Dr Greer Bennett
School of Biomedical Sciences and Pharmacy
- Phone:(02) 4924 6937
Dr Greer Bennett is a researcher interested in maternal mental health and the programming effects this can have on health behaviours in babies, children and adults. Greer has a strong background in research and behavioural neuroscience having completed her PhD with the Mothers and Babies Research Centre (Priority Research Centre for Pregnancy and Reproduction) in 2015. During her PhD studies, Greer published a number of peer reviewed publications in high ranking journals such as Developmental Neuroscience and Psychoneuroendocrinology and presented her work at over a dozen national and international conferences around the world including South America, the Netherlands and Singapore, receiving a travel award from the Australian Neuroscience Society in 2014.
In 2013 Greer concurrently took an appointment as the Convenor of the Newcastle branch of the Australian Society for Medical Research (ASMR) committee and led a number of key networking and professional development events such as Medical Research Week gala dinners and also assisted with the inaugural ASMR Scientific Meeting held in Newcastle in 2014.
Greer has also worked as a Scientific and Research Liaison with the Hunter Medical Research Institute (HMRI) creating innovative ways to promote local research and translate scientific findings to the community via the redevelopment of the HMRI website. Greer led the creation of scientific written and video content on this website redevelopment project and completed substantive interviews with research leaders across the Hunter region to develop innovative researcher profiles and research summaries now available online.
Greer holds a Bachelor of Biomedical Science (Class I Honours) from the University of Newcastle and has received an Australian Postgraduate Award (APA) to complete her PhD studies.
Dr Greer Bennett is currently a Senior Project Officer with the Hunter Institute of Mental Health (an organisation within the Hunter New England Local Health District) working to promote mental health and prevent mental illness in particularly vulnerable populations of people. As a part of the Child, Youth and Wellbeing team at this institute, she has a particular interest in promoting mental health early in life to give children the best possible start and prevent mental illnesses from occurring in adulthood.
Greer's research strengths lie in quantitative and qualitative data collection and analysis having a background in basic neuroscience and more recently, in population based research projects with the Hunter Institute of Mental Health.
- Doctor of Philosophy, University of Newcastle
- Bachelor of Biomedical Sciences, University of Newcastle
- Bachelor of Biomedical Sciences (Hons), University of Newcastle
- Brain Development
- Child Development
- Mental Health
- English (Mother)
Fields of Research
|Dates||Title||Organisation / Department|
|29/02/2016 -||Conjoint Lecturer||University of Newcastle
|Dates||Title||Organisation / Department|
Senior Project Officer
As a Senior Project Officer with the Hunter Institute of Mental Health, I am responsible for the Start Well research project which aims to identify ways to promote resilience and wellbeing in early career school teachers.
|Hunter Institute of Mental Health, Hunter Area Health Service
|24/08/2015 - 18/11/2016||
Scientific and Research Liaison (contract)
As the Scientific and Research Liaison at HMRI, I worked to foster new and innovative pathways for Hunter researchers to collaborate and progress their careers. Using my scientific training and keen interest in health promotion, I provided an informed perspective on how to best enable high quality research outcomes.
|Hunter Medical Research Institute (HMRI)
|1/01/2013 - 1/09/2014||
Committee Convenor (Newcastle Branch)
In this position I was responsible for the organisation of various events within the Hunter Region area to promote local medical research to both the scientific and lay community.
|Australian Society for Medical Research (ASMR)
|Dates||Title||Organisation / Department|
|1/03/2014 - 1/07/2015||
I have been involved with casual tutoring of the Bachelor of Biomedical Science at the University of Newcastle, providing academic help and guidance to students in class sizes of approximately 30 undergraduate students.
|The University of Newcastle - Faculty of Health and Medicine
Australian Neuroscience Society (ANS)
Australian Postgraduate Award (APA)
Department of Education
Mothers and Babies Research Centre
Deputy Vice-Chancellor Honours Scholarship
The University of Newcastle
For publications that are currently unpublished or in-press, details are shown in italics.
Chapter (1 outputs)
Palliser HK, Bennett GA, Kelleher MA, Cumberland AL, Walker DW, Hirst JJ, 'Models of perinatal compromises in the guinea pig: Their use in showing the role of neurosteroids in pregnancy and the newborn', Neuromethods 221-243 (2016) [B1]
Â© Springer Science+Business Media New York 2016. Placental progesterone production during late gestation has a major role in maintaining elevated neurosteroid levels during pregn... [more]
Â© Springer Science+Business Media New York 2016. Placental progesterone production during late gestation has a major role in maintaining elevated neurosteroid levels during pregnancy. These levels of key neurosteroids, including allopregnanolone, are critical for optimal brain development during late gestation and the early neonatal period. The long gestation period (~70), in utero brain development and placental progesterone synthesis of the guineas pig makes this species very suitable for studying the mechanisms by which pregnancy compromises impact neurosteroid pathways. We have used models of intrauterine growth restriction and preterm birth to show that these challenges may suppress neurosteroid action and this likely contributes to the adverse outcomes following these conditions. Reduced allopregnanolone levels during late gestation result in reduced myelination and injurious brain cell death suggesting supplementation treatments may improve outcomes following compromised pregnancy. Guinea pig models of episodic prenatal maternal stress have been used to examine how these events lead to adverse behavioral outcomes for the offspring. We found that prenatal stress disrupts the neurosteroid pathways between the dam and fetus. Together this work indicates that compromises and stress during pregnancy and in the early neonatal period disrupt neurotropic and protective neurosteroid pathways leading to deficiencies that contribute to the adverse neurological and behavioral outcomes following these challenges. The use of neurosteroid-based supplementation therapies may represent a future range of therapeutic approaches that could be used to improve outcomes following stressful events in pregnancy and following premature birth.
Journal article (5 outputs)
Bennett GA, Palliser HK, Shaw JC, Palazzi KL, Walker DW, Hirst JJ, 'Maternal stress in pregnancy affects myelination and neurosteroid regulatory pathways in the guinea pig cerebellum.', Stress, 20 580-588 (2017)
Bennett GA, Palliser HK, Walker D, Hirst J, 'Severity and timing: How prenatal stress exposure affects glial developmental, emotional behavioural and plasma neurosteroid responses in guinea pig offspring', Psychoneuroendocrinology, 70 47-57 (2016) [C1]
Â© 2016 Elsevier Ltd. Prenatal stress has been associated with a variety of developmental changes in offspring, notably those associated with brain development and subsequent risk... [more]
Â© 2016 Elsevier Ltd. Prenatal stress has been associated with a variety of developmental changes in offspring, notably those associated with brain development and subsequent risk for neuropathologies later in life. Recently, the importance of the timing and the severity of the stressor during pregnancy has been emphasized with neurosteroids including allopregnanolone implicated in the regulation of stress and also for endogenous neuroprotection in offspring.Prenatal stress was induced using strobe light exposure in pregnant guinea pigs (term 71 days) in three defined stress exposure groups (Gestational Age (GA)35-65, GA50-65 and GA60-65). Stress was induced for 2 h (9-11 am) every 5 days via strobe light exposure. A fetal cohort were euthanased at term with fetal brains and plasma collected. Anxiety-like behaviour was evaluated at 18 days of age in a separate cohort of offspring with brains and plasma collected at 21 days of age. Markers for mature oligodendrocytes and reactive astrocytes were measured in the CA1 region of the hippocampus and the subcortical white matter. The neurosteroid allopregnanolone was measured by radioimmunoassay in offspring plasma.In the CA1 region of the hippocampus, fetuses from all stress groups showed reduced expression of mature oligodendrocytes and reactive astrocytes. By juvenility, all male stress exposure groups had recovered to levels of unaffected controls with the exception of the GA35-65 stress group. In juvenile females, mature oligodendrocyte marker expression was reduced in all stress groups and reactive astrocyte expression was reduced in the GA35-65 and GA60-65 stress groups by juvenility. Increased reactive astrocyte expression was also apparent in the subcortical white matter in both sexes both at term and at juvenility. Prenatally stressed offspring spent less time exploring in the object exploration test and also entered the inner zone of the open field less than controls at 18 days of age. Circulating allopregnanolone concentrations were significantly reduced in GA35-65 and GA 60-65 stress exposed fetuses with those in the GA35-65 stress group remaining reduced by juvenility.This study has shown the effects of differing levels of prenatal stress severity and timing on glial development, emotional behaviour and plasma allopregnanolone concentrations in offspring.
Hirst JJ, Cumberland AL, Shaw JC, Bennett GA, Kelleher MA, Walker DW, Palliser HK, 'Loss of neurosteroid-mediated protection following stress during fetal life', Journal of Steroid Biochemistry and Molecular Biology, 160 181-188 (2016) [C1]
Â© 2015 Elsevier Ltd. All rights reserved. Elevated levels of neurosteroids during late gestation protect the fetal brain from hypoxia/ischaemia and promote neurodevelopment. Supp... [more]
Â© 2015 Elsevier Ltd. All rights reserved. Elevated levels of neurosteroids during late gestation protect the fetal brain from hypoxia/ischaemia and promote neurodevelopment. Suppression of allopregnanolone production during pregnancy leads to the onset of seizure-like activity and potentiates hypoxia-induced brain injury. Markers of myelination are reduced and astrocyte activation is increased. The placenta has a key role in maintaining allopregnanolone concentrations in the fetal circulation and brain during gestation and levels decline markedly after both normal and preterm birth. This leads to the preterm neonate developing in a neurosteroid deficient environment between delivery and term equivalence. The expression of 5a-reductases is also lower in the fetus prior to term. These deficiencies in neurosteroid exposure may contribute to the increase in incidence of the adverse patterns of behaviour seen in children that are born preterm. Repeated exposure to glucocorticoid stimulation suppresses 5a-reductase expression and allopregnanolone levels in the fetus and results in reduced myelination. Both fetal growth restriction and prenatal maternal stress lead to increased cortisol concentrations in the maternal and fetal circulation. Prenatal stress results in reduced expression of key GABA A receptor subunits that normally heighten neurosteroid sensitivity. These stressors also result in altered placental allopregnanolone metabolism pathways. These findings suggest that reduced neurosteroid production and action in the perinatal period may contribute to some of the adverse neurodevelopmental and behavioural outcomes that result from these pregnancy compromises. Studies examining perinatal steroid supplementation therapy with non-metabolisable neurosteroid analogues to improve these outcomes are warranted.
Bennett GA, Palliser HK, Shaw JC, Walker D, Hirst JJ, 'Prenatal stress alters hippocampal neuroglia and increases anxiety in childhood', Developmental Neuroscience, 37 533-545 (2015) [C1]
Â© 2015 S. Karger AG, Basel. Prenatal stress has been associated with detrimental outcomes of pregnancy, including altered brain development leading to behavioural pathologies. Th... [more]
Â© 2015 S. Karger AG, Basel. Prenatal stress has been associated with detrimental outcomes of pregnancy, including altered brain development leading to behavioural pathologies. The neurosteroid allopregnanolone has been implicated in mediating some of these adverse outcomes following prenatal stress due to its potent inhibitory and anxiolytic effects on the brain. The aims of the current study were to characterise key markers for brain development as well as behavioural parameters, adrenocortical responses to handling and possible neurosteroid influences towards outcomes in Guinea pig offspring in childhood. Preg nant Guinea pig dams were exposed to strobe light for 2 h (9-11 a.m.) on gestational days 50, 55, 60, and 65 and were left to deliver spontaneously at term and care for their litter. Behavioural testing (open-field test, object exploration test) of the offspring was performed at postnatal day 18 (with salivary cortisol and DHEA measured), and brains were collected at post-mortem on day 21. Markers of brain development myelin basic protein (MBP) and glial fibrillary acidic protein (GFAP) were assessed via immunohistochemistry, and the neurosteroid allopregnanolone and its rate-limiting enzymes 5a-reductase types 1 and 2 (5aR1/2) were measured in neonatal brains by radioimmunoassay, reverse transcriptase polymerase chain reaction (RT-PCR), and Western blot, respectively. Brain-derived neurotrophic factor protein was measured as a marker of synaptic plasticity, and GABA A receptor subunit expression was also assessed using RT-PCR. Neonates born from mothers stressed during late pregnancy showed a reduction in both MBP (p < 0.01) and GFAP (p < 0.05) expression in the CA1 region of the hippocampus at 21 days of age. Pups of prenatally stressed pregnancies also showed higher levels of anxiety and neophobic behaviours at the equivalent of childhood (p < 0.05). There were no significant changes observed in allopregnanolone levels, 5aR1/2 expression, or GABA A receptor subunit expression in prenatally stressed neonates compared to controls. This study shows alterations in markers of myelination and reactive astrocytes in the hippocampus of offspring exposed to prenatal stress. These changes are also observed in offspring that show increased anxiety behaviours at the equivalent of childhood, which indicates ongoing structural and functional postnatal changes after prenatal stress exposure.
Bennett GA, Palliser HK, Saxby B, Walker DW, Hirst JJ, 'Effects of Prenatal Stress on Fetal Neurodevelopment and Responses to Maternal Neurosteroid Treatment in Guinea Pigs', DEVELOPMENTAL NEUROSCIENCE, 35 416-426 (2013) [C1]
|Show 2 more journal articles|
Start Well: A research project supporting resilience and wellbeing in beginning teachers 2015 - 2016
|Associate Professor Frances Joy Kay-Lambkin||University of Newcastle|
Response Ability 2015 - 2016