2023 |
Jalewa J, Todd J, Michie PT, Hodgson DM, Harms L, 'The effect of schizophrenia risk factors on mismatch responses in a rat model.', Psychophysiology, 60 e14175 (2023) [C1]
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Nova |
2022 |
Cuskelly A, Hoedt EC, Harms L, Talley NJ, Tadros MA, Keely S, Hodgson DM, 'Neonatal immune challenge influences the microbiota and behaviour in a sexually dimorphic manner', BRAIN BEHAVIOR AND IMMUNITY, 103 232-242 (2022) [C1]
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Nova |
2021 |
Harms L, Parras GG, Michie PT, Malmierca MS, 'The Role of Glutamate Neurotransmission in Mismatch Negativity (MMN), A Measure of Auditory Synaptic Plasticity and Change-detection', Neuroscience, 456 106-113 (2021) [C1]
Mismatch negativity (MMN) is an electrophysiological signature that occurs in response to unexpected stimuli. It is often referred to as a measure of memory-based change detection... [more]
Mismatch negativity (MMN) is an electrophysiological signature that occurs in response to unexpected stimuli. It is often referred to as a measure of memory-based change detection, because the elicitation of a prediction error response relies on the formation of a prediction, which in turn, is dependent upon intact memory of previous auditory stimulation. As such, the MMN is altered in conditions in which memory is affected, such as Alzheimer's disease, schizophrenia and healthy aging. The most prominent pharmacological finding for MMN strengthens the link between MMN and synaptic plasticity, as glutamate N-methyl-D-aspartate receptor (NMDA-R) antagonists reduce the MMN response. However, recent data has begun to demonstrate that the link between NMDA-R function and MMN is not as clear as once thought, with low dose and low affinity NMDA-R antagonists observed to facilitate MMN.
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Nova |
2021 |
Jalewa J, Todd J, Michie PT, Hodgson DM, Harms L, 'Do rat auditory event related potentials exhibit human mismatch negativity attributes related to predictive coding?', Hearing Research, 399 (2021) [C1]
Rodent models play a significant role in understanding disease mechanisms and the screening of new treatments. With regard to psychiatric disorders such as schizophrenia, however,... [more]
Rodent models play a significant role in understanding disease mechanisms and the screening of new treatments. With regard to psychiatric disorders such as schizophrenia, however, it is difficult to replicate the human symptoms in rodents because these symptoms are often either ¿uniquely human¿ or are only conveyed via self-report. There is a growing interest in rodent mismatch responses (MMRs) as a translatable ¿biomarker¿ for disorders such as schizophrenia. In this review, we will summarize the attributes of human MMN, and discuss the scope of exploring the attributes of human MMN in rodents. Here, we examine how reliably MMRs that are measured in rats mimic human attributes, and present original data examining whether manipulations of stimulus conditions known to modulate human MMN, do the same for rat MMRs. Using surgically-implanted epidural electroencephalographic electrodes and wireless telemetry in freely-moving rats, we observed human-like modulations of MMRs, namely that larger MMRs were elicited to unexpected (deviant) stimuli that a) had a larger change in pitch compared to the expected (standard) stimulus, b) were less frequently presented (lower probability), and c) had no jitter (stable stimulus onset asynchrony) compared to high jitter. Overall, these findings contribute to the mounting evidence for rat MMRs as a good analogue of human MMN, bolstering the development of a novel approach in future to validate the preclinical models based on a translatable biomarker, MMN.
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Nova |
2021 |
Michie P, Jalewa J, Harms L, Todd J, Hodgson D, 'Mismatch Negativity (MMN) as a Promising Translational Neurophysiological Biomarker in Schizophrenia', Psychiatria et Neurologia Japonica - Seishin Shinkeigaku Zasshi, 123 824-841 (2021)
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2020 |
Dunn AL, Michie PT, Hodgson DM, Harms L, 'Adolescent cannabinoid exposure interacts with other risk factors in schizophrenia: A review of the evidence from animal models', Neuroscience and Biobehavioral Reviews, 116 202-220 (2020) [C1]
Many factors and their interaction are linked to the aetiology of schizophrenia, leading to the development of animal models of multiple risk factors and adverse exposures. Differ... [more]
Many factors and their interaction are linked to the aetiology of schizophrenia, leading to the development of animal models of multiple risk factors and adverse exposures. Differentiating between separate and combined effects for each factor could better elucidate schizophrenia pathology, and drive development of preventative strategies for high-load risk factors. An epidemiologically valid risk factor commonly associated with schizophrenia is adolescent cannabis use. The aim of this review is to evaluate how early-life adversity from various origins, in combination with adolescent cannabinoid exposure interact, and whether these interactions confer main, synergistic or protective effects in animal models of schizophrenia-like behavioural, cognitive and morphological alterations. Patterns emerge regarding which models show consistent synergistic or protective effects, particularly those models incorporating early-life exposure to maternal deprivation and maternal immune activation, and sex-specific effects are observed. It is evident that more research needs to be conducted to better understand the risks and alterations of interacting factors, with particular interest in sex differences, to better understand the translatability of these preclinical models to humans.
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Nova |
2020 |
Parras GG, Valdés-Baizabal C, Harms L, Michie PT, Malmierca MS, 'The effect of NMDA-R antagonist, MK-801, on neuronal mismatch along the rat auditory thalamocortical pathway', Scientific Reports, 10 (2020) [C1]
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Nova |
2020 |
Katz-Barber MW, Hollins SL, Cuskelly A, Leong AJW, Dunn A, Harms L, Hodgson DM, 'Investigating the gut-brain axis in a neurodevelopmental rodent model of schizophrenia.', Brain, behavior, & immunity - health, 3 100048 (2020) [C1]
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Nova |
2020 |
Rahman T, Weickert CS, Harms L, Meehan C, Schall U, Todd J, et al., 'Effect of Immune Activation during Early Gestation or Late Gestation on Inhibitory Markers in Adult Male Rats', Scientific Reports, 10 (2020) [C1]
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Nova |
2019 |
Duchatel RJ, Harms LR, Meehan CL, Michie PT, Bigland MJ, Smith DW, et al., 'Reduced cortical somatostatin gene expression in a rat model of maternal immune activation', PSYCHIATRY RESEARCH, 282 (2019) [C1]
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Nova |
2018 |
Harms L, Fulham WR, Todd J, Meehan C, Schall U, Hodgson DM, Michie PT, 'Late deviance detection in rats is reduced, while early deviance detection is augmented by the NMDA receptor antagonist MK-801', Schizophrenia Research, 191 43-50 (2018) [C1]
One of the most robust electrophysiological features of schizophrenia is reduced mismatch negativity, a component of the event related potential (ERP) induced by rare and unexpect... [more]
One of the most robust electrophysiological features of schizophrenia is reduced mismatch negativity, a component of the event related potential (ERP) induced by rare and unexpected stimuli in an otherwise regular pattern. Emerging evidence suggests that mismatch negativity (MMN) is not the only ERP index of deviance detection in the mammalian brain and that sensitivity to deviant sounds in a regular background can be observed at earlier latencies in both the human and rodent brain. Pharmacological studies in humans and rodents have previously found that MMN reductions similar to those seen in schizophrenia can be elicited by N-methyl-D-aspartate (NMDA) receptor antagonism, an observation in agreement with the hypothesised role of NMDA receptor hypofunction in schizophrenia pathogenesis. However, it is not known how NMDA receptor antagonism affects early deviance detection responses. Here, we show that NMDA antagonism impacts both early and late deviance detection responses. By recording EEG in awake, freely-moving rats in a drug-free condition and after varying doses of NMDA receptor antagonist MK-801, we found the hypothesised reduction of deviance detection for a late, negative potential (N55). However, the amplitude of an early component, P13, as well as deviance detection evident in the same component, were increased by NMDA receptor antagonism. These findings indicate that late deviance detection in rats is similar to human MMN, but the surprising effect of MK-801 in increasing ERP amplitudes as well as deviance detection at earlier latencies suggests that future studies in humans should examine ERPs over early latencies in schizophrenia and after NMDA antagonism.
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Nova |
2018 |
Duchatel RJ, Meehan CL, Harms LR, Michie PT, Bigland MJ, Smith DW, et al., 'Increased complement component 4 (
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2018 |
Duchatel RJ, Meehan CL, Harms LR, Michie PT, Bigland MJ, Smith DW, et al., 'Late gestation immune activation increases IBA1-positive immunoreactivity levels in the corpus callosum of adult rat offspring', Psychiatry Research, 266 175-185 (2018) [C1]
Animal models of maternal immune activation study the effects of infection, an environmental risk factor for schizophrenia, on brain development. Microglia activation and cytokine... [more]
Animal models of maternal immune activation study the effects of infection, an environmental risk factor for schizophrenia, on brain development. Microglia activation and cytokine upregulation may have key roles in schizophrenia neuropathology. We hypothesised that maternal immune activation induces changes in microglia and cytokines in the brains of the adult offspring. Maternal immune activation was induced by injecting polyriboinosinic:polyribocytidylic acid into pregnant rats on gestational day (GD) 10 or GD19, with brain tissue collected from the offspring at adulthood. We observed no change in Iba1, Gfap, IL1-ß and TNF-a mRNA levels in the cingulate cortex (CC) in adult offspring exposed to maternal immune activation. Prenatal exposure to immune activation had a significant main effect on microglial IBA1-positive immunoreactive material (IBA1+IRM) in the corpus callosum; post-hoc analyses identified a significant increase in GD19 offspring, but not GD10. No change in was observed in the CC. In contrast, maternal immune activation had a significant main effect on GFAP+IRM in the CC at GD19 (not GD10); post-hoc analyses only identified a strong trend towards increased GFAP+IRM in the GD19 offspring, with no white matter changes. This suggests late gestation maternal immune activation causes subtle alterations to microglia and astrocytes in the adult offspring.
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Nova |
2018 |
Hollins SL, Brock L, Barreto R, Harms L, Dunn A, Garcia-Sobrinho P, et al., 'A rodent model of anxiety: The effect of perinatal immune challenges on gastrointestinal inflammation and integrity', NeuroImmunoModulation, 25 163-175 (2018) [C1]
Objectives: Gastrointestinal (GI) inflammation and GI integrity deficits are common comorbidities of neuropsychiatric disorders. Ongoing research suggests that these aberrations m... [more]
Objectives: Gastrointestinal (GI) inflammation and GI integrity deficits are common comorbidities of neuropsychiatric disorders. Ongoing research suggests that these aberrations may be contributing to heightened immune signals that have the potential to disrupt neuronal homeostasis and exacerbate behavioural deficits. The current study aimed to determine whether the well-characterized animal model of neuropsychopathology, the maternal immune activation (MIA) model, produced GI inflammation and integrity disruptions in association with anxiety-like behaviour. Methods: Pregnant Wistar rats were exposed to the viral mimetic polyriboinosinic:polyribocytidilic acid (polyI:C) on gestational days (GD) 10 and 19. Evidence of ANS activation, GI inflammation, and GI barrier integrity was assessed in both neonatal (postnatal day, P7) and adult (P84) offspring. Anxiety-like behaviour was assessed at P100. Results: Neonatal MIA offspring exhibited an altered intestinal inflammatory profile and evidence of an increase in lymphoid aggregates. MIA neonates also displayed disruptions to GI barrier tight junction protein mRNA. In addition, adult MIA offspring exhibited an increase in anxiety-like behaviours. Conclusion: These results indicate that the MIA rat model, which is well documented to produce behavioural, neurochemical, and neuroanatomical abnormalities, also produces GI inflammation and integrity disruptions. We suggest that this model may be a useful tool to elucidate biological pathways associated with neuropsychiatric disorders.
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Nova |
2018 |
Gray A, Tattoli R, Dunn A, Hodgson DM, Michie PT, Harms L, 'Maternal immune activation in mid-late gestation alters amphetamine sensitivity and object recognition, but not other schizophrenia-related behaviours in adult rats.', Behavioural brain research, 358-364 (2018) [C1]
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Nova |
2017 |
Meehan C, Harms L, Frost JD, Barreto R, Todd J, Schall U, et al., 'Effects of immune activation during early or late gestation on schizophrenia-related behaviour in adult rat offspring', Brain, Behavior, and Immunity, 63 8-20 (2017) [C1]
Maternal exposure to infectious agents during gestation has been identified as a significant risk factor for schizophrenia. Using a mouse model, past work has demonstrated that th... [more]
Maternal exposure to infectious agents during gestation has been identified as a significant risk factor for schizophrenia. Using a mouse model, past work has demonstrated that the gestational timing of the immune-activating event can impact the behavioural phenotype and expression of dopaminergic and glutamatergic neurotransmission markers in the offspring. In order to determine the inter-species generality of this effect to rats, another commonly used model species, the current study investigated the impact of a viral mimetic Poly (I:C) at either an early (gestational day 10) or late (gestational day 19) time-point on schizophrenia-related behaviour and neurotransmitter receptor expression in rat offspring. Exposure to Poly (I:C) in late, but not early, gestation resulted in transient impairments in working memory. In addition, male rats exposed to maternal immune activation (MIA) in either early or late gestation exhibited sensorimotor gating deficits. Conversely, neither early nor late MIA exposure altered locomotor responses to MK-801 or amphetamine. In addition, increased dopamine 1 receptor mRNA levels were found in the nucleus accumbens of male rats exposed to early gestational MIA. The findings from this study diverge somewhat from previous findings in mice with MIA exposure, which were often found to exhibit a more comprehensive spectrum of schizophrenia-like phenotypes in both males and females, indicating potential differences in the neurodevelopmental vulnerability to MIA exposure in the rat with regards to schizophrenia related changes.
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Nova |
2017 |
Rahman T, Zavitsanou K, Purves-Tyson T, Harms LR, Meehan C, Schall U, et al., 'Effects of Immune Activation during Early or Late Gestation on
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Nova |
2017 |
Fuller EA, Sominsky L, Sutherland JM, Redgrove KA, Harms L, McLaughlin EA, Hodgson DM, 'Neonatal immune activation depletes the ovarian follicle reserve and alters ovarian acute inflammatory mediators in neonatal rats', BIOLOGY OF REPRODUCTION, 97 719-730 (2017) [C1]
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Nova |
2016 |
Duchatel RJ, Jobling P, Graham BA, Harms LR, Michie PT, Hodgson DM, Tooney PA, 'Increased white matter neuron density in a rat model of maternal immune activation - Implications for schizophrenia', Progress in Neuro-Psychopharmacology and Biological Psychiatry, 65 118-126 (2016) [C1]
Interstitial neurons are located among white matter tracts of the human and rodent brain. Post-mortem studies have identified increased interstitial white matter neuron (IWMN) den... [more]
Interstitial neurons are located among white matter tracts of the human and rodent brain. Post-mortem studies have identified increased interstitial white matter neuron (IWMN) density in the fibre tracts below the cortex in people with schizophrenia. The current study assesses IWMN pathology in a model of maternal immune activation (MIA); a risk factor for schizophrenia. Experimental MIA was produced by an injection of polyinosinic:polycytidylic acid (PolyI:C) into pregnant rats on gestational day (GD) 10 or GD19. A separate control group received saline injections. The density of neuronal nuclear antigen (NeuN<sup>+</sup>) and somatostatin (SST<sup>+</sup>) IWMNs was determined in the white matter of the corpus callosum in two rostrocaudally adjacent areas in the 12week old offspring of GD10 (n=10) or GD19 polyI:C dams (n=18) compared to controls (n=20). NeuN<sup>+</sup> IWMN density trended to be higher in offspring from dams exposed to polyI:C at GD19, but not GD10. A subpopulation of these NeuN<sup>+</sup> IWMNs was shown to express SST. PolyI:C treatment of dams induced a significant increase in the density of SST<sup>+</sup> IWMNs in the offspring when delivered at both gestational stages with more regionally widespread effects observed at GD19. A positive correlation was observed between NeuN<sup>+</sup> and SST<sup>+</sup> IWMN density in animals exposed to polyI:C at GD19, but not controls. This is the first study to show that MIA increases IWMN density in adult offspring in a similar manner to that seen in the brain in schizophrenia. This suggests the MIA model will be useful in future studies aimed at probing the relationship between IWMNs and schizophrenia.
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Nova |
2016 |
Michie PT, Malmierca MS, Harms L, Todd J, 'Understanding the neurobiology of MMN and its reduction in schizophrenia', BIOLOGICAL PSYCHOLOGY, 116 1-3 (2016)
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2016 |
Harms L, Michie PT, Näätänen R, 'Criteria for determining whether mismatch responses exist in animal models: Focus on rodents', Biological Psychology, 116 28-35 (2016) [C1]
The mismatch negativity (MMN) component of the auditory event-related potential, elicited in response to unexpected stimuli in the auditory environment, has great value for cognit... [more]
The mismatch negativity (MMN) component of the auditory event-related potential, elicited in response to unexpected stimuli in the auditory environment, has great value for cognitive neuroscience research. It is changed in several neuropsychiatric disorders such as schizophrenia. The ability to measure and manipulate MMN-like responses in animal models, particularly rodents, would provide an enormous opportunity to learn more about the neurobiology underlying MMN. However, the MMN in humans is a very specific phenomenon: how do we decide which features we should focus on emulating in an animal model to achieve the highest level of translational validity? Here we discuss some of the key features of MMN in humans and summarise the success with which they have been translated into rodent models. Many studies from several different labs have successfully shown that the rat brain is capable of generating deviance detection responses that satisfy of the criteria for the human MMN.
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Nova |
2016 |
Michie PT, Malmierca MS, Harms L, Todd J, 'The neurobiology of MMN and implications for schizophrenia', Biological Psychology, 116 90-97 (2016) [C1]
Although the scientific community appears to know a lot about MMN, about its neural generators and the computational processes that underlie its generation, do we have sufficient ... [more]
Although the scientific community appears to know a lot about MMN, about its neural generators and the computational processes that underlie its generation, do we have sufficient knowledge to understand what causes the reduction of MMN amplitude in schizophrenia? Here we attempt to integrate the evidence presented in this series of papers for the special issue on MMN in schizophrenia together with evidence from other new relevant research and ask-what have we learnt? While MMN research was the purview for decades of psychophysiologists interested in event-related potentials derived from scalp recorded EEG, it is now part of mainstream neuroscience research attracting the interest of basic auditory neuroscientists, neurobiologists and computational modellers. The confluence of these developments together with increasing clinical research has certainly advanced our understanding of the causes of reduced MMN in schizophrenia as this integrative review attempts to demonstrate-but much remains to be learnt. Future advances will rely on the application of multiple methodologies and approaches in order to arrive at better understanding of the neurobiology of MMN and implications for schizophrenia.
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Nova |
2016 |
Harms L, 'Mismatch responses and deviance detection in N-methyl-D-aspartate (NMDA) receptor hypofunction and developmental models of schizophrenia', Biological Psychology, 116 75-81 (2016) [C1]
Reductions in the size of the mismatch negativity (MMN), an event-related potential component elicited in response to unexpected stimuli, are arguably the most robust neurophysiol... [more]
Reductions in the size of the mismatch negativity (MMN), an event-related potential component elicited in response to unexpected stimuli, are arguably the most robust neurophysiological findings in schizophrenia. Several studies have now demonstrated that 'true' human-like deviance detection mismatch responses (MMRs) can be generated in the rodent brain and therefore that animal models can be used to examine the neurobiology of schizophrenia-like MMR impairments and investigate the efficacy of new treatments in addressing underlying neurobiological mechanisms. Two broad categories of animal models have been examined for schizophrenia-like MMRs: models involving N-methyl- D-aspartate receptor hypofunction, and models involving an insult or exposure during development. While these models have been shown to exhibit reductions in MMRs, it is still unclear whether or not these reductions involve changes to neural adaptation to repetitive stimuli or whether they reflect impairments in the response to unexpected deviations in regular patterns.
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Nova |
2014 |
Harms L, Fulham WR, Todd J, Budd TW, Hunter M, Meehan C, et al., 'Mismatch negativity (MMN) in freely-moving rats with several experimental controls', PLoS ONE, 9 (2014) [C1]
Mismatch negativity (MMN) is a scalp-recorded electrical potential that occurs in humans in response to an auditory stimulus that defies previously established patterns of regular... [more]
Mismatch negativity (MMN) is a scalp-recorded electrical potential that occurs in humans in response to an auditory stimulus that defies previously established patterns of regularity. MMN amplitude is reduced in people with schizophrenia. In this study, we aimed to develop a robust and replicable rat model of MMN, as a platform for a more thorough understanding of the neurobiology underlying MMN. One of the major concerns for animal models of MMN is whether the rodent brain is capable of producing a human-like MMN, which is not a consequence of neural adaptation to repetitive stimuli. We therefore tested several methods that have been used to control for adaptation and differential exogenous responses to stimuli within the oddball paradigm. Epidural electroencephalographic electrodes were surgically implanted over different cortical locations in adult rats. Encephalographic data were recorded using wireless telemetry while the freely-moving rats were presented with auditory oddball stimuli to assess mismatch responses. Three control sequences were utilized: the flip-flop control was used to control for differential responses to the physical characteristics of standards and deviants; the many standards control was used to control for differential adaptation, as was the cascade control. Both adaptation and adaptation-independent deviance detection were observed for high frequency (pitch), but not low frequency deviants. In addition, the many standards control method was found to be the optimal method for observing both adaptation effects and adaptation-independent mismatch responses in rats. Inconclusive results arose from the cascade control design as it is not yet clear whether rats can encode the complex pattern present in the control sequence. These data contribute to a growing body of evidence supporting the hypothesis that rat brain is indeed capable of exhibiting human-like MMN, and that the rat model is a viable platform for the further investigation of the MMN and its associated neurobiology.
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Nova |
2013 |
Todd J, Harms L, Schall U, Michie PT, 'Mismatch negativity: Translating the potential', Frontiers in Psychiatry, 4 1-22 (2013) [C1]
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Nova |
2013 |
Harms LR, Michie PT, 'Understanding the pathological mechanisms underpinning functional impairments in schizophrenia: Gamma oscillations versus mismatch negativity (MMN) as mediating factors', Clinical Neurophysiology, 124 2075-2076 (2013) [C3]
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2012 |
Harms LR, Cowin G, Eyles DW, Kurniawan ND, McGrath JJ, Burne THJ, 'Neuroanatomy and psychomimetic-induced locomotion in C57BL/6J and 129/X1SvJ mice exposed to developmental vitamin D deficiency', BEHAVIOURAL BRAIN RESEARCH, 230 125-131 (2012) [C1]
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2012 |
Harms LR, Turner KM, Eyles DW, Young JW, McGrath JJ, Burne THJ, 'Attentional Processing in C57BL/6J Mice Exposed to Developmental Vitamin D Deficiency', PLOS ONE, 7 (2012) [C1]
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2012 |
Formella I, Scott EK, Burne THJ, Harms LR, Liu P-Y, Turner KM, et al., 'Transient Knockdown of Tyrosine Hydroxylase during Development Has Persistent Effects on Behaviour in Adult Zebrafish (
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2011 |
Harms LR, Burne THJ, Eyles DW, McGrath JJ, 'Vitamin D and the brain', BEST PRACTICE & RESEARCH CLINICAL ENDOCRINOLOGY & METABOLISM, 25 657-669 (2011) [C1]
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2009 |
Eyles DW, Feron F, Cui X, Kesby JP, Harms LH, Ko P, et al., 'Developmental vitamin D deficiency causes abnormal brain development', Psychoneuroendocrinology, 34 (2009)
There is now clear evidence that vitamin D is involved in brain development. Our group is interested in environmental factors that shape brain development and how this may be rele... [more]
There is now clear evidence that vitamin D is involved in brain development. Our group is interested in environmental factors that shape brain development and how this may be relevant to neuropsychiatric diseases including schizophrenia. The origins of schizophrenia are considered developmental. We hypothesised that developmental vitamin D (DVD) deficiency may be the plausible neurobiological explanation for several important epidemiological correlates of schizophrenia namely: (1) the excess winter/spring birth rate, (2) increased incidence of the disease in 2nd generation Afro-Caribbean migrants and (3) increased urban birth rate. Moreover we have published two pieces of direct epidemiological support for this hypothesis in patients. In order to establish the "Biological Plausibility" of this hypothesis we have developed an animal model to study the effect of DVD deficiency on brain development. We do this by removing vitamin D from the diet of female rats prior to breeding. At birth we return all dams to a vitamin D containing diet. Using this procedure we impose a transient, gestational vitamin D deficiency, while maintaining normal calcium levels throughout. The brains of offspring from DVD-deficient dams are characterised by (1) a mild distortion in brain shape, (2) increased lateral ventricle volumes, (3) reduced differentiation and (4) diminished expression of neurotrophic factors. As adults, the alterations in ventricular volume persist and alterations in brain gene and protein expression emerge. Adult DVD-deficient rats also display behavioural sensitivity to agents that induce psychosis (the NMDA antagonist MK-801) and have impairments in attentional processing. In this review we summarise the literature addressing the function of vitamin D on neuronal and non-neuronal cells as well as in vivo results from DVD-deficient animals. Our conclusions from these data are that vitamin D is a plausible biological risk factor for neuropsychiatric disorders and that vitamin D acts as a neurosteroid with direct effects on brain development. Crown Copyright © 2009.
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2008 |
Harms LR, Eyles DW, McGrath JJ, Mackay-Sim A, Burne THJ, 'Developmental vitamin D deficiency alters adult behaviour in 129/SvJ and C57BL/6J mice', BEHAVIOURAL BRAIN RESEARCH, 187 343-350 (2008) [C1]
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