1. » Identification and localisation of TRP channels in the lens
  2. » Characterising the t-tubular network in the failing right ventricle
  3. » Characterisation of the Cystine/glutamate antiporter (CGAP) in the mouse ear: is it involved in protecting the cochlea from oxidative stress?
  4. » Glucose storage abnormalities in the diabetic heart
  5. » MODELLING REGULATION OF SYNAPTIC TRANSMISSION BY ENDOCANNABINOIDS IN SILICO
  6. » The impact of inflammation on the development of circadian rhythms in the preterm fetus
  7. » Sex differences in sympathetic activation in heart failure
  8. » Can we improve treatment of babies with ischemic brain injury?
  9. » Structure of the transverse tubules in ischemic heart failure
  10. » Preventing inflammation-induced brain injury in the preterm infant
  11. » Developing a model of inflammation-induced brain injury in the preterm infant
  12. » MALDI imaging of the aging ocular lens
  13. » Developmental Expression of Toll-like Receptors in the fetal sheep brain
  14. » Nerve innervation of the kidney in heart failure
  15. » Does excess extracellular hyaluronan affect the developmental morphology of hippocampal and cortical neurons?
  16. » Effects of inhibiting hyaluronan synthesis on development of cortical neurons
  17. » High Blood Pressure after Stroke - to treat or not to treat?
  18. » Developing new treatment targets for hypertension
  19. » Breathing - what does it have to do with heart function?
  20. » Elucidating the mechanism by which L-DOPA increases extracellular DA in the nigro-striatal system. Implication for understanding therapeutic effects of the drug in Parkinson’s disease

Identification and localisation of TRP channels in the lens

Project code:  MHS012

Department

  • Physiology

Location

Auckland

Supervisor

Rosica Petrova

The TRP (Transient Receptor Potential) superfamily of cation channels play critical roles in sensory physiology, which include contributions to vision, taste, olfaction, hearing, touch, and thermo- and osmosensation. In lens the channels TRPV1 and TRPV4 have been shown to reciprocally regulate the activity of the Na pump. The Na pump in turn generates a circulating flux of Na ions that drives the flow of water through the lens forms the basis of the lens circulation system. This flow of water in turn generates a hydrostatic pressure in the lens that has been shown to be modulated by activators and modulators of TRP channels. Hence TRP channels are emerging as key targets for regulation of lens function and therefore transparency yet very little is know about where they are expressed in the lens. In this project the candidate will use TRP antibodies to localise where in the lens these key regulators of lens function are expressed.

Skills

Lens dissection, Tissue fixation and sectioning, Immunolabelling, Confocal microscopy and imaging processing.

Characterising the t-tubular network in the failing right ventricle

Project code:  MHS013

Department

  • Physiology

Location

Auckland

Supervisor

Dr Denis Loiselle

The transverse tubules (t-tubules) of cardiac muscle are invaginations of the surface membrane that form an extracellular network which expedites transmission of the surface action potential to voltage-dependent Ca2+ channels deep within the myocyte. Recent evidence suggests that disruption of the tubular network occurs early in some forms of heart failure. This project aims to ascertain if a comparable situation prevails in a pharmacologically-induced rat model of right-ventricular (RV) failure. Rats will be treated with monocrotaline (MCT) to increase pulmonary resistance, thereby driving RV hypertrophy, which eventually leads to heart failure. Both RV and LV trabeculae will be dissected, fixed and their t-tubules labelled with wheat-germ agglutinin. Specimens will be examined using confocal microscopy. T-tubular disruption will be assayed using Fourier-transform-based statistical techniques and results compared with those from untreated ‘Control’ animals.

Skills

Cardiectomy & Langendorff-perfusion of the rat heart, dissection of ventricular trabeculae, histological tissue preparation, confocal microscopy, image analysis, statistical data analysis.

Characterisation of the Cystine/glutamate antiporter (CGAP) in the mouse ear: is it involved in protecting the cochlea from oxidative stress?

Project code:  MHS016

Department

  • Physiology

Location

Auckland

Aims: To map the expression of CGAP in the mouse cochlea and compare oxidative stress markers (nitrotyrosine, glutathione reductase) in young (P21) and adult (6-8 weeks) wildtype and CGAP KO mice 

Background of the project: In tissues such as the brain, the cystine/glutamate antiporter (CGAP) has an important role in providing cysteine for the synthesis of the antioxidant glutathione, in maintaining extracellular cystine (oxidised) and cysteine (reduced) concentrations, an indicator of extracellular redox balance, and in the export of the neurotransmitter glutamate.

The generation of CGAP knockout mice, has revealed that in young adult mice, there was significantly higher plasma cystine concentrations relative to cysteine indicative of an oxidative shift of the cysteine/cystine ratio. A similar shift in the cysteine/cystine ratio is also evident in humans with increasing age, and suggests that the redox imbalance observed in these knockout mice mimics accelerated aging.

These mice have been used to investigate the role of CGAP in the aging eye and discovered that CGAP is an important component of the antioxidant protection pathway in the eye.

Oxidative stress has also been implicated in hearing disorders, such as age-related and noise-induced hearing loss, however the role of CGAP in the ear has never been investigated.

Skills

Cochlear extraction and tissue processing for immunohistochemistry, Cryosectioning, Immunofluorescence, Confocal Microscopy.  

Glucose storage abnormalities in the diabetic heart

Project code:  MHS036

Department

  • Physiology

Location

Auckland

Supervisor

Dr Kimberley Mellor

Heart disease is the leading cause of morbidity and mortality in diabetic patients. In diabetes, cardiac complications are evident even in the absence of vascular abnormalities and represent a primary manifestation of the disease. Understanding the mechanisms of cardiac pathology in diabetes is important for the development of new targeted treatment therapies. We have recently reported that a specific autophagy pathway for glycogen breakdown is upregulated in diabetic hearts but an understanding of how glucose storage abnormalities contribute to cardiac pathology in diabetes is lacking. Preliminary evidence suggests that the disturbed balance of systemic glucose and insulin levels in diabetes modifies key signaling pathways involved in glycogen and autophagy induction. This project aims to identify the mechanisms involved in regulation of autophagy under normal and diabetic conditions. The ideal student for this project would have a strong background in cardiac (or cardiovascular) physiology, molecular biology and have an interest in pursuing pre-clinical research.

Skills

  • Critical analysis of the literature
  • Characterisation of diabetic model
  • Biochemical analysis of metabolic substrates and protein expression
  • Data analysis and scientific writing skills

MODELLING REGULATION OF SYNAPTIC TRANSMISSION BY ENDOCANNABINOIDS IN SILICO

Project code:  MHS039

Department

  • Physiology

Location

Auckland

Supervisor

Peter Freestone

The NEURON  simulation environment is a powerful tool that can generate and analyse computational models of neurons and connections between neurons. A computational approach enables complex biological processes – like modulation of synaptic transmission – to be modelled accurately, allowing the experimenter to answer new questions, sometimes not possible to answer with conventional in vitro or in vivo preparations.

My group studies the sub-cortical group of nuclei called the basal ganglia – a network essential to diverse functions including motor activity. In particular, we study how cannabis-like substances produced naturally by the brain – endocannabinoids – can regulate synaptic transmission to dopamine-producing cells in the substantia nigra pars compacta.

The overall aim of the wider research group is to better understand the mechanisms of dopamine release in the basal ganglia, in particular, the role of endocannabinoids in modulating that release, and explore new potential therapies for diseases affecting the dopaminergic system (e.g. Parksinson’s disease).

The aim of this project, is to create a computational model of synaptic transmission including modulation by endocannabinoids. The accuracy of the model will be compared against existing data collected during in vitro brain slice experiments. This model will be used to test the theory that activation of excitatory (glutamatergic) inputs to dopamine neurons, causing transient silencing of inhibitory (GABAergic) inputs.

Experience with electrophysiological principles (e.g. MedSci309) and/or computer programming would be favourable.

This initial project has the potential to continue to a Hons/Masters/PhD project. This project will be offered to an enthusiastic student with a cumulative GPA >6.5 and a keen interest in applying cutting-edge technologies to the study of the brain.

Skills

The first part of this project will involve learning the NEURON programming language through a series of exercises in a simple to follow handbook. The skills learnt in the first part  would then be applied to addressing the aim of the project and generating the specific computational model.

The student will also gain experience by observing in vitro electrophysiological recordings. This will provide the opportunity to see the complete workflow of data acquisition analysis modelling predictions in vitro validation.

The student will also gain skills in reporting and presentation of progress and findings, collaboration, time and project-management, computational modelling and core neuroscience principles.

The impact of inflammation on the development of circadian rhythms in the preterm fetus

Project code:  MHS041

Department

  • Physiology

Location

Auckland

Supervisor

Laura Bennet

In adults circadian rhythms are important for allowing us to co-ordinate our behaviour and physiology, including management of our energy resources, the timing of cell function, division, and growth. The fetus exhibits diurnal rhythms in behaviour and physiology cued by mum. Disruption to our rhythms is linked with increased risk of diseases such as hypertension.

Very little is known about the nature of these rhythms and their importance in the fetus, but they likely serve a similar purpose and may be very important to the physiological development of the fetus. Preterm babies are at risk of being exposed to infection and inflammation before birth. This contributes to impaired brain development and to brain injury. However, it is not known whether inflammation changes the circadian rhythms of the fetus.

The aim of this project will be to evaluate pre-clinical data on the effects of inflammation induced by exposure to the gram negative agent lipopolysaccharide on the circadian rhythms in the behaviour and physiology of preterm fetuses.

Skills

  • Physiology analysis skills: fetal behaviour, blood pressure, blood flow, heart rate, EEG activity
  • Computer skills: data assessment using Labview, data management using Excel, data graphing using Graphpad, Statistics using SPSS, data presentations using Powerpoint
  • Fetal and neonatal physiology  literature assessment,
  • Scientific writing and referencing

Sex differences in sympathetic activation in heart failure

Project code:  MHS055

Department

  • Physiology

Location

Auckland

Supervisor

Carolyn Barrett

Increased sympathetic nerve activity is a major driving force in the progression of heart failure.  While both males and females suffer from heart failure in similar numbers there are clear sex differences in the progression of the disease.  Understanding these sex differences is key to the potential of developing sex specific treatment plans.  This project will examine the changes in sympathetic innervation in the heart in an animal model of heart failure.  

Skills

  • Cardiac catheterisation and pressure volume loop analysis
  • immunohistology
  • literature review
  • data analysis 
  • report writing

Can we improve treatment of babies with ischemic brain injury?

Project code:  MHS059

Department

  • Physiology

Location

Auckland

Supervisor

Dr Joanne Davidson

Fetal ischemia, the loss of blood supply before or around the time of birth, can cause death and devastating lifelong disability. Therapeutic hypothermia (cooling of the brain) is currently the only available treatment for infants that have suffered brain injury as a result of ischemia. Whilst it significantly reduces death and disability, many infants still suffer severe brain damage, even when treated with hypothermia. It is not yet clear whether current cooling protocols are optimal and little is known about the ideal rate of rewarming of infants after hypothermia and the effect that this has on outcome. The aim of this study is to determine whether the rate of rewarming after hypothermia has an effect on the development of brain injury.

For this summer studentship, immunohistochemistry, microscopy and cell quantification will be used to determine neuronal and oligodendrocyte cell survival and the extent of inflammation in the brain after hypoxia ischemia followed by treatment with hypothermia with either rapid or slow rewarming. This research will help to establish optimal cooling protocols for treatment of babies suffering ischemic brain injury.

Please send a CV and academic transcript if interested.

Skills

  • Immunohistochemistry
  • Microscopy
  • Cellular quantification
  • Data analysis
  • Statistical analysis

Structure of the transverse tubules in ischemic heart failure

Project code:  MHS063

Department

  • Physiology

Location

Auckland

Supervisor

Dr David Crossman

The transverse tubules are projections of the plasma membrane that penetrate deep into the cardiac myocyte allowing rapid cell wide propagation of the electrical signal that synchronises contraction. Disorganisation of the transverse tubule network is thought to be a major contributor to the loss of contractility in ischaemic heart failure. However, description of this disorganisation is primarily based on the 2D data sets even though transverse tubules form a complex 3D network within the myocyte. This project seeks to rectify this knowledge gap. This will be achieved by collection and analysis of high resolution 3D confocal data sets of transverse tubules in both normal and failing myocytes. 

Skills

  • Confocal microscopy
  • Fluorescence immunohistochemistry
  • Image processing
  • 3D rendering
  • Report writing

Preventing inflammation-induced brain injury in the preterm infant

Project code:  MHS075

Department

  • Physiology

Location

Auckland

Supervisor

Robert Galinsky

Preterm brain injury, commonly manifest as cerebral palsy, is a devastating lifelong condition. Over half of very preterm babies born before 28 weeks of gestation survive with unexplained neurobehavioral and intellectual disabilities related to cognition, learning, visuospatial integration, attention deficit and socialisation. Recent data show that even subtle injury is associated with impaired brain development and disability. 

The aim of this project is to test the hypothesis that blocking key inflammatory mediators in the brain (cytokines), using an FDA approved drug, will restore normal brain growth and development in preterm fetal sheep exposed to infection/ inflammation during pregnancy. 

Skills

  • Neuropathology
  • Data analysis, presentation and statistical assessment

Developing a model of inflammation-induced brain injury in the preterm infant

Project code:  MHS077

Department

  • Physiology

Location

Auckland

Supervisor

Robert Galinsky

Preterm brain injury, commonly manifest as cerebral palsy, is a devastating lifelong condition. Over half of very preterm babies born before 28 weeks of gestation survive with unexplained neurobehavioral and intellectual disabilities related to cognition, learning, visuospatial integration, attention deficit and socialisation. Recent data show that even subtle injury is associated with impaired brain development and disability. 

While preterm brain injury is multifactorial, exposure to infection/inflammation around the time of birth is one of the strongest factors associated with brain injury and long term disability. We don't have an effective model of inflammation-induced brain injury in the preterm equivalent brain for testing potential neuroprotective agents against. 

Therefore the aim of this project is to establish a novel large animal translational model of inflammation-induced brain injury to enable future testing of potential neuroprotective agents. 

Skills

  • Cardiovascular and neuro-physiology
  • Neuropathology
  • Data analysis, presentation and statistical assessment

MALDI imaging of the aging ocular lens

Project code:  MHS093

Department

  • Physiology

Location

Auckland

Supervisor

Gus Grey

MALDI imaging is a novel, mass spectrometry-based technique that maps the spatial distribution of proteins, peptides, lipids, metabolites, or drugs in thin tissue sections. Typically, tens to hundreds of biomolecules are detected in a single experiment, and a spatial distribution plotted for each. This technique has been used to study protein and metabolite distributions in the ocular lens, with particular emphasis on characterising proteomic and metabolomic changes that take place with aging and cataract formation. The depletion of glutathione concentration in the lens nucleus is thought to play a central role in age-related nuclear cataract formation. This project aims to map the distribution of exogenous glutathione antioxidant administered in organ culture to an aged lens model to monitor glutathione movement within the lens and its efficacy in preventing proteomic and metabolomic changes that occur with cataract formation.

Skills

Lens dissection, tissue sectioning, MALDI mass spectrometry, MALDI image analysis

Developmental Expression of Toll-like Receptors in the fetal sheep brain

Project code:  MHS104

Department

  • Physiology

Location

Auckland

Background

Hypoxic brain injury occurring while in the womb or during the process of labour and delivery has profound consequences on the neurological outcome of the very premature baby. Experimental studies have demonstrated that hypoxia triggers an inflammatory reaction within the brain, including activation of the innate immune system. Toll-like receptors (TLRs) the cellular sensors of inflammation within the brain play a fundamental role in the initiation and activation of inflammatory responses.  Accumulating evidence suggests that TLRs are important mediators of brain injury. The immature brain’s TLR response to hypoxia alone remains relatively poorly defined and developmental expression may contribute to the age dependent pattern and severity of injury, namely focal and diffuse periventricular white matter lesions, observed in preterm babies.

Aims

Therefore, the overall aim of this summer studentship will be to examine through immunocytochemistry and immunofluorescence techniques the developmental expression of TLRs in fetal sheep, a species which is a well-established translational model of perinatal brain injury.

Skills

  • Critical assessment of scientific literature
  • Immunocytochemistry and Immunofluorescence analysis
  • Data collection and statistical analysis
  • Presentation of results
  • Preparation and submission of peer-reviewed manuscript for publication

Nerve innervation of the kidney in heart failure

Project code:  MHS108

Department

  • Physiology

Location

Auckland

Supervisor

Maximilian Pinkham

The kidneys control fluid and electrolyte balance and have a profound impact on the cardiovascular system. Following a heart attack, impaired kidney function is a strong predictor of poor outcome. Nerves that originate in the brain and regulate kidney function (renal nerves) are known to have increased activity following a heart attack which contributes to worse outcome. Although it is well known that the renal nerve activity is elevated following a heart attack, little is known about what happens to the anatomical structure of the nerves in the kidney. It is possible that anatomical changes in the nerve innervation of the kidneys contribute to the adverse functional effects of the nerve activity. This project will endeavour to characterize the anatomical differences in the nerve innervation of the kidneys between normal and heart failure subjects.

Skills

  • immunohistology and molecular
  • Exposure to surgical techniques
  • data analysis
  • literature review
  • report writing

Does excess extracellular hyaluronan affect the developmental morphology of hippocampal and cortical neurons?

Project code:  MHS149

Department

  • Physiology

Location

Auckland

Supervisor

Dr. Justin Dean

In the nervous system, neurons and glia are surrounded by a complex arrangement of extracellular proteins and sugars. These matrix molecules may play critical roles during neuronal development. Our group is interested in the role of hyaluronan, an unbranched sugar, in the extracellular vicinity of developing cortical and hippocampal neurons. We propose that neurons express critical hyaluronidase enzymes, which degrade excess levels of hyaluronan during extension of neurites (initially as lamellopodia and growth cones).

The aim of this study is to characterise how the degradation of excess extracellular hyaluronan relates to the morphological development of cortical and hippocampal neurons in dissociated cultures. The student will analyse the morphological properties of neurons grown on hyaluronan-coated surfaces. Comparisons will be made between cultures grown in the absence or presence of hyaluronidase inhibitors.

Skills

This project involves work with dissociated cultures of hippocampal and cortical neurons. The student will experience immunocytochemistry and confocal imaging. This study will have a strong focus on image processing and analysis methodology. The student will also gain skills necessary to design and conduct hypothesis driven-experiments.

Effects of inhibiting hyaluronan synthesis on development of cortical neurons

Project code:  MHS150

Department

  • Physiology

Location

Auckland

Supervisor

Dr. Justin Dean

In the nervous system, neurons and glia are surrounded by a complex arrangement of extracellular proteins and sugars. Our group studies the role of the sugar hyaluronan, a major component of the extracellular matrix throughout the body. Hyaluronan is produced by three enzymes called hyaluronan synthases, and is known to be important for cell structure, differentiation and signalling in many cell types. Our lab has recently shown that cortical neurons can produce their own hyaluronan matrix, and that this hyaluronan is located on structures that are critical for outgrowth of neurons. We propose that neuronal production of hyaluronan is important for controlling the growth of neuronal processes and that blocking the activity of hyaluronan synthase enzymes will impair neuronal growth.

Aims

Understand the functions of the three hyaluronan synthase enzymes in neuronal morphological development. Expression of individual hyaluronan synthase enzymes will be reduced using plasmid vectors transfected into primary cortical neuronal cultures. Neurite outgrowth analysis will be performed to assess effects of gene knockdown on neuronal growth.

Skills

This project involves work with dissociated cultures of cortical neurons. The student will experience immunocytochemistry, neuronal transfection, fluorescence and confocal imaging, image processing and analysis methodology, including neuronal tracing. The student will also gain skills necessary to design and conduct hypothesis driven-experiments.

High Blood Pressure after Stroke - to treat or not to treat?

Project code:  MHS173

Department

  • Physiology

Supervisor

Dr FD McBryde

Project aims

After stroke, over 80% of patients show a sudden increase in blood pressure, however the underlying reasons  for post-stroke hypertension are not understood. Hypertension can be pathological, causing damage to end-organs and driving tissue oedema, and increases the risk of further stroke events. Alternatively, raised blood pressure after stroke may be therapeutic, and help increase the blood supply to damaged and vulnerable brain tissue. At present we do not know whether or not blood pressure should be controlled after stroke.

This summer project in our friendly and supportive laboratory will examine the impact of therapy to lower blood pressure in an animal model of ischemic stroke. Outcomes will include chronic monitoring of blood pressure, intracranial pressure and brain tissue oxygen levels, as well as tracking the functional recovery from stroke using established behavioural testing regimes.

Prospective students with good grades, and a serious interest in enrolling for continued postgraduate studies (such as Honours or Masters) will be considered.

Skills taught

Animal handling; behavioural testing and video analysis; collection, analysis and presentation of cardiovascular data; histology to quantify stroke infarct size.

Developing new treatment targets for hypertension

Project code:  MHS017

Department

  • Physiology

Aims

Globally, 1 in 3 people suffer from high blood pressure. In spite of this, high blood pressure continues to poorly managed and it is estimated that close to half of the hypertensive patients in New Zealand do not have adequate blood pressure control. This may be related to the side-effects of current drugs and new drug treatment targets are urgently required.

We have exciting preliminary data that the peripheral chemoreceptors play an important role in modulating the increase in sympathetic drive in a large animal model of renovascular hypertension. This project will determine whether blocking the peripheral chemoreceptors using a new drug targeting this afferent mechanism can decrease blood pressure.

This project will be offered to a motivated student who is interested in cardiovascular research and has good grades in cardiovascular subjects. Preference will be given to a student intending to continue with studies towards an Honours/Masters degree.

Skills

  • Literature search and scientific writing
  • Experience with whole animal integrative experiments
  • Assistance with surgical procedures
  • Computer data analysis and data interpretation
  • Oral presentation skills

Breathing - what does it have to do with heart function?

Project code:  MHS018

Department

  • Physiology

Respiratory sinus arrhythmia (RSA) is a naturally occurring respiratory related modulation of heart rate giving rise to heart rate variability. Typically heart rate slows in early expiration and rises during inspiration. Interestingly, RSA is most prevalent in the young and in trained athletes but wanes with age. In cardiovascular disease, RSA is lost and is a prognostic indicator of mortality and morbidity. Despite its comprehensive characterization, the functional significance of RSA remains elusive.

The aim of this project is to further our understanding of how RSA might affect heart function. Recent mathematical modelling has predicted that RSA can be energy saving for the heart. Given this, together with the loss of RSA in cardiovascular disease, we wish to assess the potential therapeutic benefit of re-instating RSA in a pre-clinical animal model of heart failure. As a start to this aim, we will test the hypothesis that reinstating RSA will increase cardiac output and coronary blood flow in a control animal model.

Skills

  • Literature search and scientific writing
  • Experience with whole animal integrative experiments
  • Assistance with surgical procedures
  • Computer data analysis and data interpretation
  • Oral presentation skills

Elucidating the mechanism by which L-DOPA increases extracellular DA in the nigro-striatal system. Implication for understanding therapeutic effects of the drug in Parkinson’s disease

Project code:  MHS174

Department

  • Physiology

Supervisor

Prof Janusz Lipski

Our laboratory investigates the cellular and molecular mechanisms of neuronal damage in models of Parkinson's disease (PD) and the properties of dopaminergic neurons in the Substantia Nigra which are affected by this disease. PD is the second most common neurological disorder linked to the degeneration of nigral dopaminergic neurons and a loss of dopamine. It is most frequently treated with L-DOPA (Levodopa), the precursor to dopamine, which ameliorates motor symptoms by mainly increasing dopamine release from remaining dopaminergic neurons. However, the cellular mechanism of L-DOPA-mediated DA release is not well understood, particularly that previous studies have identified a strong inhibitory action of L-DOPA (and newly synthetized and released dopamine) on the firing frequency of nigral dopaminergic neurons. So how can L-DOPA increase dopamine release, while at the same time inhibiting the electrical activity of dopaminergic neurons? To address this paradox, this project will investigate L-DOPA-induced effects on the electrophysiological activity of dopaminergic neurons and extracellular dopamine levels using electrochemistry (‘Fast-scan controlled adsorption cyclic voltammetry’, a novel technique recently developed in our laboratory). The main hypothesis to be tested is that L-DOPA-stimulated dopamine release is independent of the electrical activity of dopaminergic neurons, and can be induced even when voltage-gated Na+ channels are blocked with tetrodotoxin.

This study will be conducted in brain slices, in which dopaminergic neurons retain most of the properties that are observed also in the intact animal. It is expected that the project will extend our knowledge of the cellular action of L-DOPA, a drug which remains the ‘gold standard’ in the treatment of PD.

This project will be offered to an enthusiastic student with a cumulative GPA ≥7, with preference given to a student intending to continue in 2017 with studies towards Honours or Masters degree.

Skills taught

  • Preparation of animal (rat) brain slices.
  • Detection of dopamine release using electrochemistry
  • Electrophysiological techniques (microelectrode recordings from Substantia Nigra neurons)
  • Computer data analysis and data interpretation
  • Literature search and scientific writing/ oral presenting skills