Models of Neurodevelopmental Abnormalities in Schizophrenia

Powell, Susan B.

doi:10.1007/7854_2010_57

Cited by 65 publications

(46 citation statements)

References 345 publications

(502 reference statements)

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“…Cognitive deficits are at the core of schizophrenia, including difficulties in problem solving, social cognition, and working memory (Powell, 2010). Therefore, rodent models have focused on tasks associated with learning and memory, working memory, and cognitive flexibility.…”

Section: Animal Models Of a Noisy Brainmentioning

confidence: 99%

Cellular and circuit models of increased resting-state network gamma activity in schizophrenia

White

Siegel

2016

Neuroscience

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Schizophrenia (SCZ) is a disorder characterized by positive symptoms (hallucinations, delusions), negative symptoms (blunted affect, alogia, reduced sociability, and anhedonia), as well as persistent cognitive deficits (memory, concentration, and learning). While the biology underlying subjective experiences is difficult to study, abnormalities in electroencephalographic (EEG) measures offer a means to dissect potential circuit and cellular changes in brain function. EEG is indispensable for studying cerebral information processing due to the introduction of techniques for the decomposition of event-related activity into its frequency components. Specifically, brain activity in the gamma frequency range (30–80Hz) is thought to underlie cognitive function and may be used as an endophenotype to aid in diagnosis and treatment of SCZ. In this review we address evidence indicating that there is increased resting state gamma power in SCZ. We address how modeling this aspect of the illness in animals may help treatment development as well as providing insight into the etiology of SCZ.

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Section: Animal Models Of a Noisy Brainmentioning

confidence: 99%

Cellular and circuit models of increased resting-state network gamma activity in schizophrenia

White

Siegel

2016

Neuroscience

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“…We can only comment selectively on this extensive literature; more comprehensive reviews can be found elsewhere (e.g. Powell, 2010; Powell and Geyer, 2002; Powell et al, 2009, 2012; Swerdlow et al, 2008). …”

Section: Introductionmentioning

confidence: 99%

Sensorimotor gating of the startle reflex: what we said 25 years ago, what has happened since then, and what comes next

2016

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Our 1992 paper, ‘The neural substrates of sensorimotor gating of the startle reflex: a review of recent findings and their implications’, reviewed a series of (then) new and preliminary findings from cross-species studies of prepulse inhibition of the startle reflex, and commented on their implications. At the time that the report was composed, PubMed listed about 40 citations for studies using the search term ‘prepulse inhibition’. In the ensuing 25 years, the field has added about 2700 such reports, reflecting the substantial growth in interest in prepulse inhibition and its utility across a number of different experimental applications. The 30th anniversary of the Journal of Psychopharmacology provides an opportunity to comment briefly on what was described in that 1992 report, how the field has progressed in the subsequent decades, and the paths forward for studies of prepulse inhibition and its use as an operational measure of sensorimotor gating. Among these future paths, we highlight the use of prepulse inhibition as: an endophenotype for genomic studies, and a biomarker for healthy brain circuitry, which may predict sensitivity to psychotherapeutics. Our 1992 report was highly speculative and based on paper-thin empirical data, yet viewed in a certain light, it appears to have contained a basic roadmap for a journey spanning the next 25 years of prepulse inhibition research… and ‘what a long, strange trip it’s been’.

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“…The terms isolation rearing or isolation housing are commonly used to denote social isolation of adolescent (post-weaning) or adult rats, respectively. The consequences of isolation are more severe in rats compared with other rodent species (Einon et al, 1981) and it has been argued that social isolation of rats has a good etiological validity to model human mental illness (Powell, 2010; Czéh et al, 2016). Given the emerging important role of BDNF in stress-related mental disorders, the aim of our investigation was to systematically summarize current evidence for altered BDNF signaling in experimental studies employing chronic social isolation of rats.…”

Section: Introductionmentioning

confidence: 99%

The Evidence for Altered BDNF Expression in the Brain of Rats Reared or Housed in Social Isolation: A Systematic Review

Murínová

Hlavacova

Chmelova

et al. 2017

Front. Behav. Neurosci.

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There is evidence that development and maintenance of neural connections are disrupted in major mental disorders, which indicates that neurotrophic factors could play a critical role in their pathogenesis. Stress is a well-established risk factor for psychopathology and recent research suggests that disrupted signaling via brain-derived neurotrophic factor (BDNF) may be involved in mediating the negative effects of stress on the brain. Social isolation of rats elicits chronic stress and is widely used as an animal model of mental disorders such as schizophrenia and depression. We carried out a systematic search of published studies to review current evidence for an altered expression of BDNF in the brain of rats reared or housed in social isolation. Across all age groups (post-weaning, adolescent, adult), majority of the identified studies (16/21) reported a decreased expression of BDNF in the hippocampus. There are far less published data on BDNF expression in other brain regions. Data are also scarce to assess the behavioral changes as a function of BDNF expression, but the downregulation of BDNF seems to be associated with increased anxiety-like symptoms. The reviewed data generally support the putative involvement of BDNF in the pathogenesis of stress-related mental illness. However, the mechanisms linking chronic social isolation, BDNF expression and the elicited behavioral alterations are currently unknown.

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Models of Neurodevelopmental Abnormalities in Schizophrenia

Cited by 65 publications

References 345 publications

Cellular and circuit models of increased resting-state network gamma activity in schizophrenia

Cellular and circuit models of increased resting-state network gamma activity in schizophrenia

Sensorimotor gating of the startle reflex: what we said 25 years ago, what has happened since then, and what comes next

The Evidence for Altered BDNF Expression in the Brain of Rats Reared or Housed in Social Isolation: A Systematic Review

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