Neuregulin 1 hypomorphic mutant mice: enhanced baseline locomotor activity but normal psychotropic drug-induced hyperlocomotion and prepulse inhibition regulation

Buuse, Maarten van den; Wischhof, Lena; Lee, Ruo Xi; Martin, Sally; Karl, Tim

doi:10.1017/s1461145709000388

Cited by 88 publications

(67 citation statements)

References 40 publications

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“…They also showed PPI and LI disruptions, as well as increased drug-dependent disruption of PPI, but no spatial memory deficits. 263,268,269 No differences were reported in terms of DA or serotonin receptor numbers. 269 These mouse models are consistent with the literature on schizophrenia in humans and elucidate some possible schizophrenia-related biomarkers that can now be specifically examined in human patients.…”

Section: Neuregulin-1 (Nrg1)mentioning

confidence: 99%

Contribution of nonprimate animal models in understanding the etiology of schizophrenia

Lazar

Neufeld²,

Cain³

2011

jpn

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Section: Neuregulin-1 (Nrg1)mentioning

confidence: 99%

Contribution of nonprimate animal models in understanding the etiology of schizophrenia

Lazar

Neufeld²,

Cain³

2011

jpn

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“…Mice were given an injection dose of 0.5 mg/kg. The drug dosage used was based on previous studies showing a high locomotor response with little stereotypic or ataxic behaviours [44,45].…”

Section: Psychomimetic Drugsmentioning

confidence: 99%

Adult vitamin D deficiency leads to behavioural and brain neurochemical alterations in C57BL/6J and BALB/c mice

Groves

Kesby

Eyles

et al. 2013

Behavioural Brain Research

124

111

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Epidemiological evidence suggests that low levels of vitamin D may predispose people to develop depression and cognitive impairment. While rodent studies have demonstrated that prenatal vitamin D deficiency is associated with altered brain development, there is a lack of research examining adult vitamin D (AVD) deficiency.The aim of this study was to examine the impact of AVD deficiency on behaviour and brain function in the mouse. Ten-week old male C57BL/6J and BALB/c mice were fed a control or vitamin D deficient diet for 10 weeks prior to, and during behavioural testing. We assessed a broad range of behavioural domains, excitatory and inhibitory neurotransmission in brain tissue, and, in separate groups of mice, locomotor response to D-amphetamine and MK-801. Overall, AVD deficiency resulted in hyperlocomotion in a novel open field and reduced GAD65/67 levels in brain tissue. AVD-deficient BALB/c mice had altered behaviour on the elevated plus maze, altered responses to heat, sound and shock, and decreased levels of glutamate and glutamine, and increased levels of GABA and glycine. By contrast C57BL/6 mice had a more subtle phenotype with no further behavioural changes but significant elevations in serine, homovanillic acid and 5-hydroxyindoleacetic acid.Although the behavioural phenotype of AVD did not seem to model a specific disorder, the overall reduction in GAD65/67 levels associated with AVD deficiency may be relevant to a number of neuropsychiatric conditions. This is the first study to show an association between AVD deficiency and prominent changes in behaviour and brain neurochemistry in the mouse.3

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“…[15,32]). In our study, hyperlocomotion was accompanied by decreased resting behaviour in baseline conditions and increased distance travelled in the periphery post restraint stress.…”

Section: R Chesworth Et Al / Neuroscience Letters 515 (2012) 82-86mentioning

confidence: 99%

The response of neuregulin 1 mutant mice to acute restraint stress

Chesworth

Yulyaningsih

Cappas

et al. 2012

Neuroscience Letters

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Stress plays a role in the development and severity of psychotic symptoms and there may be a genetic component to stress vulnerability in schizophrenia. Using an established mouse model for schizophrenia, we investigated the behavioural and endocrine response of Nrg1 transmembrane domain mutant mice (Nrg1 HET) and wild type-like (WT) littermates to acute restraint stress. Animals were screened at 3-4 months and 6-7 months of age (before and after onset of hyperlocomotion) for open field behaviour and serum corticosterone levels. In younger mice, stress reduced locomotive and explorative measures and increased anxietylike behaviour regardless of genotype. Older Nrg1 mutants were less susceptible to the effects of stress on anxiety-related behaviours. All mice responded to restraint stress with robust increases in serum corticosterone. Importantly, the stress-induced increase in corticosterone was more pronounced in Nrg1 mutant than WT mice at the younger but not the older age. Our results suggest that transmembrane domain Nrg1 has only a moderate effect on the acute stress response of mice. The behavioural differences detected between WT and Nrg1 HET mice at the older age were evident without parallel modifications to the glucocorticoid system.

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Neuregulin 1 hypomorphic mutant mice: enhanced baseline locomotor activity but normal psychotropic drug-induced hyperlocomotion and prepulse inhibition regulation

Cited by 88 publications

References 40 publications

Contribution of nonprimate animal models in understanding the etiology of schizophrenia

Contribution of nonprimate animal models in understanding the etiology of schizophrenia

Adult vitamin D deficiency leads to behavioural and brain neurochemical alterations in C57BL/6J and BALB/c mice

The response of neuregulin 1 mutant mice to acute restraint stress

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