Dr Lauren Harms
School of Biomedical Sciences and Pharmacy (Human Physiology)
- Phone:(02) 4921 5664
I'm a Lecturer with the School of Biomedical Sciences and Pharmacy. I completed my PhD in Neuroscience from The University of Queensland in 2012. In my PhD, I trained at Queensland Brain Institute, where my research was focused on how environmental risk factors for neuropsychiatric disorders such as schizophrenia impact brain development and adult behaviour.
In my postdoctoral role at the University of Newcastle's School of Psychology, as well as my current role as a Lecturer with the School of Biomedical Sciences and Pharmacy, I have continued my research into how early-life exposures can contribute to disease risk. In particular, I focus on how exposure to immune activation during gestation can affect brain development and have a long-term impact on the ability of the brain to generate electrical impulses such as mismatch negativity (MMN) and high-frequency brain wave activity. In an integrative project, I examine how early-life and adolescent factors contribute to the brain's ability to generate electrophysiological signals and how these electrical changes affect cognitive behaviour, such as attention and memory.
- PhD (Neuroscience), University of Queensland
- Bachelor of Science (Neuroscience)(Honours), University of Queensland
- Animal models
- Behavioural neuroscience
- Mismatch negativity
Fields of Research
|170101||Biological Psychology (Neuropsychology, Psychopharmacology, Physiological Psychology)||30|
|110999||Neurosciences not elsewhere classified||70|
|Title||Organisation / Department|
|Lecturer||University of Newcastle
School of Biomedical Sciences and Pharmacy
|Lecturer||University of Newcastle
School of Psychology
For publications that are currently unpublished or in-press, details are shown in italics.
Journal article (21 outputs)
Harms L, Alston M, 'Postdisaster Social Work', Australian Social Work, 71 386-391 (2018) [C1]
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]
© 2017 Elsevier B.V. One of the most robust electrophysiological features of schizophrenia is reduced mismatch negativity, a component of the event related potential (ERP) induced... [more]
© 2017 Elsevier B.V. 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.
Duchatel RJ, Meehan CL, Harms LR, Michie PT, Bigland MJ, Smith DW, et al., 'Increased complement component 4 (C4) gene expression in the cingulate cortex of rats exposed to late gestation immune activation', SCHIZOPHRENIA RESEARCH, 199 442-444 (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]
© 2018 Animal models of maternal immune activation study the effects of infection, an environmental risk factor for schizophrenia, on brain development. Microglia activation and c... [more]
© 2018 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.
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]
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]
© 2016 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 ... [more]
© 2016 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.
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 N-Methyl-D-Aspartate Receptor Measures in Adult Rat Offspring', FRONTIERS IN PSYCHIATRY, 8 (2017) [C1]
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]
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]
© 2015. Interstitial neurons are located among white matter tracts of the human and rodent brain. Post-mortem studies have identified increased interstitial white matter neuron (I... [more]
© 2015. 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.
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]
© 2015 Elsevier B.V. The mismatch negativity (MMN) component of the auditory event-related potential, elicited in response to unexpected stimuli in the auditory environment, has g... [more]
© 2015 Elsevier B.V. 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.
Michie PT, Malmierca MS, Harms L, Todd J, 'The neurobiology of MMN and implications for schizophrenia', Biological Psychology, 116 90-97 (2016) [C1]
© 2016 Elsevier B.V. Although the scientific community appears to know a lot about MMN, about its neural generators and the computational processes that underlie its generation, d... [more]
© 2016 Elsevier B.V. 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.
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]
© 2015. 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 neur... [more]
© 2015. 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.
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]
© 2014 Harms et al. Mismatch negativity (MMN) is a scalp-recorded electrical potential that occurs in humans in response to an auditory stimulus that defies previously established... [more]
© 2014 Harms et al. 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.
Todd J, Harms L, Schall U, Michie PT, 'Mismatch negativity: Translating the potential', Frontiers in Psychiatry, 4 1-22 (2013) [C1]
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]
|Show 18 more journal articles|
Conference (6 outputs)
Rahman T, Zavitsanou K, Purves-Tyson T, Harms L, Meehan C, Schall U, et al., 'Maternal immune activation alters molecular indices of the NMDA receptor in the striatum', JOURNAL OF NEUROCHEMISTRY, Cairns, AUSTRALIA (2015) [E3]
Harms L, Zavitsanou K, Meehan C, Wong A, Fullham R, Todd J, et al., 'Examination of mismatch negativity, oscillatory activity and related neurochemistry in a developmental rat model of Schizophrenia', JOURNAL OF NEUROCHEMISTRY, Cairns, AUSTRALIA (2015) [E3]
Duchatel R, Jobling P, Graham B, Harms L, Michie P, Hodgson D, Tooney P, 'Modelling white matter neuron pathology in schizophrenia using maternal immune activation', JOURNAL OF NEUROCHEMISTRY, Cairns, AUSTRALIA (2015) [E3]
Harms LR, Hodgson D, Fulham W, Hunter M, Penttonen M, Schall U, et al., 'THE EFFECTS OF MATERNAL IMMUNE ACTIVATION AND MK-801 ON MISMATCH RESPONSES IN AWAKE, FREELY MOVING RATS', SCHIZOPHRENIA RESEARCH (2014)
Michie PT, Harms LR, Fulham WR, Penttonen M, Todd J, Hunter M, et al., 'Is the rodent brain capable of auditory deviance detection and MMN-like responses?', ACNS2012 - The 3rd Australasian Cognitive Neuroscience Conference. Program Book, Brisbane, Qld (2012) [E3]
Nakamura T, Harms LR, Fulham WR, Todd J, Schall UA, Michie PT, Hodgson DM, 'Advances in modeling an endophenotype of schizophrenia in rodents: Mismatch responses to frequency deviants', Abstract Book. Biological Psychiatry Australia Scientific Meeting, Parkville, Vic (2012) [E3]
|Show 3 more conferences|
Grants and Funding
|Number of grants||6|
Click on a grant title below to expand the full details for that specific grant.
20163 grants / $683,953
Maternal immune activation and adolescent exposure to cannabis in rodents: Do two developmental “hits” lead to schizophrenia-like changes in brain and behaviour?$654,403
Funding body: NHMRC (National Health & Medical Research Council)
|Funding body||NHMRC (National Health & Medical Research Council)|
|Project Team||Professor Deborah Hodgson, Emeritus Professor Patricia Michie, Professor Cynthia Weickert, Doctor Lauren Harms, Professor Ulli Schall, Associate Professor Juanita Todd|
|Type Of Funding||Aust Competitive - Commonwealth|
The impact of gamma oscillation disturbances on cognition: relevance for schizophrenia and possible treatment options$23,750
Funding body: Yakiti Family Trust
Funding body: Keats Endowment Research Fund
|Funding body||Keats Endowment Research Fund|
|Project Team||Doctor Lauren Harms, Professor Scott Brown, Professor Deborah Hodgson, Emeritus Professor Patricia Michie|
|Type Of Funding||C3112 - Aust Not for profit|
20151 grants / $22,000
Electrophysiology rig for the study of schizophrenia-related changes in white matter neurons after maternal infection$22,000
Funding body: Rebecca L Cooper Medical Research Foundation Ltd
|Funding body||Rebecca L Cooper Medical Research Foundation Ltd|
|Project Team||Associate Professor Paul Tooney, Doctor Phil Jobling, Associate Professor Brett Graham, Professor Deborah Hodgson, Emeritus Professor Patricia Michie, Doctor Lauren Harms|
|Type Of Funding||Grant - Aust Non Government|
20141 grants / $2,000
Funding body: University of Newcastle - Faculty of Science & IT
|Funding body||University of Newcastle - Faculty of Science & IT|
|Project Team||Doctor Lauren Harms|
|Scheme||PVC Conference Assistance Grant|
|Type Of Funding||Internal|
20131 grants / $3,000
Funding body: ATSE (Australian Academy of Technological Sciences and Engineering)
|Funding body||ATSE (Australian Academy of Technological Sciences and Engineering)|
|Project Team||Doctor Lauren Harms|
|Scheme||Australian Israel Research Exchange|
|Type Of Funding||Other Public Sector - Commonwealth|
Number of supervisions
|Commenced||Level of Study||Research Title||Program||Supervisor Type|
|2017||PhD||Exploring Electrophysiological Biomarkers of Schizophrenia in a Rat Model - Impact of Pharmacological Intervention on Cognition.||PhD (Psychology - Science), Faculty of Science, The University of Newcastle||Principal Supervisor|
|2017||PhD||The combined impact of two developmental risk factors for schizophrenia on inhibitory and excitatory systems in a rat model||PhD (Psychology - Science), Faculty of Science, The University of Newcastle||Co-Supervisor|
|2016||PhD||Effects of Prenatal Maternal Immune Activation and Adolescent Cannabis Exposure on Neurophysiology, Cognition and Behaviour||PhD (Psychology - Science), Faculty of Science, The University of Newcastle||Co-Supervisor|
|Year||Level of Study||Research Title||Program||Supervisor Type|
|2018||PhD||Perinatal Programming of Female Subfertility: The Impact of Neonatal Immune Activation on Behaviour, Ovarian Development, and the Brain||PhD (Psychology - Science), Faculty of Science, The University of Newcastle||Co-Supervisor|
|2018||PhD||The Role of Early Versus Late Gestational Maternal Immune Activation in the Aetiology of Schizophrenia: Establishing a Rat Model with a Focus on Cognitive Symptomology and Neuroinflammation||PhD (Psychology - Science), Faculty of Science, The University of Newcastle||Co-Supervisor|
The map is a representation of a researchers co-authorship with collaborators across the globe. The map displays the number of publications against a country, where there is at least one co-author based in that country. Data is sourced from the University of Newcastle research publication management system (NURO) and may not fully represent the authors complete body of work.
|Country||Count of Publications|
Dr Lauren Harms
School of Biomedical Sciences and Pharmacy
Faculty of Health and Medicine
|Phone||(02) 4921 5664|
Callaghan, NSW 2308