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Hyperlocomotion

From Wikipedia, the free encyclopedia

Hyperlocomotion, also known as locomotor hyperactivity, hyperactivity, or increased locomotor activity, is an effect of certain drugs in animals in which locomotor activity is increased.[1] More specifically, it is an effect induced by dopamine releasing agents and psychostimulants like amphetamine and methamphetamine and by NMDA receptor antagonists and dissociative hallucinogens like dizocilpine (MK-801) and phencyclidine (PCP).[1][2][3][4] Stimulation of locomotor activity is thought to be mediated by increased signaling in the nucleus accumbens.[5][6]

Drug-induced hyperlocomotion can be reversed by various drugs, such as antipsychotics acting as dopamine D2 receptor antagonists.[1][3] Reversal of drug-induced hyperlocomotion has been used as an animal test of drug antipsychotic-like activity.[1][3] Amphetamines and NMDA receptor antagonists likewise induce stereotypies, and reversal of these stereotypies is also employed as a test of drug antipsychotic-like activity.[1][3]

Certain antidepressants, including the dopamine reuptake inhibitors amineptine, bupropion, and nomifensine, also increase spontaneous locomotor activity in animals.[7][8] Conversely, most other antidepressants do not do so, and instead often actually show behavioral sedation in this test.[7][5][9] The dopamine reuptake inhibitor cocaine increases locomotor activity similarly to amphetamines.[4] Atypical dopamine reuptake inhibitors like modafinil do not produce hyperlocomotion in animals.[4] Direct dopamine receptor agonists like apomorphine show biphasic effects, decreasing locomotor activity at low doses and increasing locomotor activity at high doses.[5]

Other similar effects include stereotypy, exploratory behavior, climbing behavior, and jumping behavior.[10][2][3] Amphetamines induce stereotypies in addition to hyperlocomotion.[2][3] Apomorphine induces stereotypy and climbing behavior.[2] The dopamine precursor levodopa (L-DOPA) induces jumping behavior.[2] These effects can all be reversed by antipsychotics.[2]

See also

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References

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  1. ^ a b c d e Castagné, Vincent; Moser, Paul C.; Porsolt, Roger D. (2009). "Preclinical Behavioral Models for Predicting Antipsychotic Activity". Advances in Pharmacology. Elsevier. p. 381–418. doi:10.1016/s1054-3589(08)57010-4. ISSN 1054-3589.
  2. ^ a b c d e f Ayyar P, Ravinder JR (June 2023). "Animal models for the evaluation of antipsychotic agents". Fundam Clin Pharmacol. 37 (3): 447–460. doi:10.1111/fcp.12855. PMID 36410728.
  3. ^ a b c d e f Yee BK, Singer P (October 2013). "A conceptual and practical guide to the behavioural evaluation of animal models of the symptomatology and therapy of schizophrenia". Cell Tissue Res. 354 (1): 221–246. doi:10.1007/s00441-013-1611-0. PMC 3791321. PMID 23579553.
  4. ^ a b c Nishino, Seiji; Kotorii, Nozomu (2016). "Modes of Action of Drugs Related to Narcolepsy: Pharmacology of Wake-Promoting Compounds and Anticataplectics". Narcolepsy. Cham: Springer International Publishing. p. 307–329. doi:10.1007/978-3-319-23739-8_22. ISBN 978-3-319-23738-1.
  5. ^ a b c D'Aquila PS, Collu M, Gessa GL, Serra G (September 2000). "The role of dopamine in the mechanism of action of antidepressant drugs". Eur J Pharmacol. 405 (1–3): 365–373. doi:10.1016/s0014-2999(00)00566-5. PMID 11033341.
  6. ^ Ikemoto S, Panksepp J (December 1999). "The role of nucleus accumbens dopamine in motivated behavior: a unifying interpretation with special reference to reward-seeking". Brain Res Brain Res Rev. 31 (1): 6–41. doi:10.1016/s0165-0173(99)00023-5. PMID 10611493.
  7. ^ a b Tucker JC, File SE (1986). "The effects of tricyclic and 'atypical' antidepressants on spontaneous locomotor activity in rodents". Neurosci Biobehav Rev. 10 (2): 115–121. doi:10.1016/0149-7634(86)90022-9. PMID 3737024.
  8. ^ Rampello, Liborio; Nicoletti, Ferdinando; Nicoletti, Francesco (2000). "Dopamine and Depression". CNS Drugs. 13 (1). Springer Science and Business Media LLC: 35–45. doi:10.2165/00023210-200013010-00004. ISSN 1172-7047.
  9. ^ File SE, Tucker JC (1986). "Behavioral consequences of antidepressant treatment in rodents". Neurosci Biobehav Rev. 10 (2): 123–134. doi:10.1016/0149-7634(86)90023-0. PMID 3526203.
  10. ^ McCarson KE (2020). "Strategies for Behaviorally Phenotyping the Transgenic Mouse". Methods Mol Biol. 2066: 171–194. doi:10.1007/978-1-4939-9837-1_15. PMID 31512217.