Mice expressing only the VGV isoform of 5-HT2C receptors displayed a high level of conspecific aggression [174]. (4) The association between Htr2c gene polymorphism and criminal behavior in humans was demonstrated [175]. (5) Recently, a novel 5-HT2C agonist, lorcaserin, has been demonstrated to have antiaggressive properties in human subjects with impulsive aggressive behavior. Lorcaserin attenuated provoked, but not unprovoked, aggression in impulsively aggressive individuals indicating that 5-HT2C receptor may be a putative target for the treatment of impulsive aggressive behavior in human subjects [176]."
12. ^ Desilva, Nilifa; Hollander, Eric (2023). "Impulse Control Disorders: Intermittent Explosive Disorder, Kleptomania, Pyromania". Tasman's Psychiatry. Cham: Springer International Publishing. p. 1–49. doi:10.1007/978-3-030-42825-9_165-1. ISBN 978-3-030-42825-9. "Based on evidence from a recent pilot study, lorcaserin, a selective 5-HT2c agonist, was found to have anti-aggressive effects in humans with high levels of impulsive aggression like in those diagnosed with IED."
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