A serenic, or antiaggressive agent, is a type of
drug which reduces the capacity for
irritability and
aggression.[1]
Examples
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]
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.[13][14][15] 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.[16]
^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.
PMID10917407.
^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.
LCCN2006244001.
OCLC69984013.
PMID19562632.
S2CID12310995.
^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.
LCCN73644949.
OCLC1787728.
PMID23872370.
S2CID19772247.
^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.
LCCNsf97001017.
OCLC01568459.
PMID16310183.
^Calcagnoli F, de Boer SF, Althaus M, den Boer JA, Koolhaas JM (October 2013). de Witt H, Curran VH, Morrow AL, Hashimoto K, Howes O, Floresco SB, D'Souza D (eds.). "Antiaggressive activity of central oxytocin in male rats". Psychopharmacology. 229 (4).
Geneva, Switzerland: European Behavioural Pharmacology Society (EBPS)/
Springer: 639–651.
doi:
10.1007/s00213-013-3124-7.
PMID23624810.
S2CID481042.
^Ferris CF, Lu SF, Messenger T, Guillon CD, Heindel N, Miller M, et al. (February 2006). Griebel G, Arends MA, Izenwasser S (eds.). "Orally active vasopressin V1a receptor antagonist, SRX251, selectively blocks aggressive behavior". Pharmacology, Biochemistry, and Behavior. 83 (2).
Amsterdam, Netherlands: 169–174.
doi:
10.1016/j.pbb.2006.01.001.
OCLC67271683.
PMID16504276.
S2CID24199104.
^Pinna G, Agis-Balboa RC, Pibiri F, Nelson M, Guidotti A, Costa E (October 2008). Schousboe A (ed.). "Neurosteroid biosynthesis regulates sexually dimorphic fear and aggressive behavior in mice". Neurochemical Research. 33 (10).
Geneva, Switzerland:
Springer: 1990–2007.
doi:
10.1007/s11064-008-9718-5.
PMID18473173.
S2CID19338424.