A follow-up study: acute behavioural effects of Δ9-THC in female heterozygous Neuregulin 1 transmembrane domain mutant mice

Long, Leonora E.; Chesworth, Rose; Arnold, Jonathon C.; Karl, Tim

doi:10.1007/s00213-010-1896-6

Cited by 61 publications

(45 citation statements)

References 52 publications

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“…Furthermore, EH and EC animals similarly traveled and crossed the central area of the arena. Noteworthy, a pattern featured by increased central traveling is retained to be linked to reduced anxiety levels [58,59]. Thus, it is possible that the ameliorative effects of the environmental enrichment we observed on various parameters of the behavioral tasks were related to diminished levels of anxiety of animals exposed to a complex environment [60].…”

Section: Discussionmentioning

confidence: 95%

Exposure to an Enriched Environment Accelerates Recovery from Cerebellar Lesion

et al. 2010

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The exposure to enriched environments allows the maintenance of normal cognitive functioning even in the presence of brain pathology. Up until now, clinical and experimental studies have investigated environmental effects mainly on the symptoms linked to the presence of neuro-degenerative diseases, and no study has yet analyzed whether prolonged exposure to complex environments allows modifying the clinical expression and compensation of deficits of cerebellar origin. In animals previously exposed to complex stimulations, the effects of cerebellar lesions have been analyzed to verify whether a prolonged and intense exposure to complex stimulations affected the compensation of motor and cognitive functions following a cerebellar lesion. Hemicerebellectomized or intact animals housed in enriched or standard conditions were administered spatial tests. Postural asymmetries and motor behavior were also assessed. Exposure to the enriched environment almost completely compensated the effects of the hemicerebellectomy. In fact, the motor and cognitive performances of the enriched hemicerebellectomized animals were similar to those of the intact animals. The plastic changes induced by enhanced mental and physical activity seem to provide the development of compensatory responses against the disrupting motor and cognitive consequences of the cerebellar damage.

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Section: Discussionmentioning

confidence: 95%

Exposure to an Enriched Environment Accelerates Recovery from Cerebellar Lesion

et al. 2010

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“…Schneider and Koch (2003) observed no impairment with a 2-h delay. Neither acute nor subchronic THC treatment during adulthood impaired SOR with a 1-h delay (Long et al 2010;Quinn et al 2008) but chronic hippocampal infusion of the cannabinoid agonist WIN 55,212-2 did impair performance (1 h; Barna et al 2007). Post-sample infusion of WIN 55,212-2 into CA1 had no effect in adult rats when the delay was 3 h, but did impair performance with a 24-h delay (Clarke et al 2008).…”

Section: Cannabinoidsmentioning

confidence: 96%

“…Many of the GM mice tested to date display impaired SOR, although results can vary between laboratories, perhaps highlighting the interaction between genotype and small differences in environmental/testing conditions or genetic background (Crabbe et al 1999) (Table 5). Mice heterozygous for a mutation in the transmembrane domain (TM) of neuregulin 1 (NRG1), for example, have been reported to be unimpaired with a 60-min delay (Long et al 2010) but impaired with a 10-min delay (Duffy et al 2010). This apparent discrepancy may reflect the use of male mice in one study and females in the other, as the effects of NRG1 disruption may be sex-specific (Taylor et al 2011;O'Tuathaigh et al 2006).…”

Section: Genetically Modified (Gm) Micementioning

confidence: 98%

Spontaneous object recognition and its relevance to schizophrenia: a review of findings from pharmacological, genetic, lesion and developmental rodent models

2011

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“…enhancement of prepulse inhibition (PPI), hypolocomotive and anxiogenic effects, selective increases in c-Fos expression ; Boucher et al 2007a, b]. This phenomenon is sex-specific, since female Nrg1 TM HET mice do not show increased behavioural sensitivity to acute THC treatment (Long et al 2010a). The role of Nrg1 in the response to cannabinoid agonists is further exemplified by altered rates of tolerance in adult Nrg1 TM HET mice to the locomotor and anxiogenic effects of the synthetic cannabinoid CP 55 940 (Boucher et al 2011).…”

Section: Introductionmentioning

confidence: 94%

Transmembrane domain Nrg1 mutant mice show altered susceptibility to the neurobehavioural actions of repeated THC exposure in adolescence

Long

Chesworth

Huang

et al. 2013

International Journal of Neuropsychopharmacology

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Heavy cannabis abuse increases the risk of developing schizophrenia. Adolescents appear particularly vulnerable to the development of psychosis-like symptoms after cannabis use. To test whether the schizophrenia candidate gene neuregulin 1 (NRG1) modulates the effects of cannabinoids in adolescence, we tested male adolescent heterozygous transmembrane domain Nrg1 mutant (Nrg1 TM HET) mice and wild type-like littermates (WT) for their neurobehavioural response to repeated Δ(9)-tetrahydrocannabinol (THC, 10 mg/kg i.p. for 21 d starting on post-natal day 31). During treatment and 48 h after treatment withdrawal, we assessed several behavioural parameters relevant to schizophrenia. After behavioural testing we measured autoradiographic CB(1), 5-HT(2A) and NMDA receptor binding. The hyperlocomotor phenotype typical of Nrg1 mutants emerged after drug withdrawal and was more pronounced in vehicle than THC-treated Nrg1 TM HET mice. All mice were equally sensitive to THC-induced suppression of locomotion. However, mutant mice appeared protected against inhibiting effects of repeated THC on investigative social behaviours. Neither THC nor Nrg1 genotype altered prepulse inhibition. Repeated adolescent THC promoted differential effects on CB(1) and 5-HT(2A) receptor binding in the substantia nigra and insular cortex respectively, decreasing binding in WT while increasing it in Nrg1 TM HET mice. THC also selectively affected 5-HT(2A) receptor binding in several other regions in WT mice, whereas NMDA receptor binding was only affected in mutant mice. Overall, Nrg1 mutation does not appear to increase the induction of psychotomimetic symptoms by repeated adolescent THC exposure but may attenuate some of its actions on social behaviour and schizophrenia-relevant neurotransmitter receptor profiles.

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A follow-up study: acute behavioural effects of Δ9-THC in female heterozygous Neuregulin 1 transmembrane domain mutant mice

Cited by 61 publications

References 52 publications

Exposure to an Enriched Environment Accelerates Recovery from Cerebellar Lesion

Exposure to an Enriched Environment Accelerates Recovery from Cerebellar Lesion

Spontaneous object recognition and its relevance to schizophrenia: a review of findings from pharmacological, genetic, lesion and developmental rodent models

Transmembrane domain Nrg1 mutant mice show altered susceptibility to the neurobehavioural actions of repeated THC exposure in adolescence

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