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Article: Chronic ketamine exposure induces permanent impairment of brain functions in adolescent cynomolgus monkeys

TitleChronic ketamine exposure induces permanent impairment of brain functions in adolescent cynomolgus monkeys
Authors
KeywordsApoptosis
Behavioral depression
Cynomolgus monkeys
Ketamine
Prefrontal cortex
Issue Date2014
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.addiction-ssa.org/ssa_aj.htm
Citation
Addiction Biology, 2014, v. 19 n. 2, p. 185-194 How to Cite?
AbstractKetamine, a non‐competitive N‐methyl‐D‐aspartic acid receptor antagonist, has emerged as an increasingly popular drug among young drug abusers worldwide. Available evidence suggests that ketamine produces acute impairments of working, episodic and semantic memory along with psychotogenic and dissociative effects when a single dose is given to healthy volunteers. However, understanding of the possible chronic effects of ketamine on behavior, cognitive anomalies and neurochemical homeostasis is still incomplete. Although previous human studies demonstrate that ketamine could impair a range of cognitive skills, investigation using non‐human models would permit more precise exploration of the neurochemical mechanisms which may underlie the detrimental effects. The current study examined the abnormalities in behavior (move, walk, jump and climb) and apoptosis of the prefrontal cortex using terminal deoxynucleotidyl transferase‐mediated biotinylated dUTP nick end labeling (TUNEL) and apoptotic markers, including Bax, Bcl‐2 and caspase‐3 in adolescent male cynomolgus monkeys (Macaca fascicularis) after 1 or 6 months of sub‐anesthetic ketamine administration (1 mg/kg, i.v.). Results showed that ketamine decreased locomotor activity and increased cell death in the prefrontal cortex of monkeys with 6 months of ketamine treatment when compared with the control monkeys. Such decreases were not found in the 1‐month ketamine‐treated group. Our study suggested that ketamine administration of recreational dose in monkeys might produce permanent and irreversible deficits in brain functions due to neurotoxic effects, involving the activation of apoptotic pathways in the prefrontal cortex.
Persistent Identifierhttp://hdl.handle.net/10722/186209
ISSN
2019 Impact Factor: 4.121
2015 SCImago Journal Rankings: 2.091
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSun, L-
dc.contributor.authorLi, Q-
dc.contributor.authorLi, Q-
dc.contributor.authorZhang, Y-
dc.contributor.authorLiu, D-
dc.contributor.authorJiang, H-
dc.contributor.authorPan, F-
dc.contributor.authorYew, DT-
dc.date.accessioned2013-08-20T11:59:39Z-
dc.date.available2013-08-20T11:59:39Z-
dc.date.issued2014-
dc.identifier.citationAddiction Biology, 2014, v. 19 n. 2, p. 185-194-
dc.identifier.issn1355-6215-
dc.identifier.urihttp://hdl.handle.net/10722/186209-
dc.description.abstractKetamine, a non‐competitive N‐methyl‐D‐aspartic acid receptor antagonist, has emerged as an increasingly popular drug among young drug abusers worldwide. Available evidence suggests that ketamine produces acute impairments of working, episodic and semantic memory along with psychotogenic and dissociative effects when a single dose is given to healthy volunteers. However, understanding of the possible chronic effects of ketamine on behavior, cognitive anomalies and neurochemical homeostasis is still incomplete. Although previous human studies demonstrate that ketamine could impair a range of cognitive skills, investigation using non‐human models would permit more precise exploration of the neurochemical mechanisms which may underlie the detrimental effects. The current study examined the abnormalities in behavior (move, walk, jump and climb) and apoptosis of the prefrontal cortex using terminal deoxynucleotidyl transferase‐mediated biotinylated dUTP nick end labeling (TUNEL) and apoptotic markers, including Bax, Bcl‐2 and caspase‐3 in adolescent male cynomolgus monkeys (Macaca fascicularis) after 1 or 6 months of sub‐anesthetic ketamine administration (1 mg/kg, i.v.). Results showed that ketamine decreased locomotor activity and increased cell death in the prefrontal cortex of monkeys with 6 months of ketamine treatment when compared with the control monkeys. Such decreases were not found in the 1‐month ketamine‐treated group. Our study suggested that ketamine administration of recreational dose in monkeys might produce permanent and irreversible deficits in brain functions due to neurotoxic effects, involving the activation of apoptotic pathways in the prefrontal cortex.-
dc.languageeng-
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.addiction-ssa.org/ssa_aj.htm-
dc.relation.ispartofAddiction Biology-
dc.subjectApoptosis-
dc.subjectBehavioral depression-
dc.subjectCynomolgus monkeys-
dc.subjectKetamine-
dc.subjectPrefrontal cortex-
dc.titleChronic ketamine exposure induces permanent impairment of brain functions in adolescent cynomolgus monkeys-
dc.typeArticle-
dc.identifier.emailLi, Q: liqi@hkucc.hku.hk-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/adb.12004-
dc.identifier.pmid23145560-
dc.identifier.scopuseid_2-s2.0-84894432563-
dc.identifier.hkuros217888-
dc.identifier.volume19-
dc.identifier.issue2-
dc.identifier.spage185-
dc.identifier.epage194-
dc.identifier.isiWOS:000331529100005-
dc.publisher.placeUnited Kingdom-

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