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The '''head-twitch response''' ('''HTR''') is a rapid side-to-side head movement that occurs in mice and rats after the [[serotonin]] [[5-HT2A receptor]] is activated.<ref>{{cite journal |last1=Nakagawasai |first1=O |last2=Arai |first2=Y |last3=Satoh |first3=SE |last4=Satoh |first4=N |last5=Neda |first5=M |last6=Hozumi |first6=M |last7=Oka|first7=R|last8=Hiraga|first8=H|last9=Tadano|first9=T|title=Monoamine Oxidase and Head-Twitch Response in Mice Mechanisms of α-Methylated Substrate Derivatives|journal=NeuroToxicology|date=January 2004|volume=25|issue=1–2|pages=223–232|doi=10.1016/S0161-813X(03)00101-3|pmid=14697897}}</ref> The [[prefrontal cortex]] may be the neuroanatomical locus mediating the HTR.<ref>{{cite journal |last1=Willins |first1=DL |last2=Meltzer|first2=HY|title=Direct injection of 5-HT2A receptor agonists into the medial prefrontal cortex produces a head-twitch response in rats.|journal=The Journal of Pharmacology and Experimental Therapeutics|date=August 1997|volume=282|issue=2|pages=699–706|pmid=9262333}}</ref> Many serotonergic hallucinogens, including [[lysergic acid diethylamide]] (LSD), induce the head-twitch response, and so the HTR is used as a behavioral model of hallucinogen effects. However while there is generally a good correlation between compounds that induce head twitch in mice and compounds that are hallucinogenic in humans, it is unclear whether the head twitch response is primarily caused by [[5-HT2A receptor]]s, [[5-HT2C receptor]]s or both, but recent evidence shows that the HTR is mediated by the 5-HT2A receptor and modulated by the 5-HT2C receptor.<ref>Modulation by 5- |
The '''head-twitch response''' ('''HTR''') is a rapid side-to-side head movement that occurs in mice and rats after the [[serotonin]] [[5-HT2A receptor]] is activated.<ref>{{cite journal |last1=Nakagawasai |first1=O |last2=Arai |first2=Y |last3=Satoh |first3=SE |last4=Satoh |first4=N |last5=Neda |first5=M |last6=Hozumi |first6=M |last7=Oka|first7=R|last8=Hiraga|first8=H|last9=Tadano|first9=T|title=Monoamine Oxidase and Head-Twitch Response in Mice Mechanisms of α-Methylated Substrate Derivatives|journal=NeuroToxicology|date=January 2004|volume=25|issue=1–2|pages=223–232|doi=10.1016/S0161-813X(03)00101-3|pmid=14697897}}</ref> The [[prefrontal cortex]] may be the neuroanatomical locus mediating the HTR.<ref>{{cite journal |last1=Willins |first1=DL |last2=Meltzer|first2=HY|title=Direct injection of 5-HT2A receptor agonists into the medial prefrontal cortex produces a head-twitch response in rats.|journal=The Journal of Pharmacology and Experimental Therapeutics|date=August 1997|volume=282|issue=2|pages=699–706|pmid=9262333}}</ref> Many serotonergic hallucinogens, including [[lysergic acid diethylamide]] (LSD), induce the head-twitch response, and so the HTR is used as a behavioral model of hallucinogen effects. However while there is generally a good correlation between compounds that induce head twitch in mice and compounds that are hallucinogenic in humans, it is unclear whether the head twitch response is primarily caused by [[5-HT2A receptor]]s, [[5-HT2C receptor]]s or both, but recent evidence shows that the HTR is mediated by the 5-HT2A receptor and modulated by the 5-HT2C receptor.<ref>{{cite journal | pmid = 12083749 | doi=10.1254/jjp.89.89 | volume=89 | title=Modulation by 5-hT2A receptors of aggressive behavior in isolated mice | year=2002 | journal=Jpn J Pharmacol | pages=89–92 | last1 = Sakaue | first1 = M | last2 = Ago | first2 = Y | last3 = Sowa | first3 = C | last4 = Sakamoto | first4 = Y | last5 = Nishihara | first5 = B | last6 = Koyama | first6 = Y | last7 = Baba | first7 = A | last8 = Matsuda | first8 = T}}</ref><ref>{{cite journal|last1=Carbonaro|first1=Theresa M.|title=The role of 5-HT2A, 5-HT2C and mGlu2 receptors in the behavioral effects of tryptamine hallucinogens N,N-dimethyltryptamine and N,N-diisopropyltryptamine in rats and mice|date=July 3, 2014|volume=232|issue=1|pages=275–284|doi=10.1007/s00213-014-3658-3|journal=Psychopharmacology|pmid=24985890|pmc=4282596}}</ref> Also, the effect can be non-specific, with head twitch responses also produced by some drugs that do not act through 5-HT<sub>2</sub> receptors, such as [[phencyclidine]], [[yohimbine]], [[atropine]] and [[cannabinoid receptor antagonist]]s. As well, compounds such as [[5-HTP]], [[fenfluramine]] and [[1-Methylpsilocin]] can also produce head twitch and do stimulate serotonin receptors, but are not hallucinogenic in humans. This means that while the head twitch response can be a useful indicator as to whether a compound is likely to display hallucinogenic activity in humans, the induction of a head twitch response does not necessarily mean that a compound will be hallucinogenic, and caution should be exercised when interpreting such results.<ref>{{cite journal|last1=Canal|first1=Clint E.|last2=Morgan|first2=Drake|title=Head-twitch response in rodents induced by the hallucinogen 2,5-dimethoxy-4-iodoamphetamine: a comprehensive history, a re-evaluation of mechanisms, and its utility as a model|journal=Drug Testing and Analysis|date=July 2012|volume=4|issue=7–8|pages=556–576|doi=10.1002/dta.1333|pmid=22517680|pmc=3722587}}</ref> |
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==References== |
==References== |
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Revision as of 10:52, 12 April 2020
The head-twitch response (HTR) is a rapid side-to-side head movement that occurs in mice and rats after the serotonin 5-HT2A receptor is activated.[1] The prefrontal cortex may be the neuroanatomical locus mediating the HTR.[2] Many serotonergic hallucinogens, including lysergic acid diethylamide (LSD), induce the head-twitch response, and so the HTR is used as a behavioral model of hallucinogen effects. However while there is generally a good correlation between compounds that induce head twitch in mice and compounds that are hallucinogenic in humans, it is unclear whether the head twitch response is primarily caused by 5-HT2A receptors, 5-HT2C receptors or both, but recent evidence shows that the HTR is mediated by the 5-HT2A receptor and modulated by the 5-HT2C receptor.[3][4] Also, the effect can be non-specific, with head twitch responses also produced by some drugs that do not act through 5-HT2 receptors, such as phencyclidine, yohimbine, atropine and cannabinoid receptor antagonists. As well, compounds such as 5-HTP, fenfluramine and 1-Methylpsilocin can also produce head twitch and do stimulate serotonin receptors, but are not hallucinogenic in humans. This means that while the head twitch response can be a useful indicator as to whether a compound is likely to display hallucinogenic activity in humans, the induction of a head twitch response does not necessarily mean that a compound will be hallucinogenic, and caution should be exercised when interpreting such results.[5]
References
- ^ Nakagawasai, O; Arai, Y; Satoh, SE; Satoh, N; Neda, M; Hozumi, M; Oka, R; Hiraga, H; Tadano, T (January 2004). "Monoamine Oxidase and Head-Twitch Response in Mice Mechanisms of α-Methylated Substrate Derivatives". NeuroToxicology. 25 (1–2): 223–232. doi:10.1016/S0161-813X(03)00101-3. PMID 14697897.
- ^ Willins, DL; Meltzer, HY (August 1997). "Direct injection of 5-HT2A receptor agonists into the medial prefrontal cortex produces a head-twitch response in rats". The Journal of Pharmacology and Experimental Therapeutics. 282 (2): 699–706. PMID 9262333.
- ^ Sakaue, M; Ago, Y; Sowa, C; Sakamoto, Y; Nishihara, B; Koyama, Y; Baba, A; Matsuda, T (2002). "Modulation by 5-hT2A receptors of aggressive behavior in isolated mice". Jpn J Pharmacol. 89: 89–92. doi:10.1254/jjp.89.89. PMID 12083749.
- ^ Carbonaro, Theresa M. (July 3, 2014). "The role of 5-HT2A, 5-HT2C and mGlu2 receptors in the behavioral effects of tryptamine hallucinogens N,N-dimethyltryptamine and N,N-diisopropyltryptamine in rats and mice". Psychopharmacology. 232 (1): 275–284. doi:10.1007/s00213-014-3658-3. PMC 4282596. PMID 24985890.
- ^ Canal, Clint E.; Morgan, Drake (July 2012). "Head-twitch response in rodents induced by the hallucinogen 2,5-dimethoxy-4-iodoamphetamine: a comprehensive history, a re-evaluation of mechanisms, and its utility as a model". Drug Testing and Analysis. 4 (7–8): 556–576. doi:10.1002/dta.1333. PMC 3722587. PMID 22517680.